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Base URL:  http://orca.cf.ac.uk/cgi/oai2
Sample date:  2017-01-30
Sample size:  100 records harvested

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ID: oai:http://orca.cf.ac.uk:1
Date: 2016-12-13

RIOXX

Base RIOXX scheme designed for low-level interoperability
This is not a valid RIOXX record
PropertyError
dc:identifierMinimum of 1 value(s) required for dc:identifier - found 0 values

RCUK-RIOXX

RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
This is not a valid RCUK-RIOXX record
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rioxxterms:projectMinimum of 1 value(s) required for rioxxterms:project - found 0 values
dcterms:dateAcceptedMinimum of 1 value(s) required for dcterms:dateAccepted - found 0 values
dc:identifierMinimum of 1 value(s) required for dc:identifier - found 0 values
ali:license_refMinimum of 1 value(s) required for ali:license_ref - found 0 values
<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:1</identifier>
      <datestamp>2016-12-13T02:31:51Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>BACKGROUND: Low folate status and elevated plasma homocysteine are associated with increased risk of neural tube defects and cardiovascular disease. Homocysteine responses to folate may be influenced by genetic variants in folate metabolism.&#13;
OBJECTIVE: We determined the effect of folate-enhancing dietary interventions on plasma folate and plasma total homocysteine (tHcy) with respect to the methylenetetrahydrofolate reductase 677C--&gt;T genotype.&#13;
DESIGN: A total of 126 healthy subjects (42 TT, 42 CT, and 42 CC genotypes) completed 3 dietary interventions (4 mo each) in random order: 1) exclusion diet (avoidance of folic acid-fortified foods and ingestion of a placebo daily), 2) folate-rich diet (increased intake of fortified and naturally folate-rich foods to achieve 400 microg folate/d), and 3) supplement (exclusion diet plus a folate supplement of 400 microg/d).&#13;
RESULTS: Plasma folate was higher (P &lt; or = 0.001) and plasma tHcy lower (P &lt; or = 0.001) after the folate-rich and supplement interventions than after the exclusion diet. Plasma folate was significantly greater after supplementation than after the folate-rich diet, but there was no significant difference in tHcy concentration (P = 0.72). TT homozygotes had higher plasma tHcy (14.5 compared with 8.9 micromol/L, P &lt; or = 0.001) and lower plasma folate (14.8 compared with 19.0 nmol/L, P &lt; or = 0.01) than did subjects with the CC genotype after the exclusion diet. CT heterozygotes had intermediate concentrations. The trend toward higher tHcy in TT homozygotes persisted throughout the study but was less marked with increasing folate intake (TT compared with CC after supplementation, P = 0.097).&#13;
CONCLUSIONS: A folate-rich diet including folic acid-fortified foods or low-dose supplements effectively increases folate status. TT homozygotes require higher folate intakes than do individuals with the CT or CC genotype to achieve similar tHcy concentrations but are responsive to folate intervention.</dc:description><dc:language>en</dc:language><dc:source>0002-9165</dc:source><dc:subject>R1</dc:subject><dc:title>Methylenetetrahydrofolate reductase 677CT genotype modulates homocysteine responses to a folate-rich diet or a low-dose folic acid supplement: a randomized controlled trial</dc:title><rioxxterms:author>Ashfield-Watt, Pauline Annie L.</rioxxterms:author><rioxxterms:author>Pullin, C. H.</rioxxterms:author><rioxxterms:author>Whiting, Jane Margaret Anne</rioxxterms:author><rioxxterms:author>Clark, Zoe Elizabeth</rioxxterms:author><rioxxterms:author>Moat, Stuart James</rioxxterms:author><rioxxterms:author>Newcombe, Robert Gordon</rioxxterms:author><rioxxterms:author>Burr, Michael Leslie</rioxxterms:author><rioxxterms:author>Lewis, Malcolm John</rioxxterms:author><rioxxterms:author>Powers, H. J.</rioxxterms:author><rioxxterms:author>McDowell, Ian Frederick</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:2
Date: 2016-02-12

RIOXX

Base RIOXX scheme designed for low-level interoperability
This is not a valid RIOXX record
PropertyError
dc:identifierMinimum of 1 value(s) required for dc:identifier - found 0 values

RCUK-RIOXX

RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
This is not a valid RCUK-RIOXX record
PropertyError
rioxxterms:projectMinimum of 1 value(s) required for rioxxterms:project - found 0 values
dcterms:dateAcceptedMinimum of 1 value(s) required for dcterms:dateAccepted - found 0 values
dc:identifierMinimum of 1 value(s) required for dc:identifier - found 0 values
ali:license_refMinimum of 1 value(s) required for ali:license_ref - found 0 values
<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:2</identifier>
      <datestamp>2016-02-12T22:00:06Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>The exact mechanism(s) by which hyperhomocysteinaemia promotes vascular disease remains unclear. Moreover, recent evidence suggests that the beneficial effect of folic acid on endothelial function is independent of homocysteine-lowering. In the present study the effect of a low (400 microg/70 kg/day) and high (5 mg/70 kg/day) dose folic acid supplement on endothelium-dependent relaxation in the isolated perfused mesenteric bed of heterozygous cystathionine beta-synthase deficient mice was investigated. Elevated total plasma homocysteine and impaired relaxation responses to methacholine were observed in heterozygous mice. In the presence of N(G)-nitro-L-arginine methyl ester relaxation responses in wild-type tissues were reduced, but in heterozygous tissues were abolished. Clotrimazole and 18alpha-glycyrrhetinic acid, both inhibitors of non-nitric oxide/non-prostanoid-induced endothelium-dependent relaxation, reduced responses to methacholine in wild-type but not heterozygous tissues. The combination of N(G)-nitro-L-arginine methyl ester and either clotrimazole or 18alpha-glycyrrhetinic acid completely inhibited relaxation responses in wild-type tissues. Both low and high dose folic acid increased plasma folate, reduced total plasma homocysteine and reversed endothelial dysfunction in heterozygous mice. A greater increase in plasma folate in the high dose group was accompanied by a more significant effect on endothelial function. In the presence of N(G)-nitro-L-arginine methyl ester, a significant residual relaxation response was evident in tissues from low and high dose folic acid treated heterozygous mice. These data suggest that the impaired mesenteric relaxation in heterozygous mice is largely due to loss of the non-nitric oxide/non-prostanoid component. While low dose folic acid may restore this response in a homocysteine-dependent manner, the higher dose has an additional effect on nitric oxide-mediated relaxation that would appear to be independent of homocysteine lowering.</dc:description><dc:language>en</dc:language><dc:publisher>Elsevier</dc:publisher><dc:source>0014-2999</dc:source><dc:title>Differential effects of low and high dose folic acid on endothelial dysfunction in a murine model of mild hyperhomocysteinaemia</dc:title><rioxxterms:author>Clarke, Zoe L.</rioxxterms:author><rioxxterms:author>Moat, Stuart James</rioxxterms:author><rioxxterms:author>Miller, Alastair L.</rioxxterms:author><rioxxterms:author>Randall, Michael D.</rioxxterms:author><rioxxterms:author>Lewis, Malcolm John</rioxxterms:author><rioxxterms:author>Lang, Derek</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/j.ejphar.2006.08.085</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:3
Date: 2016-03-19

RIOXX

Base RIOXX scheme designed for low-level interoperability
This is not a valid RIOXX record
PropertyError
dc:identifierMinimum of 1 value(s) required for dc:identifier - found 0 values

RCUK-RIOXX

RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
This is not a valid RCUK-RIOXX record
PropertyError
rioxxterms:projectMinimum of 1 value(s) required for rioxxterms:project - found 0 values
dcterms:dateAcceptedMinimum of 1 value(s) required for dcterms:dateAccepted - found 0 values
dc:identifierMinimum of 1 value(s) required for dc:identifier - found 0 values
ali:license_refMinimum of 1 value(s) required for ali:license_ref - found 0 values
<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:3</identifier>
      <datestamp>2016-03-19T22:00:05Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:language>en</dc:language><dc:source>10959319</dc:source><dc:title>Relative contributions of NO and gap junctional communication to endothelium-dependent relaxations of rabbit resistance arteries vary with vessel size</dc:title><rioxxterms:author>Berman, Rodney Simon</rioxxterms:author><rioxxterms:author>Martin, Patricia Esther Mary</rioxxterms:author><rioxxterms:author>Evans, William Howard</rioxxterms:author><rioxxterms:author>Griffith, Tudor Morley</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1006/mvre.2001.2352</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:4
Date: 2016-02-12

RIOXX

Base RIOXX scheme designed for low-level interoperability
This is not a valid RIOXX record
PropertyError
dc:identifierMinimum of 1 value(s) required for dc:identifier - found 0 values

RCUK-RIOXX

RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
This is not a valid RCUK-RIOXX record
PropertyError
rioxxterms:projectMinimum of 1 value(s) required for rioxxterms:project - found 0 values
dcterms:dateAcceptedMinimum of 1 value(s) required for dcterms:dateAccepted - found 0 values
dc:identifierMinimum of 1 value(s) required for dc:identifier - found 0 values
ali:license_refMinimum of 1 value(s) required for ali:license_ref - found 0 values
<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:4</identifier>
      <datestamp>2016-02-12T22:00:07Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Specific interactions between adjacent ryanodine receptor (RyR) molecules to form ordered two-dimensional arrays in the membrane have been demonstrated using electron microscopy both in situ, in tissues and cells, and in vitro, with the purified protein. RyR interoligomeric association has also been inferred from observations of simultaneous channel gating during multi-RyR channel recordings in lipid bilayers. In this study, we report experiments designed to identify the region(s) of the RyR molecule, participating in this reciprocal interaction. Using epitope-specific antibodies, we identified a RyR tryptic fragment that specifically bound the intact immobilized RyR. Three overlapping RyR fragments encompassing this epitope, expressed using an in vitro mammalian expression system, were immunoprecipitated by RyR. To refine the binding regions, smaller RyR fragments were expressed as glutathione S-transferase (GST) fusion proteins, and their binding to RyR was monitored using a "sandwich" enzyme-linked immunosorbent assay. Three GST-RyR fusion proteins demonstrated specific binding, dependent upon ionic strength. Binding was greatest at 50–150 mM NaCl for two GST-RyR constructs, and a third GST-RyR construct demonstrated maximum binding between 150 and 450 mM NaCl. The binding at high NaCl concentration suggested involvement of a hydrophobic interaction. In silico analysis of secondary structure showed evidence of coil regions in two of these RyR fragment sequences, which might explain these data. In GST pull-down assays, these same three fragments captured RyR2, and two of them retained RyR1. These results identify a region at the center of the linear RyR (residues 2540–3207 of human RyR2) which is able to bind to the RyR oligomer. This region may constitute a specific subdomain participating in RyR-RyR interaction.</dc:description><dc:language>en</dc:language><dc:publisher>American Society for Biochemistry and Molecular Biology</dc:publisher><dc:source>1083-351X</dc:source><dc:title>Ryanodine receptor oligomeric interaction: identification of a putative binding region</dc:title><rioxxterms:author>Blayney, Lynda Mary</rioxxterms:author><rioxxterms:author>Zissimopoulos, Spyros</rioxxterms:author><rioxxterms:author>Ralph, Emma</rioxxterms:author><rioxxterms:author>Abbot, Eleanor</rioxxterms:author><rioxxterms:author>Matthews, Laura</rioxxterms:author><rioxxterms:author>Lai, Francis Anthony</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1074/jbc.M308014200</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:5
Date: 2016-06-15

RIOXX

Base RIOXX scheme designed for low-level interoperability
This is not a valid RIOXX record
PropertyError
dc:identifierMinimum of 1 value(s) required for dc:identifier - found 0 values

RCUK-RIOXX

RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
This is not a valid RCUK-RIOXX record
PropertyError
rioxxterms:projectMinimum of 1 value(s) required for rioxxterms:project - found 0 values
dcterms:dateAcceptedMinimum of 1 value(s) required for dcterms:dateAccepted - found 0 values
dc:identifierMinimum of 1 value(s) required for dc:identifier - found 0 values
ali:license_refMinimum of 1 value(s) required for ali:license_ref - found 0 values
<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:5</identifier>
      <datestamp>2016-06-15T12:56:56Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:language>en</dc:language><dc:source>15387836</dc:source><dc:title>An influence of ABO blood group on the rate of proteolysis of von Willebrand factor by ADAMTS13</dc:title><rioxxterms:author>Bowen, Derrick John</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1046/j.1538-7836.2003.00007.x</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:6
Date: 2016-06-15

RIOXX

Base RIOXX scheme designed for low-level interoperability
This is not a valid RIOXX record
PropertyError
dc:identifierMinimum of 1 value(s) required for dc:identifier - found 0 values

RCUK-RIOXX

RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
This is not a valid RCUK-RIOXX record
PropertyError
rioxxterms:projectMinimum of 1 value(s) required for rioxxterms:project - found 0 values
dcterms:dateAcceptedMinimum of 1 value(s) required for dcterms:dateAccepted - found 0 values
dc:identifierMinimum of 1 value(s) required for dc:identifier - found 0 values
ali:license_refMinimum of 1 value(s) required for ali:license_ref - found 0 values
<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:6</identifier>
      <datestamp>2016-06-15T12:56:55Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D51:5150</setSpec>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>The hypothesis that increased ADAMTS13 (a disintegrin and metalloprotease with thrombospondin repeats) activity or increased susceptibility of von Willebrand factor (VWF) to proteolysis by ADAMTS13 may underlie type I von Willebrand disease (VWD) in some patients was investigated. Plasma from 4 patients with type I VWD was cryoprecipitated. ADAMTS13 activity in the VWF-poor cryodepleted fraction was assessed by incubation with purified VWF; susceptibility to proteolysis of the VWF in the VWF-rich cryoprecipitate was assessed by incubation with a normal, group O cryodepleted plasma. ADAMTS13 activity was similar in all 4 type I VWD cryodepleted plasmas and comparable to a normal control plasma. In contrast, the VWF of one patient showed increased susceptibility to proteolysis by ADAMTS13. Investigation of additional family members indicated that increased susceptibility was heritable, but it did not track uniquely with type I VWD. Sequence analysis of VWF exon 28 indicated that increased susceptibility to proteolysis tracked with the "G" allele of the A/G polymorphism at position 24/1282, encoding the amino acid polymorphism Tyr/Cys1584 ("G" = Cys1584). A prospective study of 200 individuals yielded 2 Tyr/Cys1584 heterozygotes; for both, plasma VWF showed increased susceptibility to proteolysis. The finding that an amino acid polymorphism in VWF may influence susceptibility to ADAMTS13 has potentially significant implications in diverse areas.</dc:description><dc:language>en</dc:language><dc:publisher>American Society of Hematology</dc:publisher><dc:source>0006-4971</dc:source><dc:subject>QP</dc:subject><dc:title>An amino acid polymorphism in von Willebrand factor correlates with increased susceptibility to proteolysis by ADAMTS13</dc:title><rioxxterms:author>Bowen, Derrick John</rioxxterms:author><rioxxterms:author>Collins, Peter William</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1182/blood-2003-05-1505</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:8
Date: 2016-06-15

RIOXX

Base RIOXX scheme designed for low-level interoperability
This is not a valid RIOXX record
PropertyError
dc:identifierMinimum of 1 value(s) required for dc:identifier - found 0 values

RCUK-RIOXX

RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
This is not a valid RCUK-RIOXX record
PropertyError
rioxxterms:projectMinimum of 1 value(s) required for rioxxterms:project - found 0 values
dcterms:dateAcceptedMinimum of 1 value(s) required for dcterms:dateAccepted - found 0 values
dc:identifierMinimum of 1 value(s) required for dc:identifier - found 0 values
ali:license_refMinimum of 1 value(s) required for ali:license_ref - found 0 values
<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:8</identifier>
      <datestamp>2016-06-15T12:56:57Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:language>en</dc:language><dc:source>0340-6245</dc:source><dc:title>Factor VIIa induced release of von Willebrand factor from human umbilical vein endothelial cells by a tyrosine kinase dependent pathway</dc:title><rioxxterms:author>Brown, Simon A.</rioxxterms:author><rioxxterms:author>Bowen, Derrick John</rioxxterms:author><rioxxterms:author>Hallett, Maurice Bartlett</rioxxterms:author><rioxxterms:author>Giddings, John Charles</rioxxterms:author><rioxxterms:author>Collins, Peter William</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:9
Date: 2016-06-15

RIOXX

Base RIOXX scheme designed for low-level interoperability
This is not a valid RIOXX record
PropertyError
dc:identifierMinimum of 1 value(s) required for dc:identifier - found 0 values

RCUK-RIOXX

RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
This is not a valid RCUK-RIOXX record
PropertyError
rioxxterms:projectMinimum of 1 value(s) required for rioxxterms:project - found 0 values
dcterms:dateAcceptedMinimum of 1 value(s) required for dcterms:dateAccepted - found 0 values
dc:identifierMinimum of 1 value(s) required for dc:identifier - found 0 values
ali:license_refMinimum of 1 value(s) required for ali:license_ref - found 0 values
<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:9</identifier>
      <datestamp>2016-06-15T12:56:57Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>The exact function of the carbohydrate component of von Willebrand factor (VWF) is unknown. ABO blood group antigens are present as integral structures on the oligosaccharide side chains and it has long been recognised that ABO blood group is a determinant of VWF levels. The mechanism for this is not known. Using a monoclonal antibody against the A-antigen, we investigated the presence of this antigen on VWF from plasma, platelets, human umbilical vein endothelial cells (HUVEC) and saphenous vein endothelial cells. Initial studies on plasma VWF revealed that 23.5% of samples appeared to be negative for the A-antigen. This was shown to correlate with the A2 subtype of the A-antigen (p &lt; 0.01). Analysis of intracellular VWF from saphenous vein endothelial cells revealed low levels of A-antigen to be present in comparison to the corresponding plasma VWF. In contrast, VWF from platelets and HUVEC gave no detectable A-antigen. However, within 1 h of administration of DDAVP to type 1 VWD patients, there was a &gt; 2-fold increase in the A-antigen/VWF: Ag ratio for VWF in the plasma. In vitro experiments with serum N-acetlygalactosaminyltransferase failed to demonstrate any addition of A-antigen to platelet or HUVEC VWF. These data are consistent with heterogeneity in the content of A-antigen on VWF from different physiological compartments. Also, they are consistent with either a change in the A-antigen content of VWF after release from the intracellular compartment or a difference in the intracellular addition of A-antigen to VWF by endo thelium from different vascular beds.</dc:description><dc:language>en</dc:language><dc:publisher>Schattauer</dc:publisher><dc:source>0340-6245</dc:source><dc:title>Heterogeneous detection of A-antigen on von Willebrand factor derived from platelets, endothelial cells and plasma</dc:title><rioxxterms:author>Brown, Simon A.</rioxxterms:author><rioxxterms:author>Collins, Peter William</rioxxterms:author><rioxxterms:author>Bowen, Derrick John</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:10
Date: 2016-06-15

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    <header>
      <identifier>oai:http://orca.cf.ac.uk:10</identifier>
      <datestamp>2016-06-15T12:56:56Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>The mechanism of von Willebrand factor (VWF) clearance is not fully understood. The factors that affect VWF clearance, and the normal in vivo mechanism of clearance, may be relevant to the pathogenesis of Type 1 von Willebrand disease (VWD), in which there is a partial deficiency of VWF. In order to investigate the clearance of VWF in Type 1 VWD, the current study assessed the half-life of VWF antigen (t(1/2) VWF:Ag) in Type 1 VWD patients and individuals with mild hemophilia A following the administration of 1-deamino-8-d-arginine vasopressin (DDAVP; desmopressin). To date 20 individuals have been assessed, 13 with Type 1 VWD and seven with mild hemophilia A. The median t(1/2) VWF:Ag in the Type 1 VWD and mild hemophilia A groups were 4.6 h and 9.5 h, respectively. The difference between the t(1/2) VWF:Ag for the two groups was significant, P &lt; 0.02. Analysis of the data showed a correlation between the t(1/2) VWF:Ag and the baseline VWF:Ag level prior to administration of DDAVP: lower baseline VWF:Ag levels were associated with a shorter t(1/2) VWF:Ag. These data suggest that increased clearance of VWF may be the pathogenic mechanism in some cases of Type 1 VWD.</dc:description><dc:language>en</dc:language><dc:publisher>Blackwell Publishing</dc:publisher><dc:source>1538-7836</dc:source><dc:title>Increased clearance of von Willebrand factor antigen post-DDAVP in Type 1 von Willebrand disease: is it a potential pathogenic process?</dc:title><rioxxterms:author>Brown, Simon A.</rioxxterms:author><rioxxterms:author>Eldridge, Adam</rioxxterms:author><rioxxterms:author>Collins, Peter William</rioxxterms:author><rioxxterms:author>Bowen, Derrick John</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1046/j.1538-7836.2003.00359.x</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:11
Date: 2016-03-19

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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
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    <header>
      <identifier>oai:http://orca.cf.ac.uk:11</identifier>
      <datestamp>2016-03-19T22:00:06Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:language>en</dc:language><dc:source>0002-9149</dc:source><dc:title>Differentiation between pathologic and physiologic left ventricular hypertrophy by tissue Doppler assessment of long-axis function in patients with hypertrophic cardiomyopathy or systemic hypertension and in athletes</dc:title><rioxxterms:author>Vinereanu, Dragos</rioxxterms:author><rioxxterms:author>Florescu, Nicolae</rioxxterms:author><rioxxterms:author>Sculthorpe, Nicholas</rioxxterms:author><rioxxterms:author>Tweddel, Ann C.</rioxxterms:author><rioxxterms:author>Stephens, Michael R.</rioxxterms:author><rioxxterms:author>Fraser, Alan Gordon</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/S0002-9149(01)01585-5</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:13
Date: 2016-03-19

RIOXX

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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:13</identifier>
      <datestamp>2016-03-19T22:00:07Z</datestamp>
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      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:language>en</dc:language><dc:source>14765381</dc:source><dc:title>Connexin-mimetic peptides dissociate electrotonic EDHF-type signalling via myoendothelial and smooth muscle gap junctions in the rabbit iliac artery</dc:title><rioxxterms:author>Chaytor, Andrew Thomas</rioxxterms:author><rioxxterms:author>Bakker, Linda Margaretha</rioxxterms:author><rioxxterms:author>Edwards, David Hughes</rioxxterms:author><rioxxterms:author>Griffith, Tudor Morley</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1038/sj.bjp.0706046</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:14
Date: 2016-03-19

RIOXX

Base RIOXX scheme designed for low-level interoperability
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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:14</identifier>
      <datestamp>2016-03-19T22:00:07Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:language>en</dc:language><dc:source>10916490</dc:source><dc:title>Distinct hyperpolarizing and relaxant roles for gap junctions and endothelium-derived H2O2 in NO-independent relaxations of rabbit arteries</dc:title><rioxxterms:author>Chaytor, Andrew Thomas</rioxxterms:author><rioxxterms:author>Edwards, David Hughes</rioxxterms:author><rioxxterms:author>Bakker, Linda Margaretha</rioxxterms:author><rioxxterms:author>Griffith, Tudor Morley</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1073/pnas.2435030100</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:15
Date: 2016-03-19

RIOXX

Base RIOXX scheme designed for low-level interoperability
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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
This is not a valid RCUK-RIOXX record
PropertyError
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:15</identifier>
      <datestamp>2016-03-19T22:00:07Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Synthetic peptides homologous to the Gap 26 and Gap 27 domains of the first and second extracellular loops of the major vascular connexins (Cx37, Cx40, and Cx43) have been used to investigate the role of gap junctions in endothelium-derived hyperpolarizing factor (EDHF)-type relaxations of the rat hepatic artery. These peptides were designated 37,40Gap 26, 43Gap 26, 37,43Gap 27, and 40Gap 27, according to connexin specificity. When administered at 600 microM, none of the peptides individually affected maximal EDHF-type relaxations to ACh. By contrast, at 300 microM each, paired peptide combinations targeting more than one connexin subtype attenuated relaxation by up to 50%, and responses were abolished by the triple peptide combination 43Gap 26 + 40Gap 27 + 37,43Gap 27. In parallel experiments with A7r5 cells expressing Cx40 and Cx43, neither 43Gap 26 nor 40Gap 27 affected intercellular diffusion of Lucifer yellow individually but, in combination, significantly attenuated dye transfer. The findings confirm that functional cell-cell coupling may depend on more than one connexin subtype and demonstrate that direct intercellular communication via gap junctions constructed from Cx37, Cx40, and Cx43 underpins EDHF-type responses in the rat hepatic artery.</dc:description><dc:language>en</dc:language><dc:source>0363-6135</dc:source><dc:title>Gap junctional communication underpins EDHF-type relaxations evoked by ACh in the rat hepatic artery</dc:title><rioxxterms:author>Chaytor, Andrew Thomas</rioxxterms:author><rioxxterms:author>Martin, Patricia Esther Mary</rioxxterms:author><rioxxterms:author>Edwards, David Hughes</rioxxterms:author><rioxxterms:author>Griffith, Tudor Morley</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:16
Date: 2016-02-12

RIOXX

Base RIOXX scheme designed for low-level interoperability
This is a valid RIOXX record

RCUK-RIOXX

RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
This is not a valid RCUK-RIOXX record
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:16</identifier>
      <datestamp>2016-02-12T22:00:08Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><ali:free_to_read/><dc:description>Lipoxygenases (LOX) contribute to vascular disease and inflammation through generation of bioactive lipids, including 12-hydro(pero)xyeicosatetraenoic acid (12-H(P)ETE). The physiological mechanisms that acutely control LOX product generation in mammalian cells are uncharacterized. Human platelets that contain a 12-LOX isoform (p12-LOX) were used to define pathways that activate H(P)ETE synthesis in the vasculature. Collagen and collagen-related peptide (CRP) (1 to 10 µg/mL) acutely induced platelet 12-H(P)ETE synthesis. This implicated the collagen receptor glycoprotein VI (GPVI), which signals via the immunoreceptor-based activatory motif (ITAM)-containing FcR chain. Conversely, thrombin only activated at high concentrations (&gt; 0.2 U/mL), whereas U46619 and ADP alone were ineffective. Collagen or CRP-stimulated 12-H(P)ETE generation was inhibited by staurosporine, PP2, wortmannin, BAPTA/AM, EGTA, and L-655238, implicating src-tyrosine kinases, PI3-kinase, Ca2+ mobilization, and p12-LOX translocation. In contrast, protein kinase C (PKC) inhibition potentiated 12-H(P)ETE generation. Finally, activation of the immunoreceptor tyrosine-based inhibitory motif (ITIM)–containing platelet endothelial cell adhesion molecule (PECAM-1) inhibited p12-LOX product generation. This study characterizes a receptor-dependent pathway for 12-H(P)ETE synthesis via the collagen receptor GPVI, which is negatively regulated by PECAM-1 and PKC, and demonstrates a novel link between immune receptor signaling and lipid mediator generation in the vasculature.</dc:description><dc:format>application/pdf</dc:format><dc:identifier>http://orca.cf.ac.uk/16/1/Coffey%202004.pdf</dc:identifier><dc:language>en</dc:language><dc:publisher>American Heart Association</dc:publisher><dc:relation>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=15142951</dc:relation><dc:source>0009-7330</dc:source><dc:title>Platelet 12-lipoxygenase activation via glycoprotein VI: involvement of multiple signaling pathways in agonist control of H(P)ETE synthesis</dc:title><rioxxterms:author>Coffey, Marcus Jonathan</rioxxterms:author><rioxxterms:author>Jarvis, Gavin E</rioxxterms:author><rioxxterms:author>Gibbins, Jonathan M.</rioxxterms:author><rioxxterms:author>Coles, Barbara</rioxxterms:author><rioxxterms:author>Barrett, Natasha E.</rioxxterms:author><rioxxterms:author>Wylie, Oliver R.E.</rioxxterms:author><rioxxterms:author>O'Donnell, Valerie Bridget</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>VoR</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1161/01.RES.0000132281.78948.65</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:18
Date: 2016-02-12

RIOXX

Base RIOXX scheme designed for low-level interoperability
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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
This is not a valid RCUK-RIOXX record
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:18</identifier>
      <datestamp>2016-02-12T22:00:08Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Recent studies implicate the collagen receptor, glycoprotein VI (GPVI) in activation of platelet 12-lipoxygenase (p12-LOX). Herein, we show that GPVI-stimulated 12-hydro(peroxy)eicosatetraenoic acid (H(P)ETE) synthesis is inhibited by palmityl trifluromethyl ketone or oleyloxyethylphosphocholine , but not bromoenol lactone, implicating secretory and cytosolic, but not calcium-independent phospholipase A2 (PLA2) isoforms. Also, following GPVI activation, 12-LOX co-immunoprecipitates with both cytosolic and secretory PLA2 (sPLA2). Finally, venoms containing sPLA2 acutely activate p12-LOX in a dose-dependent manner. This study shows that platelet 12-H(P)ETE generation utilizes arachidonate substrate from both c- and sPLA2 and that 12-LOX functionally associates with both PLA2 isoforms.</dc:description><dc:language>en</dc:language><dc:publisher>Elsevier</dc:publisher><dc:source>0014-5793</dc:source><dc:title>Interactions of 12-lipoxygenase with phospholipase A2 isoforms following platelet activation through the glycoprotein VI collagen receptor</dc:title><rioxxterms:author>Coffey, Marcus Jonathan</rioxxterms:author><rioxxterms:author>Coles, Barbara</rioxxterms:author><rioxxterms:author>Locke, Matthew</rioxxterms:author><rioxxterms:author>Bermudez-Fajardo, Alexandra</rioxxterms:author><rioxxterms:author>Williams, Paula Claire</rioxxterms:author><rioxxterms:author>Jarvis, Gavin E.</rioxxterms:author><rioxxterms:author>O'Donnell, Valerie Bridget</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/j.febslet.2004.09.007</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:19
Date: 2016-02-12

RIOXX

Base RIOXX scheme designed for low-level interoperability
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RCUK-RIOXX

RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
This is not a valid RCUK-RIOXX record
PropertyError
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<record>
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      <identifier>oai:http://orca.cf.ac.uk:19</identifier>
      <datestamp>2016-02-12T22:00:08Z</datestamp>
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      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>12/15-Lipoxygenase (LOX) activity is elevated in vascular diseases associated with impaired nitric oxide (( small middle dot)NO) bioactivity, such as hypertension and atherosclerosis. In this study, primary porcine monocytes expressing 12/15-LOX, rat A10 smooth muscle cells transfected with murine 12/15-LOX, and purified porcine 12/15-LOX all consumed *NO in the presence of lipid substrate. Suppression of LOX diene conjugation by *NO was also found, although the lipid product profile was unchanged. *NO consumption by porcine monocytes was inhibited by the LOX inhibitor, eicosatetraynoic acid. Rates of arachidonate (AA)- or linoleate (LA)-dependent *NO depletion by porcine monocytes (2.68 +/- 0.03 nmol x min(-1) x 10(6) cells(-1) and 1.5 +/- 0.25 nmol x min(-1) x 10(6) cells(-1), respectively) were several-fold greater than rates of *NO generation by cytokine-activated macrophages (0.1-0.2 nmol x min(-1) x 10(6) cells(-1)) and LA-dependent *NO consumption by primary porcine monocytes inhibited *NO activation of soluble guanylate cyclase. These data indicate that catalytic *NO consumption by 12/15-LOX modulates monocyte *NO signaling and suggest that LOXs may contribute to vascular dysfunction not only by the bioactivity of their lipid products, but also by serving as catalytic sinks for *NO in the vasculature.</dc:description><dc:language>en</dc:language><dc:publisher>National Academy of Sciences</dc:publisher><dc:source>1091-6490</dc:source><dc:title>Catalytic consumption of nitric oxide by 12/15- lipoxygenase: inhibition of monocyte soluble guanylate cyclase activation</dc:title><rioxxterms:author>Coffey, Marcus Jonathan</rioxxterms:author><rioxxterms:author>Natarajan, Rama</rioxxterms:author><rioxxterms:author>Chumley, Philip H.</rioxxterms:author><rioxxterms:author>Coles, Barbara</rioxxterms:author><rioxxterms:author>Thimmalapura, Pushpa-Rekha</rioxxterms:author><rioxxterms:author>Nowell, Mari Ann</rioxxterms:author><rioxxterms:author>Kühn, Hartmut</rioxxterms:author><rioxxterms:author>Lewis, Malcolm John</rioxxterms:author><rioxxterms:author>Freeman, Bruce A.</rioxxterms:author><rioxxterms:author>O'Donnell, Valerie Bridget</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1073/pnas.141136098</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:20
Date: 2016-10-25

RIOXX

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    <header>
      <identifier>oai:http://orca.cf.ac.uk:20</identifier>
      <datestamp>2016-10-25T01:30:11Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><ali:free_to_read/><dc:description>Nitration of unsaturated fatty acids such as linoleate by NO-derived reactive species forms novel derivatives (including nitrolinoleate [LNO2]) that can stimulate smooth muscle relaxation and block platelet activation by either NO/cGMP or cAMP-dependent mechanisms. Here, LNO2 was observed to inhibit human neutrophil function. LNO2, but not linoleic acid or the nitrated amino acid 3-nitrotyrosine, dose-dependently (0.2 to 1 µmol/L) inhibited superoxide (O2·-) generation, Ca2+ influx, elastase release, and CD11b expression in response to either phorbol 12-myristate 13-acetate or N-formyl-Met-Leu-Phe. LNO2 did not elevate cGMP, and inhibition of guanylate cyclase by 1H-[1,2,4]oxadiazole[4,3-a]quinoxalin-1-one did not restore neutrophil responses, ruling out a role for NO. In contrast, LNO2 caused elevations in intracellular cAMP in the presence and absence of phosphodiesterase inhibition, suggesting activation of adenylate cyclase. Compared with phorbol 12-myristate 13-acetate–activated neutrophils, N-formyl-Met-Leu-Phe–activated neutrophils were more susceptible to the inhibitory effects of LNO2, indicating that LNO2 may inhibit signaling both upstream and downstream of protein kinase C. These data suggest novel signaling actions for LNO2 in mediating its potent inhibitory actions. Thus, nitration of lipids by NO-derived reactive species yields products with antiinflammatory properties, revealing a novel mechanism by which NO-derived nitrated biomolecules can influence the progression of vascular disease.</dc:description><dc:format>application/pdf</dc:format><dc:identifier>http://orca.cf.ac.uk/20/1/Coles%202002.pdf</dc:identifier><dc:language>en</dc:language><dc:publisher>American Heart Association</dc:publisher><dc:relation>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=12215485</dc:relation><dc:source>0009-7330</dc:source><dc:title>Nitrolinoleate inhibits superoxide generation, degranulation, and integrin expression by human neutrophils: novel antiinflammatory properties of nitric oxide-derived reactive species in vascular cells</dc:title><rioxxterms:author>Coles, Barbara</rioxxterms:author><rioxxterms:author>Bloodsworth, Allison</rioxxterms:author><rioxxterms:author>Clark, Stephen Robert</rioxxterms:author><rioxxterms:author>Lewis, Malcolm John</rioxxterms:author><rioxxterms:author>Cross, Andrew R.</rioxxterms:author><rioxxterms:author>Freeman, Bruce A.</rioxxterms:author><rioxxterms:author>O'Donnell, Valerie Bridget</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>VoR</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1161/01.RES.0000032114.68919.EF</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:21
Date: 2015-11-05

RIOXX

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    <header>
      <identifier>oai:http://orca.cf.ac.uk:21</identifier>
      <datestamp>2015-11-05T15:50:36Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:language>en</dc:language><dc:source>15280020</dc:source><dc:title>Acquired hemophilia A in the United Kingdom: a 2-year national surveillance study by the United Kingdom Haemophilia Centre Doctors' Organisation</dc:title><rioxxterms:author>Collins, Peter William</rioxxterms:author><rioxxterms:author>Dolan, G.</rioxxterms:author><rioxxterms:author>Hirsch, S.</rioxxterms:author><rioxxterms:author>Baglin, T. P.</rioxxterms:author><rioxxterms:author>Hanley, J</rioxxterms:author><rioxxterms:author>Makris, M</rioxxterms:author><rioxxterms:author>Keeling, D. M.</rioxxterms:author><rioxxterms:author>Liesner, R.</rioxxterms:author><rioxxterms:author>Brown, S. A.</rioxxterms:author><rioxxterms:author>Hay, C. R.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1182/blood-2006-06-029850</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:22
Date: 2016-06-15

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:22</identifier>
      <datestamp>2016-06-15T12:56:55Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:language>en</dc:language><dc:source>0340-6245</dc:source><dc:title>An investigation of the von Willebrand factor genotype in UK patients diagnosed to have type 1 von Willebrand disease</dc:title><rioxxterms:author>Cumming, Anthony</rioxxterms:author><rioxxterms:author>Grundy, Pamela</rioxxterms:author><rioxxterms:author>Keeney, Stephen</rioxxterms:author><rioxxterms:author>Lester, William</rioxxterms:author><rioxxterms:author>Enayat, Said</rioxxterms:author><rioxxterms:author>Guilliatt, Andrea</rioxxterms:author><rioxxterms:author>Bowen, Derrick John</rioxxterms:author><rioxxterms:author>Pasi, John</rioxxterms:author><rioxxterms:author>Keeling, David</rioxxterms:author><rioxxterms:author>Hill, Frank</rioxxterms:author><rioxxterms:author>Bolton-Maggs, Paula H. B.</rioxxterms:author><rioxxterms:author>Hay, Charles</rioxxterms:author><rioxxterms:author>Collins, Peter William</rioxxterms:author><rioxxterms:author>UK Haemophilia Centre Doctors’ Organisation</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1160/TH06-07-0383</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:23
Date: 2016-03-19

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:23</identifier>
      <datestamp>2016-03-19T22:00:08Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5231</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Background— A respiratory cycle for nitric oxide (NO) would involve the formation of vasoactive metabolites between NO and hemoglobin during pulmonary oxygenation. We investigated the role of these metabolites in hypoxic tissue in vitro and in vivo in healthy subjects and patients with congestive heart failure (CHF).&#13;
&#13;
Methods and Results— We investigated the capacity for red blood cells (RBCs) to dilate preconstricted aortic rings under various O2 tensions. RBCs induced cyclic guanylyl monophosphate–dependent vasorelaxation during hypoxia (35±4% at 1% O2, 4.7±1.6% at 95% O2; P&lt;0.05). RBC-induced relaxations during hypoxia correlated with S-nitrosohemoglobin (SNO-Hb) (R2=0.88) but not iron nitrosylhemoglobin (HbFeNO) content. Relaxation responses for RBCs were compared with S-nitrosoglutathione across a range of O2 tensions. The fold increases in relaxation evoked by RBCs were significantly greater at 1% and 2% O2 compared with relaxations induced at 95% (P&lt;0.05), consistent with an allosteric mechanism of hypoxic vasodilation. We also measured transpulmonary gradients of NO metabolites in healthy control subjects and in patients with CHF. In CHF patients but not control subjects, levels of SNO-Hb increase from 0.00293±0.00089 to 0.00585±0.00137 mol NO/mol hemoglobin tetramer (P=0.005), whereas HbFeNO decreases from 0.00361±0.00109 to 0.00081±0.00040 mol NO/mol hemoglobin tetramer (P=0.03) as hemoglobin is oxygenated in the pulmonary circulation. These metabolite gradients correlated with the hemoglobin O2 saturation gradient (P&lt;0.05) and inversely with cardiac index (P&lt;0.05) for both CHF patients and control subjects.&#13;
&#13;
Conclusions— We confirm that RBC-bound NO mediates hypoxic vasodilation in vitro. Transpulmonary gradients of hemoglobin-bound NO are evident in CHF patients and are inversely dependent on cardiac index. Hemoglobin may transport and release NO bioactivity to areas of tissue hypoxia or during increased peripheral oxygen extraction via an allosteric mechanism.</dc:description><dc:language>en</dc:language><dc:source>1524-4539</dc:source><dc:subject>R1</dc:subject><dc:title>Red blood cell nitric oxide as an endocrine vasoregulator: a potential role in congestive heart failure</dc:title><rioxxterms:author>Datta, Borunendra</rioxxterms:author><rioxxterms:author>Tufnell-Barrett, Timothy</rioxxterms:author><rioxxterms:author>James, Philip Eurig</rioxxterms:author><rioxxterms:author>Bleasdale, Robert Anthony</rioxxterms:author><rioxxterms:author>Jones, Christopher John Hugh</rioxxterms:author><rioxxterms:author>Beeton, Ian</rioxxterms:author><rioxxterms:author>Paul, Vincent</rioxxterms:author><rioxxterms:author>Frenneaux, Michael Paul</rioxxterms:author><rioxxterms:author>James, Philip Eurig</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1161/01.CIR.0000124450.07016.1D</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:24
Date: 2016-06-15

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:24</identifier>
      <datestamp>2016-06-15T12:56:54Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Blood group O and the cysteine allele of the Y/C1584 change in von Willebrand factor (VWF) are enriched in type 1 VWD, but neither causes disease. We investigated the effect of C1584, alone and in combination with the ABO blood group, on the level and properties of plasma VWF. A cohort of 5052 blood donors was recruited: 50 donors were heterozygous for Y/C1584 and 5002 were homozygous for Y/Y1584. Mean VWF antigen (VWF:Ag) for heterozygotes (82 +/- 35 IUdL(-1)) was significantly lower than for homozygotes (111 +/- 37 IUdL(-1)) (P &lt; .001). Foreach ABO blood group, VWF:Ag was decreased among Y/C1584 heterozygotes compared with Y/Y1584 homozygotes; a larger decrease was observed for group O. Among donors with VWF:Ag levels of 50 IUdL(-1) or lower, Y/C1584 heterozygosity was markedly enriched (18%) compared with the entire cohort (1.5%). Blood group O was enriched to a lesser extent (2.4%), but Y/C1584 in conjunction with group O was strikingly enriched (34.8%). VWF collagen binding activity (VWF:CB) and ristocetin cofactor activity (VWF:RCo) were significantly lower for Y/C1584 heterozygotes than for Y/Y1584 homozygotes, and a qualitative difference in Y/C1584 plasma VWF multimer profile was observed compared with that for Y/Y1584 VWF. The data support a multifactorial basis for low VWF levels in some individuals.</dc:description><dc:language>en</dc:language><dc:publisher>American Society of Hematology</dc:publisher><dc:source>0006-4971</dc:source><dc:title>The effect of von Willebrand factor Y/C1584 on in vivo protein level and function, and interaction with ABO blood group</dc:title><rioxxterms:author>Davies, James Anthony</rioxxterms:author><rioxxterms:author>Collins, Peter William</rioxxterms:author><rioxxterms:author>Hathaway, Lee Sarah</rioxxterms:author><rioxxterms:author>Bowen, Derrick John</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1182/blood-2006-07-035105</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:26
Date: 2016-12-13

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      <identifier>oai:http://orca.cf.ac.uk:26</identifier>
      <datestamp>2016-12-13T02:31:54Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:language>en</dc:language><dc:source>00260495</dc:source><dc:title>Relationship between S-adenosylmethionine, S-adenosylhomocysteine, asymmetric dimethylarginine, and endothelial function in healthy human subjects during experimental hyper- and hypohomocysteinemia</dc:title><rioxxterms:author>Doshi, Sagar Navin</rioxxterms:author><rioxxterms:author>McDowell, Ian Frederick</rioxxterms:author><rioxxterms:author>Goodfellow, Jonathan</rioxxterms:author><rioxxterms:author>Stabler, Sally</rioxxterms:author><rioxxterms:author>Boger, Rainer</rioxxterms:author><rioxxterms:author>Allen, Robert</rioxxterms:author><rioxxterms:author>Newcombe, Robert Gordon</rioxxterms:author><rioxxterms:author>Lewis, Malcolm John</rioxxterms:author><rioxxterms:author>Moat, Stuart James</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/j.metabol.2004.09.015</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:27
Date: 2016-12-13

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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><ali:free_to_read/><dc:description>Homocysteine is a risk factor for coronary artery disease (CAD). Folic acid lowers homocysteine and may improve endothelial function in CAD, although the mechanism is unclear. We investigated the effect of folic acid on endothelial function, homocysteine, and oxidative stress in patients with CAD. We also examined the acute effect of 5-methyltetrahydrofolate (5-MTHF), the principal circulating folate, on endothelial function in vivo and on intracellular superoxide in cultured endothelial cells. A randomized crossover study of folic acid (5 mg daily) for 6 weeks was undertaken in 52 patients with CAD. Ten further patients were given intra-arterial 5-MTHF. Endothelial function was assessed by flow-mediated dilatation (FMD). Folic acid increased plasma folate (P&lt;0.001), lowered homocysteine by 19% (P&lt;0.001), and improved FMD (P&lt;0.001). FMD improvement did not correlate with homocysteine reduction. Malondialdehyde and total plasma antioxidant capacity, markers of oxidative stress, were unchanged. 5-MTHF acutely improved FMD (P&lt;0.001) without altering homocysteine (P=0.47). In vitro, 5-MTHF abolished homocysteine-induced intracellular superoxide increase (P&lt;0.001); this effect was also observed with folic acid and tetrahydrobiopterin. Our data support the beneficial effect of folic acid on endothelial function in CAD but suggest that the mechanism is independent of homocysteine. Reduction of intracellular endothelial superoxide may have contributed to the effect.</dc:description><dc:format>application/pdf</dc:format><dc:identifier>http://orca.cf.ac.uk/27/1/Doshi%202001.pdf</dc:identifier><dc:language>en</dc:language><dc:publisher>American Heart Association</dc:publisher><dc:relation>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=11451751</dc:relation><dc:source>15244636</dc:source><dc:title>Folate improves endothelial function in coronary artery disease: an effect mediated by reduction of intracellular superoxide?</dc:title><rioxxterms:author>Doshi, Sagar Navin</rioxxterms:author><rioxxterms:author>McDowell, Ian Frederick</rioxxterms:author><rioxxterms:author>Moat, Stuart</rioxxterms:author><rioxxterms:author>Lang, Derek</rioxxterms:author><rioxxterms:author>Newcombe, Robert</rioxxterms:author><rioxxterms:author>Kredan, Mahmud B.</rioxxterms:author><rioxxterms:author>Lewis, Malcolm John</rioxxterms:author><rioxxterms:author>Goodfellow, Jonathan</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>VoR</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1161/hq0701.092000</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:28
Date: 2016-02-12

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:28</identifier>
      <datestamp>2016-02-12T22:00:11Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><ali:free_to_read/><dc:description>Background— Homocysteine is a risk factor for coronary artery disease (CAD), although a causal relation remains to be proven. The importance of determining direct causality rests in the fact that plasma homocysteine can be safely and inexpensively reduced by 25% with folic acid. This reduction is maximally achieved by doses of 0.4 mg/d. High-dose folic acid (5 mg/d) improves endothelial function in CAD, although the mechanism is controversial. It has been proposed that improvement occurs through reduction in total (tHcy) or free (non–protein bound) homocysteine (fHcy). We investigated the effects of folic acid on endothelial function before a change in homocysteine in patients with CAD. &#13;
&#13;
Methods and Results— A randomized, placebo-controlled study of folic acid (5 mg/d) for 6 weeks was undertaken in 33 patients. Endothelial function, assessed by flow-mediated dilatation (FMD), was measured before, at 2 and 4 hours after the first dose of folic acid, and after 6 weeks of treatment. Plasma folate increased markedly by 1 hour (200 compared with 25.8 nmol/L; P&lt;0.001). FMD improved at 2 hours (83 compared with 47 µm; P&lt;0.001) and was largely complete by 4 hours (101 compared with 51 µm; P&lt;0.001). tHcy did not significantly differ acutely (4-hour tHcy, 9.56 compared with 9.79 µmol/L; P=NS). fHcy did not differ at 3 hours but was slightly reduced at 4 hours (1.55 compared with 1.78 µmol/L; P=0.02). FMD improvement did not correlate with reductions in either fHcy or tHcy at any time. &#13;
&#13;
Conclusions— These data suggest that folic acid improves endothelial function in CAD acutely by a mechanism largely independent of homocysteine.</dc:description><dc:format>application/pdf</dc:format><dc:identifier>http://orca.cf.ac.uk/28/1/Doshi%202002.pdf</dc:identifier><dc:language>en</dc:language><dc:publisher>American Heart Association</dc:publisher><dc:relation>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=11772871</dc:relation><dc:source>1524-4539</dc:source><dc:title>Folic acid improves endothelial function in coronary artery disease via mechanisms largely independent of homocysteine lowering</dc:title><rioxxterms:author>Doshi, Sagar Navin</rioxxterms:author><rioxxterms:author>McDowell, Ian Frederick</rioxxterms:author><rioxxterms:author>Moat, Stuart James</rioxxterms:author><rioxxterms:author>Payne, Nicola</rioxxterms:author><rioxxterms:author>Durrant, Hilary J.</rioxxterms:author><rioxxterms:author>Lewis, Malcolm John</rioxxterms:author><rioxxterms:author>Goodfellow, Jonathan</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>VoR</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1161/hc0102.101388</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:30
Date: 2016-02-12

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:30</identifier>
      <datestamp>2016-02-12T22:00:11Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Ca2+ release from the sarcoplasmic reticulum mediated by the cardiac ryanodine receptor (RyR2) is a fundamental event in cardiac muscle contraction. RyR2 mutations suggested to cause defective Ca2+ channel function have recently been identified in catecholaminergic polymorphic ventricular tachycardia (CPVT) and arrhythmogenic right ventricular dysplasia (ARVD) affected individuals. We report expression of three CPVT-linked human RyR2 (hRyR2) mutations (S2246L, N4104K, and R4497C) in HL-1 cardiomyocytes displaying correct targeting to the endoplasmic reticulum. N4104K also localized to the Golgi apparatus. Phenotypic characteristics including intracellular Ca2+ handling, proliferation, viability, RyR2:FKBP12.6 interaction, and beat rate in resting HL-1 cells expressing mutant hRyR2 were indistinguishable from wild-type (WT) hRyR2. However, Ca2+ release was augmented in cells expressing mutant hRyR2 after RyR activation (caffeine and 4-chloro-m-cresol) or</dc:description><dc:language>en</dc:language><dc:source>1524-4571</dc:source><dc:subject>R1</dc:subject><dc:title>Ryanodine receptor mutations associated with stress-induced ventricular tachycardia mediate increased calcium release in stimulated cardiomyocytes</dc:title><rioxxterms:author>George, Christopher H.</rioxxterms:author><rioxxterms:author>Higgs, Gemma</rioxxterms:author><rioxxterms:author>Lai, Francis Anthony</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1161/01.RES.0000091335.07574.86</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:31
Date: 2016-02-12

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:31</identifier>
      <datestamp>2016-02-12T22:00:11Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Ca2+ homeostasis is a vital cellular control mechanism in which Ca2+ release from intracellular stores plays a central role. Ryanodine receptor (RyR)-mediated Ca2+ release is a key modulator of Ca2+ homeostasis, and the defective regulation of RyR is pathogenic. However, the molecular events underlying RyR-mediated pathology remain undefined. Cells stably expressing recombinant human RyR2 (Chinese hamster ovary cells, CHOhRyR2) had similar resting cytoplasmic Ca2+ levels ([Ca2+]c) to wild-type CHO cells (CHOWT) but exhibited increased cytoplasmic Ca2+ flux associated with decreased cell viability and proliferation. Intracellular Ca2+ flux increased with human RyR2 (hRyR2) expression levels and determined the extent of phenotypic modulation. Co-expression of FKBP12.6, but not FKBP12, or incubation of cells with ryanodine suppressed intracellular Ca2+ flux and restored normal cell viability and proliferation. Restoration of normal phenotype was independent of the status of resting [Ca2+]c or ER Ca2+ load. Heparin inhibition of endogenous inositol trisphosphate receptors (IP3R) had little effect on intracellular Ca2+ handling or viability. However, purinergic stimulation of endogenous IP3R resulted in apoptotic cell death mediated by hRyR2 suggesting functional interaction occurred between IP3R and hRyR2 Ca2+ release channels. These data demonstrate that defective regulation of RyR causes altered cellular phenotype via profound perturbations in intracellular Ca2+ signaling and highlight a key modulatory role of FKBP12.6 in hRyR2 Ca2+ channel function.</dc:description><dc:language>en</dc:language><dc:source>1083-351X</dc:source><dc:title>Dysregulated ryanodine receptors mediate cellular toxicity: restoration of normal phenotype by FKBP12.6</dc:title><rioxxterms:author>George, Christopher</rioxxterms:author><rioxxterms:author>Higgs, Gemma</rioxxterms:author><rioxxterms:author>Mackrill, John J.</rioxxterms:author><rioxxterms:author>Lai, Francis Anthony</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1074/jbc.M212440200</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:32
Date: 2016-03-19

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:32</identifier>
      <datestamp>2016-03-19T22:00:09Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Arrhythmogenic cardiac ryanodine receptor (RyR2) mutations are associated with stress-induced malignant tachycardia, frequently leading to sudden cardiac death (SCD). The causative mechanisms of RyR2 Ca2+ release dysregulation are complex and remain controversial. We investigated the functional impact of clinically-severe RyR2 mutations occurring in the central domain, and the C-terminal I domain, a key locus of RyR2 autoregulation, on interdomain interactions and Ca2+ release in living cells. Using high-resolution confocal microscopy and fluorescence resonance energy transfer (FRET) analysis of interaction between fusion proteins corresponding to amino- (N-) and carboxyl- (C-) terminal RyR2 domains, we determined that in resting cells, RyR2 interdomain interaction remained unaltered after introduction of SCD-linked mutations and normal Ca2+ regulation was maintained. In contrast, after channel activation, the abnormal Ca2+ release via mutant RyR2 was intrinsically linked to altered interdomain interaction that was equivalent with all mutations and exhibited threshold characteristics (caffeine &gt;2.5 mmol/L; Ca2+ &gt;150 nmol/L). Noise analysis revealed that I domain mutations introduced a distinct pattern of conformational instability in Ca2+ handling and interdomain interaction after channel activation that was absent in signals obtained from the central domain mutation. I domain–linked channel instability also occurred in intact RyR2 expressed in CHO cells and in HL-1 cardiomyocytes. These new insights highlight a critical role for mutation-linked defects in channel autoregulation, and may contribute to a molecular explanation for the augmented Ca2+ release following RyR2 channel activation. Our findings also suggest that the mutational locus may be an important mechanistic determinant of Ca2+ release channel dysfunction in arrhythmia and SCD.</dc:description><dc:language>en</dc:language><dc:source>1524-4571</dc:source><dc:subject>R1</dc:subject><dc:title>Arrhythmogenic mutation-linked defects in ryanodine receptor autoregulation reveal a novel mechanism of Ca2+ release channel dysfunction</dc:title><rioxxterms:author>George, Christopher</rioxxterms:author><rioxxterms:author>Jundi, Hala</rioxxterms:author><rioxxterms:author>Walters, Nicola</rioxxterms:author><rioxxterms:author>Thomas, Nia Lowri</rioxxterms:author><rioxxterms:author>West, Robert Raynard</rioxxterms:author><rioxxterms:author>Lai, Francis Anthony</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1161/01.RES.0000199296.70534.7c</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:34
Date: 2016-03-19

RIOXX

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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:34</identifier>
      <datestamp>2016-03-19T22:00:09Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:language>en</dc:language><dc:source>10916490</dc:source><dc:title>5-Methyltetrahydrofolate and tetrahydrobiopterin can modulate electrotonically mediated endothelium-dependent vascular relaxation</dc:title><rioxxterms:author>Griffith, Tudor Morley</rioxxterms:author><rioxxterms:author>Chaytor, Andrew Thomas</rioxxterms:author><rioxxterms:author>Edwards, David Hughes</rioxxterms:author><rioxxterms:author>Bakker, Linda Margaretha</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1073/pnas.0408919102</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:35
Date: 2016-03-19

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:35</identifier>
      <datestamp>2016-03-19T22:00:09Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>We have investigated the role of cAMP in NO- and prostanoid-independent relaxations that are widely attributed to an endothelium-derived hyperpolarizing factor (EDHF). Under control conditions EDHF-type relaxations evoked by acetylcholine (ACh) in rabbit iliac arteries were transient, but in the presence of the cAMP phosphodiesterase inhibitor isobutylmethylxanthine (IBMX) or the cell permeant cAMP analog 8-bromo-cAMP, relaxations became sustained with their maxima potentiated ≈2-fold. Relaxation was associated with transient ≈1.5-fold elevations in smooth muscle cAMP levels with both mechanical and nucleotide responses being abolished by interrupting gap junctional communication with the connexin-mimetic peptide Gap 27 and by endothelial denudation. However, IBMX induced a sustained endothelium-independent ≈2-fold rise in cAMP levels, which was not further amplified by ACh, suggesting that the contribution of cAMP to the EDHF phenomenon is permissive. After selective loading of the endothelium with calcein AM, direct transfer of dye from the endothelium to the media was enhanced by IBMX or 8-bromo-cAMP, but not by 8-bromo-cGMP, whereas Gap 27 promoted sequestration within the intima. ACh-induced hyperpolarizations of subintimal smooth muscle in arterial strips with intact endothelium were abolished by Gap 27 and the adenylyl cyclase inhibitor 2′,5′-dideoxyadenosine but were unaffected by IBMX. By contrast, in strips partially denuded of endothelium, IBMX enhanced the transmission of hyperpolarization from the endothelium to remote smooth muscle cells. These findings support the hypothesis that endothelial hyperpolarization underpins the EDHF phenomenon, with cAMP governing subsequent electrotonic signaling via both myoendothelial and homocellular smooth muscle gap junctions.</dc:description><dc:language>en</dc:language><dc:source>1091-6490</dc:source><dc:subject>R1</dc:subject><dc:title>cAMP facilitates EDHF-type relaxations in conduit arteries by enhancing electrotonic conduction via gap junctions</dc:title><rioxxterms:author>Griffith, Tudor Morley</rioxxterms:author><rioxxterms:author>Chaytor, Andrew Thomas</rioxxterms:author><rioxxterms:author>Taylor, Hannah J.</rioxxterms:author><rioxxterms:author>Giddings, Beverley Diane</rioxxterms:author><rioxxterms:author>Edwards, David Hughes</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1073/pnas.092089799</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:36
Date: 2016-03-19

RIOXX

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<record>
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      <identifier>oai:http://orca.cf.ac.uk:36</identifier>
      <datestamp>2016-03-19T22:00:10Z</datestamp>
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      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Vascular dysfunction in diabetes is attributed to lack of bioavailable nitric oxide (NO) and is postulated as a primary cause of small vessel complications as a result of poor glycemic control. Although it has been proposed that NO is bound by red blood cells (RBCs) and can induce relaxation of blood vessels distal to its site of production in the normal circulation, the effect of RBC glycation on NO binding and relaxation of hypoxic vessels is unknown. We confirm RBC-induced vessel relaxation is inversely related to tissue oxygenation and is proportional to RBC S-nitrosohemoglobin (HbSNO) content (but not nitrosylhemoglobin content). We show more total NO bound inside highly glycated RBCs (0.0134 versus 0.0119 NO/Hb, respectively; P&lt;0.05) although proportionally less HbSNO (0.0053 versus 0.0088 NO/Hb, respectively; P&lt;0.05). We also show glycosylation impairs the vasodilator function of RBCs within a physiological range of tissue oxygenation. These findings may represent an important contribution to reduced NO bioavailability in the microvasculature in diabetes.</dc:description><dc:language>en</dc:language><dc:publisher>Lippincott, Williams &amp; Wilkins</dc:publisher><dc:source>0009-7330</dc:source><dc:title>Vasorelaxation by red blood cells and impairment in diabetes: reduced nitric oxide and oxygen delivery by glycated hemoglobin</dc:title><rioxxterms:author>James, Philip Eurig</rioxxterms:author><rioxxterms:author>Lang, Derek</rioxxterms:author><rioxxterms:author>Tufnell-Barret, Timothy</rioxxterms:author><rioxxterms:author>Milsom, Alexandra Barrie</rioxxterms:author><rioxxterms:author>Frenneaux, Michael Paul</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1161/01.RES.0000122044.21787.01</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:37
Date: 2016-02-12

RIOXX

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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:37</identifier>
      <datestamp>2016-02-12T22:00:12Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5231</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>BACKGROUND: While folic acid (FA) reduces plasma homocysteine (Hcy), whether the simultaneous improvement in endothelial function is dependent on Hcy lowering per se is questionable. In the present study the relationship between FA dose, Hcy lowering and endothelial function in patients with coronary artery disease (CAD) was investigated. MATERIALS AND METHODS: Eighty-four patients with CAD received either 400 microg FA or 5 mg placebo daily for a 6-week treatment period. A further 44 patients with CAD received either 100 mg kg(-1) day(-1) of betaine or placebo for a 6-week treatment period. Flow-mediated dilatation (FMD), a measure of endothelial function, was assessed before and after the 6-week periods. Isometric tension and Western blotting were used to investigate the effect of FA on endothelial function and endothelial nitric oxide synthase (eNOS) dimerization in isolated rabbit aortic rings and cultured porcine aortic endothelial cells (PAEC), respectively. RESULTS: Both 400 micro g day(-1) and 5 mg day(-1) FA significantly increased plasma folate and decreased plasma Hcy. The FMD improved significantly after 6 weeks' treatment of 5 mg day(-1) FA but did not correlate with the reduction in Hcy. There was no change in FMD in either the 400 micro g FA or placebo group. In a subgroup analysis of 11 patients in the betaine group, despite a reduced Hcy, a significant impairment in FMD was observed. In the in vitro studies FA, but not betaine, reversed methionine-induced endothelial dysfunction. Moreover, the FA promoted eNOS dimerization in cultured PAEC. CONCLUSIONS: These data suggest that FA dose-dependently improves endothelial function in CAD via a mechanism independently of Hcy lowering. It may involve promotion of eNOS dimerization.</dc:description><dc:language>en</dc:language><dc:publisher>Blackwell Publishing</dc:publisher><dc:source>1365-2362</dc:source><dc:subject>R1</dc:subject><dc:title>High- but not low-dose folic acid improves endothelial function in coronary artery disease</dc:title><rioxxterms:author>Moat, Stuart James</rioxxterms:author><rioxxterms:author>Madhavan, Anil Kumar</rioxxterms:author><rioxxterms:author>Taylor, Sarah Yvonne</rioxxterms:author><rioxxterms:author>Payne, Nichola</rioxxterms:author><rioxxterms:author>Allen, R. H.</rioxxterms:author><rioxxterms:author>Stabler, Sally P.</rioxxterms:author><rioxxterms:author>Goodfellow, Jonathan</rioxxterms:author><rioxxterms:author>McDowell, Ian Frederick</rioxxterms:author><rioxxterms:author>Lewis, Malcolm John</rioxxterms:author><rioxxterms:author>Lang, Derek</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1111/j.1365-2362.2006.01739.x</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:38
Date: 2016-02-12

RIOXX

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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:38</identifier>
      <datestamp>2016-02-12T22:00:12Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Ryanodine receptor (RyR) Ca2+ release channels undergo a conformational change between the open and closed states. Its protein modulator, FK506 binding protein 12 (FKBP12), stabilises the channel gating between the four subunits that surround a central Ca2+-conducting pore. To understand the interdependence of RyR and FKBP12 binding, physiological and pharmacological agents were used to modulate the RyR open/closed state. ELISA sandwich binding assays showed that FKBP12 binding was dependent on the free Ca2+ and was lower at 1-10 µM free Ca2+ compared with 1 mM EGTA and 1 mM Ca2+, and this effect was enhanced by the inclusion of 1 mM ATP. Ruthenium red increased the binding of FKBP12. [3H]Ryanodine binding confirmed that 1 mM EGTA, 1 mM Ca2+ and 1 µM ruthenium red closed the channel, whereas 1 µM free Ca2+, 1 µM free Ca2+ + 1 mM ATP, or 10 mM caffeine opened it. These binding conditions were used in surface plasmon resonance studies to measure equilibrium binding kinetics. The affinity constant KA was significantly greater for the closed than the open channel, a change mediated by a decreased dissociation rate constant, kd. The results show that surface plasmon resonance is a powerful technique that can measure differences in RyR1 equilibrium binding kinetics with FKBP12.</dc:description><dc:language>en</dc:language><dc:publisher>Company of Biologists</dc:publisher><dc:source>1477-9137</dc:source><dc:title>Ryanodine receptor binding to FKBP12 is modulated by channel activation state</dc:title><rioxxterms:author>Jones, Jonathan-Lee</rioxxterms:author><rioxxterms:author>Reynolds, Deborah Fidelis</rioxxterms:author><rioxxterms:author>Lai, Francis Anthony</rioxxterms:author><rioxxterms:author>Blayney, Lynda Mary</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1242/jcs.02582</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:39
Date: 2016-02-12

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:39</identifier>
      <datestamp>2016-02-12T22:00:13Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>The skeletal muscle Ca2+ release channel (ryanodine receptor 1, RYR1) plays an important role in the excitation–contraction coupling process. We purified ryanodine receptor type 1 from rabbit white muscle and adsorbed it to mica sheets with the cytoplasmic side facing up. Single receptors of uniformly distributed size and shape of 10–12 nm height and 40–50 nm width, and occasionally some aggregates were seen in contact mode AFM images. These immobilized RYR1 were specifically recognized by rabbit anti-RYR1 (antibody#8) with at least 30% efficiency, as measured by an enzyme immunoassay with goat-anti-rabbit. Single specific antibody–antigen recognition events were detected with AFM tips to which an antibody#8 was tethered. In linear scans, the occurrence of antibody–antigen binding showed significant lateral dependence, which allowed for the localization of binding sites with nm resolution. Variation of the loading rate in force spectroscopy experiments revealed a logarithmic dependence of the unbinding forces, ranging from 42 to 73 pN. From this dependence, a bond width of the binding pocket of L=0.2 nm and a kinetic off-rate of koff=12.7 s−1 was determined.</dc:description><dc:language>en</dc:language><dc:source>0304-3991</dc:source><dc:title>Recognition force microscopy/spectroscopy of ion channels: applications to the skeletal muscle Ca2+ release channel (RYR1)</dc:title><rioxxterms:author>Kada, G.</rioxxterms:author><rioxxterms:author>Blayney, Lynda Mary</rioxxterms:author><rioxxterms:author>Jeyakumar, L. H.</rioxxterms:author><rioxxterms:author>Kienberger, F.</rioxxterms:author><rioxxterms:author>Pastushenko, V. Ph.</rioxxterms:author><rioxxterms:author>Fleischer, S.</rioxxterms:author><rioxxterms:author>Schindler, H.</rioxxterms:author><rioxxterms:author>Lai, Francis Anthony</rioxxterms:author><rioxxterms:author>Hinterdorfer, P.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/S0304-3991(00)00070-X</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:44
Date: 2016-03-19

RIOXX

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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:44</identifier>
      <datestamp>2016-03-19T22:00:11Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5231</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Aims/hypothesis. Reduced bioavailability of endothelium-derived nitric oxide is implicated in diabetic macrovascular and microvascular disease. In patients with diabetes, we hypothesised that protein glycosylation can alter nitric oxide binding affinity of haemoglobin and plasma proteins, hence reducing nitric oxide availability and causing an alteration in nitric oxide metabolism.&#13;
&#13;
Methods. Binding of nitric oxide to haemoglobin was studied across a range of glycosylation levels in vitro (HbA1c 5.9 to 9.8%). In clinical studies nitrate, nitrite, nitrosyl haemoglobin and plasma nitrosothiols were measured in venous blood from 23 patients with uncomplicated Type I (insulin-dependent) diabetes mellitus and 17 non-diabetic control subjects. Samples were analysed at baseline and after nitric oxide was added ex vivo.&#13;
&#13;
Results. Nitric oxide-haemoglobin binding was increased at a HbA1c greater than 8.5% compared with 5.9% (p&lt;0.01). Basal nitrosyl haemoglobin was higher in diabetic patients compared with the control subjects (0.59-0.12</dc:description><dc:language>en</dc:language><dc:source>1432-0428</dc:source><dc:subject>R1</dc:subject><dc:title>Abnormal metabolic fate of nitric oxide in Type I diabetes mellitus</dc:title><rioxxterms:author>Milsom, Alexandra Barrie</rioxxterms:author><rioxxterms:author>Jones, Christopher John Hugh</rioxxterms:author><rioxxterms:author>Goodfellow, Jonathan</rioxxterms:author><rioxxterms:author>Frenneaux, Michael Paul</rioxxterms:author><rioxxterms:author>Peters, J. R.</rioxxterms:author><rioxxterms:author>James, Philip Eurig</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1007/s00125-002-0956-9</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:45
Date: 2016-12-13

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:45</identifier>
      <datestamp>2016-12-13T02:31:56Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Background: Riboflavin (vitamin B2) is the precursor for FAD, the cofactor for methylenetetrahydrofolate reductase (MTHFR). MTHFR catalyzes the formation of 5-methyltetrahydrofolate, which acts as a methyl donor for homocysteine remethylation. Individuals with the MTHFR 677CT mutation have increased plasma total homocysteine (tHcy) concentrations, particularly in association with low folate status. It has been proposed that riboflavin may act together with folate to lower plasma tHcy, particularly in individuals with the thermolabile MTHFR T variant. &#13;
&#13;
Methods: We measured B-vitamin status and plasma tHcy in 126 healthy individuals 20–63 years of age (42 CC, 42 CT, and 42 TT MTHFR genotypes) at baseline and after three interventions (4 months): placebo plus natural diet; daily 400 µg folic acid supplement plus natural diet; and increased dietary folate to 400 µg/day. &#13;
&#13;
Results: At baseline and after nutritional intervention, lower riboflavin status was associated with increased plasma tHcy concentrations. Plasma tHcy was 2.6 µmol/L higher in the lowest plasma riboflavin quartile compared with the highest (P &lt;0.02) and was 4.2 µmol/L higher in the highest erythrocyte glutathione reductase activation coefficient (EGRAC) quartile compared with the lowest (P &lt;0.001). This effect was not restricted to those with the T allele. Folic acid given as a 400 µg/day supplement appeared to exacerbate a tendency toward riboflavin deficiency, as suggested by an increase in the proportion of individuals with EGRAC 1.4 from 52% to 65% after supplementation (P &lt;0.05). &#13;
&#13;
Conclusions: Folate and riboflavin interact to lower plasma tHcy, possibly by maximizing the catalytic activity of MTHFR. The effect may be unrelated to MTHFR genotype.</dc:description><dc:language>en</dc:language><dc:publisher>American Association for Clinical Chemistry</dc:publisher><dc:relation>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=12560354</dc:relation><dc:source>15308561</dc:source><dc:title>Effect of riboflavin status on the homocysteine-lowering effect of folate in relation to the MTHFR (C677T) genotype</dc:title><rioxxterms:author>Moat, Stuart James</rioxxterms:author><rioxxterms:author>Ashfield-Watt, Pauline Annie L.</rioxxterms:author><rioxxterms:author>Powers, Hilary J.</rioxxterms:author><rioxxterms:author>Newcombe, Robert Gordon</rioxxterms:author><rioxxterms:author>McDowell, Ian Frederick</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1373/49.2.295</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:46
Date: 2016-02-12

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:46</identifier>
      <datestamp>2016-02-12T22:00:13Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>While folic acid has been shown to reverse endothelial dysfunction, the exact underlying mechanism remains elusive. Here, folic acid reversed both the endothelial dysfunction and increased production of superoxide following depletion of rabbit aortic ring tetrahydrobiopterin (BH4) levels with 2,4-diamino-6-hydroxy-pyrimidine (DAHP) and N-acetyl-5-hydroxy-tryptamine (NAS). Incubation with l-nitroarginine methyl ester also attenuated the production of superoxide. DAHP and NAS reduced BH4 concentrations in both aorta and cultured porcine aortic endothelial cells. Folic acid had no effect on BH4 concentrations in either preparation. The superoxide anion scavenger Tiron but not folic acid reversed the endothelial dysfunction produced in aortic rings by inhibition of copper-zinc superoxide dismutase with diethyldithiocarbamic acid. Neither folic acid nor its metabolite 5-methyltetrahydrofolate prevented the in vitro oxidation of BH4. This study demonstrates that folic acid reverses the endothelial dysfunction induced by BH4 depletion independently of either the regeneration or stabilization of BH4 or an antioxidant effect.</dc:description><dc:language>en</dc:language><dc:publisher>Elsevier</dc:publisher><dc:source>0014-2999</dc:source><dc:title>Folic acid reverses endothelial dysfunction induced by inhibition of tetrahydrobiopterin biosynthesis</dc:title><rioxxterms:author>Moat, Stuart James</rioxxterms:author><rioxxterms:author>Clarke, Zoe L.</rioxxterms:author><rioxxterms:author>Madhavan, Anil Kumar</rioxxterms:author><rioxxterms:author>Lewis, Malcolm John</rioxxterms:author><rioxxterms:author>Lang, Derek</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/j.ejphar.2005.11.047</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:47
Date: 2016-03-19

RIOXX

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    <header>
      <identifier>oai:http://orca.cf.ac.uk:47</identifier>
      <datestamp>2016-03-19T22:00:12Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><ali:free_to_read/><dc:description>The effects of pharmacological interventions that modulate Ca2+ homeodynamics and membrane potential in rat isolated cerebral vessels during vasomotion (i.e., rhythmic fluctuations in arterial diameter) were simulated by a third-order system of nonlinear differential equations. Independent control variables employed in the model were [Ca2+] in the cytosol, [Ca2+] in intracellular stores, and smooth muscle membrane potential. Interactions between ryanodine- and inositol 1,4,5-trisphosphate-sensitive intracellular Ca2+ stores and transmembrane ion fluxes via K+ channels, Cl? channels, and voltage-operated Ca2+ channels were studied by comparing simulations of oscillatory behavior with experimental measurements of membrane potential, intracellular free [Ca2+] and vessel diameter during a range of pharmacological interventions. The main conclusion of the study is that a general model of vasomotion that predicts experimental data can be constructed by a low-order system that incorporates nonlinear interactions between dynamical control variables.</dc:description><dc:format>application/pdf</dc:format><dc:identifier>http://orca.cf.ac.uk/47/1/Dynamicsofthreevariable.pdf</dc:identifier><dc:language>en</dc:language><dc:source>1542-0086</dc:source><dc:subject>R1</dc:subject><dc:title>Dynamics of a three-variable nonlinear model of vasomotion:  comparison of theory and experiment</dc:title><rioxxterms:author>Parthimos, Dimitris</rioxxterms:author><rioxxterms:author>Haddock, R. E.</rioxxterms:author><rioxxterms:author>Hill, C. E.</rioxxterms:author><rioxxterms:author>Griffith, Tudor Morley</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1529/biophysj.107.106278</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:48
Date: 2016-03-19

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    <header>
      <identifier>oai:http://orca.cf.ac.uk:48</identifier>
      <datestamp>2016-03-19T22:00:12Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Spontaneous fluctuations in flow in isolated rabbit ear resistance arteries may exhibit almost-periodic behavior interrupted by chaotic bursts that can be classified as type-I Pomeau-Manneville intermittency. This conclusion was supported by the construction of parabolic return maps and identification of the characteristic probability distributions for the number of oscillations per laminar segment (n) associated with the type-I scenario. Pharmacological inhibition of nitric oxide (NO) synthesis by the vascular endothelium modulated the dynamics of the reinjection mechanism, and thus the generic shape of the probability distribution for n. Nevertheless, average laminar length was related to a derived bifurcation parameter ɛ according to power-law scaling of the form 〈n〉∼ɛβ, where the estimated critical exponent β was close to the theoretical value of -0.5 both in the presence and absence of NO synthesis.</dc:description><dc:language>en</dc:language><dc:publisher>American Physical Society</dc:publisher><dc:source>1539-3755</dc:source><dc:title>Universal scaling properties of type-I intermittent chaos in isolated resistance arteries are unaffected by endogenous nitric oxide synthesis</dc:title><rioxxterms:author>Parthimos, Dimitris</rioxxterms:author><rioxxterms:author>Edwards, David Hughes</rioxxterms:author><rioxxterms:author>Griffith, Tudor Morley</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1103/PhysRevE.64.061906</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:49
Date: 2016-03-19

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:49</identifier>
      <datestamp>2016-03-19T22:00:13Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>We provide experimental evidence for the existence of Shil’nikov homoclinic chaos in the fluctuations in flow which can be observed in isolated perfused rabbit ear arteries, and establish a close association between homoclinicity and type-III Pomeau-Manneville intermittent behavior. The transition between the homoclinic scenario and type-III intermittency is clarified by a mathematical model of the arterial smooth muscle cell. Simulations of the effects of nitric oxide (NO) by the vascular endothelium on these patterns of behavior closely match experimental observations.</dc:description><dc:language>en</dc:language><dc:publisher>American Physical Society</dc:publisher><dc:source>1539-3755</dc:source><dc:title>Shil'nikov homoclinic chaos is intimately related to type-III intermittency in isolated rabbit arteries: role of nitric oxide</dc:title><rioxxterms:author>Parthimos, Dimitris</rioxxterms:author><rioxxterms:author>Edwards, David Hughes</rioxxterms:author><rioxxterms:author>Griffith, Tudor Morley</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1103/PhysRevE.67.051922</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:50
Date: 2016-03-19

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    <header>
      <identifier>oai:http://orca.cf.ac.uk:50</identifier>
      <datestamp>2016-03-19T22:00:13Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>We have performed a nonlinear analysis of fluctuations in red cell velocity and arteriolar calibre in the mesenteric bed of the anaesthetized rat. Measurements were obtained under control conditions and during local superfusion with NG-nitro-L-arginine (L-NNA, 30 µM) and tetrabutylammonium (TBA, 0.1 mM), which suppress NO synthesis and block Ca2+ activated K+ channels (KCa), respectively. Time series were analysed by calculating correlation dimensions and largest Lyapunov exponents. Both statistics were higher for red cell velocity than diameter fluctuations, thereby potentially differentiating between global and local mechanisms that regulate microvascular flow. Evidence for underlying nonlinear structure was provided by analysis of surrogate time series generated from the experimental data following randomization of Fourier phase. Complexity indices characterizing time series under control conditions were in general higher than those derived from data obtained during superfusion with L-NNA and TBA.</dc:description><dc:language>en</dc:language><dc:source>13616560</dc:source><dc:title>Deterministic nonlinear characteristics of in vivo blood flow velocity and arteriolar diameter fluctuations</dc:title><rioxxterms:author>Parthimos, Dimitris</rioxxterms:author><rioxxterms:author>Osterloh, K.</rioxxterms:author><rioxxterms:author>Pries, A. R.</rioxxterms:author><rioxxterms:author>Griffith, Tudor Morley</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1088/0031-9155/49/9/014</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:51
Date: 2016-12-13

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:51</identifier>
      <datestamp>2016-12-13T02:31:57Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>OBJECTIVES&#13;
&#13;
We sought to study the effect of low-dose folic acid supplementation or optimization of dietary folate intake on plasma homocysteine and endothelial function in healthy adults.&#13;
&#13;
BACKGROUND&#13;
&#13;
Elevated homocysteine is associated with cardiovascular disease, but it is not known whether this relationship is causal. Individuals homozygous (TT) for the C677T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene (12% of the population) have increased homocysteine levels, particularly in association with suboptimal folate intake.&#13;
&#13;
METHODS&#13;
&#13;
Healthy subjects (n = 126; 42 of each MTHFR genotype) were included in this cross-over study of three interventions of four months each: 1) placebo plus natural diet; 2) daily 400-?g folic acid supplement plus natural diet; and 3) increased dietary folate intake to 400 ?g/day.&#13;
&#13;
RESULTS&#13;
&#13;
At baseline, homocysteine was inversely related to plasma folate and was higher in TT homozygotes. For the whole group, plasma folate increased by 46% after dietary folate and by 79% after supplementation, with reductions of homocysteine of 14% and 16%, respectively. Within the genotype, TT homozygotes exhibited the most marked changes in these variables. Brachial artery endothelial function, as determined by a change in end-diastolic diameter in response to increased flow, was not changed by increased folate intake (98</dc:description><dc:language>en</dc:language><dc:source>0735-1097</dc:source><dc:subject>R1</dc:subject><dc:title>Optimization of dietary folate or low-dose folic acid supplements lower homocysteine but do not enhance endothelial function in healthy adults, irrespective of the methylenetetrahydrofolate reductase (C677T) genotype</dc:title><rioxxterms:author>Pullin, Catherine H.</rioxxterms:author><rioxxterms:author>Ashfield-Watt, Pauline Annie Lorraine</rioxxterms:author><rioxxterms:author>Burr, Michael Leslie</rioxxterms:author><rioxxterms:author>Clark, Zoe Elizabeth</rioxxterms:author><rioxxterms:author>Lewis, Malcolm John</rioxxterms:author><rioxxterms:author>Moat, Stuart James</rioxxterms:author><rioxxterms:author>Newcombe, Robert Gordon</rioxxterms:author><rioxxterms:author>Powers, Hilary J.</rioxxterms:author><rioxxterms:author>Whiting, Jenny M.</rioxxterms:author><rioxxterms:author>McDowell, Ian Frederick</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/S0735-1097(01)01668-0</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:53
Date: 2016-03-19

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:53</identifier>
      <datestamp>2016-03-19T22:00:13Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5231</setSpec>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Major disparities in reported levels of basal human nitric oxide metabolites have resulted in a recent literature focusing almost exclusively on methods. We chose to analyze triiodide chemiluminescence, drawn by the prospect of identifying why the most commonly employed assay in nitric oxide biology typically yielded lower metabolite values, compared with several other techniques. We found that the sensitivity of triiodide was greatly affected by the auto-capture of nitric oxide by deoxygenated cell-free heme in the reaction chamber. Potential contaminants and signal losses were also associated with standard sample purification procedures and the chemistry involved in nitrite removal. To inhibit heme nitric oxide auto-capture, we added potassium ferricyanide to the triiodide reagent, reasoning this would provide a more complete detection of any liberated nitric oxide. From human venous blood samples, we established nitric oxide levels ranging from 0.000178 to 0.00024 mol nitric oxide/mol hemoglobin. We went on to find significantly elevated nitric oxide levels in venous blood taken from diabetic patients in comparison to healthy controls (p &lt; 0.0001). We concluded that the lack of signals reported of late by several groups using triiodide chemiluminescence for the detection of hemoglobin-bound nitric oxide may not represent levels on the border of assay sensitivity but rather underestimated values because of methodological limitations. We therefore stress the need for assay systems to be developed that differentiate between individual nitric oxide metabolite species and overcome the limitations we outline, allowing accurate conclusions to be drawn regarding physiological nitric oxide metabolite levels.</dc:description><dc:language>en</dc:language><dc:source>1083-351X</dc:source><dc:subject>R1</dc:subject><dc:title>Detection of human red blood cell-bound nitric oxide</dc:title><rioxxterms:author>Rogers, Stephen C.</rioxxterms:author><rioxxterms:author>Khalatbari, Afshin</rioxxterms:author><rioxxterms:author>Gapper, Peter William James</rioxxterms:author><rioxxterms:author>Frenneaux, Michael Paul</rioxxterms:author><rioxxterms:author>James, Philip Eurig</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1074/jbc.M501179200</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:56
Date: 2016-03-19

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:56</identifier>
      <datestamp>2016-03-19T22:00:13Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5231</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Objective— C-reactive protein (CRP) has been proposed to be an independent risk factor for cardiovascular disease. In vitro studies investigating the mechanism behind this have used purified commercial CRP (cCRP) and endothelial cells. We investigated the role of contaminants in cCRP preparations. &#13;
&#13;
Methods and Results— Human umbilical vein endothelial cells and the human endothelial cell line EA.hy926 were incubated with Escherichia coli–derived cCRP, in-house–generated azide-free recombinant, and ascites-purified CRP, azide, or lipopolysaccharide (LPS) equivalent to the concentration present in cCRP preparations. Cells were investigated for change in cell proliferation, morphology, apoptosis, and expression of endothelial NO synthase and intercellular adhesion molecule-1. Cell supernatants were assessed for monocyte chemoattractant protein-1 (MCP-1), interleukin-8, von Willebrand factor secretion, and pH change. Only cCRP was able to induce all activation events analyzed; however, this ability was lost on extensive dialysis, suggesting that low molecular weight contaminants were responsible for these events. Indeed, the effects of cCRP were mirrored by azide or LPS. &#13;
&#13;
Conclusions— We investigated a wide range of effects on endothelial cells ascribed to CRP; however, azide and LPS, but never CRP itself, were responsible for the cell activation events. We conclude that CRP, per se, does not activate endothelial cells. &#13;
&#13;
We investigated the validity of the numerous responses of endothelial cells attributed to CRP and demonstrate here that the reported effects are caused by low molecular weight contaminants, like azide and LPS, which are present in commercial CRP preparations.</dc:description><dc:language>en</dc:language><dc:source>15244636</dc:source><dc:subject>R1</dc:subject><dc:title>C-reactive protein-induced in vitro endothelial cell activation is an artefact caused by azide and lipopolysaccharide</dc:title><rioxxterms:author>Taylor, Karolina E.</rioxxterms:author><rioxxterms:author>Giddings, John Charles</rioxxterms:author><rioxxterms:author>Van Den Berg, Carmen Wilma</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1161/01.ATV.0000164623.41250.28</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:58
Date: 2016-03-19

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:58</identifier>
      <datestamp>2016-03-19T22:00:14Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5231</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Background— Resynchronization pacing is an effective symptomatic treatment for heart failure patients with prolongation of the QRS duration (QRSd). Dyssynchronous contraction of the left ventricle is also observed with normal QRSd. We set out to determine how electrical activation of the left ventricular (LV) free wall differed between patients with left bundle-branch block (LBBB) and normal QRSd and if synchrony improved during pacing in patients with normal QRSd. &#13;
&#13;
Methods and Results— Twenty-two patients were implanted with resynchronization pacemakers, 13 with LBBB (mean QRS, 171 ms) and 9 with normal QRSd &lt;120 ms (mean, 100 ms). LV lead electrograms and surface ECGs in sinus rhythm (unpaced) were recorded. Conventional and tissue Doppler echocardiography were performed without pacing, with LV and biventricular pacing at optimal atrioventricular delay. Lead electrograms from the LV free wall were later in the LBBB patients in absolute terms (155 ms [SD 23] versus 65.5 ms [SD 25]; P=0.05) and also relative to the surface QRS (90.5% [SD 8] versus 65.5% [SD 24]). Improved synchrony of the left and right ventricles (interventricular synchrony) and of the LV myocardial segments (intraventricular synchrony) was observed for patients with LBBB and normal QRSd. Baseline LV synchrony correlated with timing of LV free-wall electrical activation. Improved intraventricular synchrony during pacing also correlated with LV free-wall electrical activation time. &#13;
&#13;
Conclusions— Resynchronization of systole can be achieved for patients with normal QRSd and LBBB during biventricular and LV pacing. The timing of LV free-wall electrical activation correlated with the improvement in synchrony.</dc:description><dc:language>en</dc:language><dc:source>1524-4539</dc:source><dc:subject>R1</dc:subject><dc:title>Electrical and mechanical components of dyssynchrony in heart failure patients with normal QRS duration and left bundle-branch block: impact of left and biventricular pacing</dc:title><rioxxterms:author>Turner, Mark Stephen</rioxxterms:author><rioxxterms:author>Bleasdale, Robert Anthony</rioxxterms:author><rioxxterms:author>Vinereanu, Dragos</rioxxterms:author><rioxxterms:author>Mumford, Catherine E.</rioxxterms:author><rioxxterms:author>Paul, Vince</rioxxterms:author><rioxxterms:author>Fraser, Alan Gordon</rioxxterms:author><rioxxterms:author>Frenneaux, Michael Paul</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1161/01.CIR.0000131184.40893.40</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:60
Date: 2016-03-19

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      <identifier>oai:http://orca.cf.ac.uk:60</identifier>
      <datestamp>2016-03-19T22:00:14Z</datestamp>
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ID: oai:http://orca.cf.ac.uk:61
Date: 2016-03-19

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      <identifier>oai:http://orca.cf.ac.uk:61</identifier>
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ID: oai:http://orca.cf.ac.uk:66
Date: 2016-03-19

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      <datestamp>2016-03-19T22:00:15Z</datestamp>
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ID: oai:http://orca.cf.ac.uk:68
Date: 2016-02-12

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:68</identifier>
      <datestamp>2016-02-12T22:00:17Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Antiplatelet therapies improve endothelial function in atherosclerosis, suggesting that platelets regulate vascular nitric oxide (NO) bioactivity in vivo. Herein, washed platelets consumed NO on activation in an aspirin-sensitive manner, and aspirin enhanced platelet NO responses in vitro. To examine whether in vivo aspirin can inhibit platelet NO consumption, a double-blind placebo-controlled study was conducted. After a 2-week nonsteroidal anti-inflammatory drug (NSAID)–free period, healthy men were randomly assigned and administered aspirin (75 mg/d orally) or identical placebo for 14 days, then crossed over to the opposite arm. Following in vivo aspirin, NO consumption by platelets was inhibited 91%. Rate of onset and recovery following aspirin withdrawal was consistent with cyclooxygenase 1 (COX-1) inhibition. In a small substudy, NO consumption by platelets from postmenopausal women was faster in hypercholesterolemics and less sensitive to aspirin (ie, 39% versus 76% inhibition for hypercholesterolemics or normocholesterolemics, respectively). However, 150 mg aspirin/day increased inhibition of NO consumption by platelets of hypercholesterolemics to 80%. Comparisons of platelet COX-1 or -2 expression and urinary 11-dehydro-thromboxane B2 excretion suggested that aspirin was less able to block platelet activation in vivo in hypercholesterolemia. In conclusion, aspirin inhibits NO consumption by platelets from healthy subjects, but its beneficial effects on NO bioactivity may be compromised in some hypercholesterolemic patients.</dc:description><dc:language>en</dc:language><dc:publisher>American Society of Hematology</dc:publisher><dc:source>0006-4971</dc:source><dc:title>In vivo aspirin supplementation inhibits nitric oxide consumption by human platelets</dc:title><rioxxterms:author>Williams, Paula Claire</rioxxterms:author><rioxxterms:author>Coffey, Marcus Jonathan</rioxxterms:author><rioxxterms:author>Coles, Barbara</rioxxterms:author><rioxxterms:author>Sanchez, Stephanie</rioxxterms:author><rioxxterms:author>Morrow, Jason D.</rioxxterms:author><rioxxterms:author>Cockcroft, John Ronald</rioxxterms:author><rioxxterms:author>Lewis, Malcolm John</rioxxterms:author><rioxxterms:author>O'Donnell, Valerie Bridget</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1182/blood-2005-02-0664</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:69
Date: 2016-02-12

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<record>
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      <identifier>oai:http://orca.cf.ac.uk:69</identifier>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Ryanodine receptor–calcium release channels play a pivotal role in the calcium signaling that mediates muscle excitation–contraction coupling. Their membrane organization into regular patterns, functional gating studies and theoretical analysis of receptor clustering have led to models that invoke allosteric interaction between individual channel oligomers as a critical mechanism for control of calcium release. Here we show that in reconstituted “checkerboard-like� lattices that mimic in situ membrane channel arrays, each oligomer is interlocked physically with four adjacent oligomers via a specific domain–domain interaction. Direct physical coupling between ryanodine receptors provides structural evidence for an inter-oligomer allosteric mechanism in channel regulation. Therefore, in addition to established cytosolic and luminal regulation of function, these observations indicate that channel–channel communication through physical coupling provides a novel mode of regulation of intracellular calcium release channels.</dc:description><dc:language>en</dc:language><dc:publisher>Elsevier</dc:publisher><dc:source>1089-8638</dc:source><dc:title>Physical coupling between ryanodine receptor-calcium release channels</dc:title><rioxxterms:author>Yin, Chang-Cheng</rioxxterms:author><rioxxterms:author>Blayney, Lynda Mary</rioxxterms:author><rioxxterms:author>Lai, Francis Anthony</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/j.jmb.2005.04.002</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:71
Date: 2016-03-19

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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><ali:free_to_read/><dc:description>Ryanodine receptors (RyR) function as Ca2+ channels that regulate Ca2+ release from intracellular stores to control a diverse array of cellular processes. The massive cytoplasmic domain of RyR is believed to be responsible for regulating channel function. We investigated interaction between the transmembrane Ca2+-releasing pore and a panel of cytoplasmic domains of the human cardiac RyR in living cells. Expression of eGFP-tagged RyR constructs encoding distinct transmembrane topological models profoundly altered intracellular Ca2+ handling and was refractory to modulation by ryanodine, FKBP12.6 and caffeine. The impact of coexpressing dsRed-tagged cytoplasmic domains of RyR2 on intracellular Ca2+ phenotype was assessed using confocal microscopy coupled with parallel determination of in situ protein: protein interaction using fluorescence resonance energy transfer (FRET). Dynamic interactions between RyR cytoplasmic and transmembrane domains were mediated by amino acids 3722-4610 (Interacting or "I"-domain) which critically modulated intracellular Ca2+ handling and restored RyR sensitivity to caffeine activation. These results provide compelling evidence that specific interaction between cytoplasmic and transmembrane domains is an important mechanism in the intrinsic modulation of RyR Ca2+ release channels.</dc:description><dc:format>application/pdf</dc:format><dc:identifier>http://orca.cf.ac.uk/71/2/Ryanodine_Receptor_Regulation.pdf</dc:identifier><dc:language>en</dc:language><dc:source>1059-1524</dc:source><dc:title>Ryanodine receptor regulation by intramolecular interaction between cytoplasmic and transmembrane domains</dc:title><rioxxterms:author>George, Christopher</rioxxterms:author><rioxxterms:author>Jundi, Hala</rioxxterms:author><rioxxterms:author>Thomas, Nia Lowri</rioxxterms:author><rioxxterms:author>Scoote, Mark</rioxxterms:author><rioxxterms:author>Walters, Nicola</rioxxterms:author><rioxxterms:author>Williams, Alan John</rioxxterms:author><rioxxterms:author>Lai, Francis Anthony</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1091/mbc.E03-09-0688</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:72
Date: 2016-02-12

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<record>
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      <identifier>oai:http://orca.cf.ac.uk:72</identifier>
      <datestamp>2016-02-12T22:00:17Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Ca2+ release via type 2 ryanodine receptors (RyR2) regulates cardiac function. Molecular cloning of human&#13;
RyR2 identified 2 alternatively spliced variants, comprising 30- and 24-bp sequence insertions; yet their role in shaping cardiomyocyte Ca2+ signaling and cell phenotype is unknown. We profiled the developmental regulation and the tissue and species specificity of these variants and showed that their recombinant expression in HL-1 cardiomyocytes profoundly modulated nuclear and cytoplasmic Ca2+ release. All splice variants localized to the sarcoplasmic reticulum, perinuclear Golgi apparatus, and to finger-like invaginations of the nuclear envelope (nucleoplasmic reticulum).&#13;
Strikingly, the 24-bp splice insertion that was present at low levels in embryonic and adult hearts was essential for&#13;
targeting RyR2 to an intranuclear Golgi apparatus and promoted the intracellular segregation of this variant. The&#13;
amplitude variability of nuclear and cytoplasmic Ca2+ fluxes were reduced in nonstimulated cardiomyocytes expressing both 30- and 24-bp splice variants and were associated with lower basal levels of apoptosis. Expression of RyR2 containing the 24-bp insertion also suppressed intracellular Ca2+ fluxes following prolonged caffeine exposure (1 mmol/L, 16 hours) that protected cells from apoptosis. The antiapoptotic effects of this variant were linked to increased levels of Bcl-2 phosphorylation. In contrast, RyR2 containing the 30-bp insertion, which was abundant in human embryonic heart but was decreased during cardiac development, did not protect cardiomyocytes from&#13;
caffeine-evoked apoptosis. Thus, we provide the first evidence that RyR2 splice variants exquisitely modulate&#13;
intracellular Ca2+ signaling and are key determinants of cardiomyocyte apoptotic susceptibility.</dc:description><dc:language>en</dc:language><dc:source>15244571</dc:source><dc:subject>QP</dc:subject><dc:subject>R1</dc:subject><dc:title>Alternative splicing of ryanodine receptors modulates cardiomyocyte Ca2+ signalling and susceptibility to apoptosis</dc:title><rioxxterms:author>George, Christopher H.</rioxxterms:author><rioxxterms:author>Rogers, Sarah Ann</rioxxterms:author><rioxxterms:author>Bertrand, Benedicte M.A.</rioxxterms:author><rioxxterms:author>Tunwell, Richard E.A.</rioxxterms:author><rioxxterms:author>Thomas, Nia Lowri</rioxxterms:author><rioxxterms:author>Steele, Derek S.</rioxxterms:author><rioxxterms:author>Cox, Eryl Vanessa</rioxxterms:author><rioxxterms:author>Pepper, Christopher John</rioxxterms:author><rioxxterms:author>Hazeel, Carolyn Jean</rioxxterms:author><rioxxterms:author>Claycomb, William C.</rioxxterms:author><rioxxterms:author>Lai, Francis Anthony</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1161/01.RES.0000260804.77807.cf</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:73
Date: 2016-02-12

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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>The ryanodine receptor (RyR) calcium release channel functions as a redox sensor that is sensitive to channel modulators. The FK506-binding protein (FKBP) is an important regulator of channel activity, and disruption of the RyR2-FKBP12.6 association has been implicated in cardiac disease. In the present study, we investigated whether the RyR-FKBP association is redox-regulated. Using co-immunoprecipitation assays of solubilized native RyR2 from cardiac muscle sarcoplasmic reticulum (SR) with recombinant [35S]FKBP12.6, we found that the sulfydryl-oxidizing agents, H2O2 and diamide, result in diminished RyR2-FKBP12.6 binding. Co-sedimentation experiments of cardiac SR vesicles with [35S]FKBP12.6 also demonstrated that oxidizing reagents decreased FKBP binding. Matching results were obtained with skeletal muscle SR. Notably, H2O2 and diamide differentially affected the RyR2-FKBP12.6 interaction, decreasing binding to 75 and 50% of control, respectively. In addition, the effect of H2O2 was negligible when the channel was in its closed state or when applied after FKBP binding had occurred, whereas diamide was always effective. A cysteine-null mutant FKBP12.6 retained redox-sensitive interaction with RyR2, suggesting that the effect of the redox reagents is exclusively via sites on the ryanodine receptor. K201 (or JTV519), a drug that has been proposed to prevent FKBP12.6 dissociation from the RyR2 channel complex, did not restore normal FKBP binding under oxidizing conditions. Our results indicate that the redox state of the RyR is intimately connected with FKBP binding affinity.</dc:description><dc:language>en</dc:language><dc:publisher>American Society for Biochemistry and Molecular Biology</dc:publisher><dc:source>1083-351X</dc:source><dc:title>Redox sensitivity of the ryanodine receptor interaction with FK506-binding protein</dc:title><rioxxterms:author>Zissimopoulos, Spyros</rioxxterms:author><rioxxterms:author>Docrat, Naadiya</rioxxterms:author><rioxxterms:author>Lai, Francis Anthony</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1074/jbc.M607590200</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:74
Date: 2016-02-12

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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:74</identifier>
      <datestamp>2016-02-12T22:00:17Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>The ryanodine receptor (RyR) is a widely expressed intracellular calcium (Ca2+)-release channel regulating processes such as muscle contraction and neurotransmission. Snapin, a ubiquitously expressed SNARE-associated protein, has been implicated in neurotransmission. Here, we report the identification of snapin as a novel RyR2-interacting protein. Snapin binds to a 170-residue predicted ryanodine receptor cytosolic loop (RyR2 residues 4596-4765), containing a hydrophobic segment required for snapin interaction. Ryanodine receptor binding of snapin is not isoform specific and is conserved in homologous RyR1 and RyR3 fragments. Consistent with peptide fragment studies, snapin interacts with the native ryanodine receptor from skeletal muscle, heart and brain. The snapin-RyR1 association appears to sensitise the channel to Ca2+ activation in [3H]ryanodine-binding studies. Deletion analysis indicates that the ryanodine receptor interacts with the snapin C-terminus, the same region as the SNAP25-binding site. Competition experiments with native ryanodine receptor and SNAP25 suggest that these two proteins share an overlapping binding site on snapin. Thus, regulation of the association between ryanodine receptor and snapin might constitute part of the elusive molecular mechanism by which ryanodine-sensitive Ca2+ stores modulate neurosecretion.</dc:description><dc:language>en</dc:language><dc:publisher>Company of Biologists</dc:publisher><dc:source>1477-9137</dc:source><dc:title>Ryanodine receptor interaction with the SNARE-associated protein snapin</dc:title><rioxxterms:author>Zissimopoulos, Spyros</rioxxterms:author><rioxxterms:author>West, Duncan J.</rioxxterms:author><rioxxterms:author>Williams, Alan John</rioxxterms:author><rioxxterms:author>Lai, Francis Anthony</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1242/jcs.02936</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:75
Date: 2016-02-12

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:75</identifier>
      <datestamp>2016-02-12T22:00:18Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:language>en</dc:language><dc:source>15244571</dc:source><dc:title>Arrhythmogenesis in catecholaminergic polymorphic ventricular tachycardia: insights from a RyR2 R4496C knock-in mouse model</dc:title><rioxxterms:author>Liu, Nian</rioxxterms:author><rioxxterms:author>Colombi, Barbara</rioxxterms:author><rioxxterms:author>Memmi, Mirella</rioxxterms:author><rioxxterms:author>Zissimopoulos, Spyros</rioxxterms:author><rioxxterms:author>Rizzi, Nicoletta</rioxxterms:author><rioxxterms:author>Negri, Sara</rioxxterms:author><rioxxterms:author>Imbriani, Marcello</rioxxterms:author><rioxxterms:author>Napolitano, Carlo</rioxxterms:author><rioxxterms:author>Lai, Francis Anthony</rioxxterms:author><rioxxterms:author>Priori, Silvia G.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1161/01.RES.0000235869.50747.e1</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:76
Date: 2016-02-12

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:76</identifier>
      <datestamp>2016-02-12T22:00:18Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>The ryanodine receptor-calcium release channel complex (RyR) plays a pivotal role in excitation-contraction coupling in skeletal and cardiac muscle. RyR channel activity is modulated by interaction with FK506-binding protein (FKBP), and disruption of the RyR-FKBP association has been implicated in cardiomyopathy, cardiac hypertrophy, and heart failure. Evidence for an interaction between RyR and FKBP is well documented, both in skeletal muscle (RyR1-FKBP12) and in cardiac muscle (RyR2-FKBP12.6), however definition of the FKBP-binding site remains elusive. Early reports proposed interaction of a short RyR central domain with FKBP12/12.6, however this site has been questioned, and recently an alternative FKBP12.6 interaction site has been identified within the N-terminal half of RyR2. In this study, we report evidence for the human RyR2 C-terminal domain as a novel FKBP12.6-binding site. Using competition binding assays, we find that short C-terminal RyR2 fragments can displace bound FKBP12.6 from the native RyR2, although they are unable to exclusively support interaction with FKBP12.6. However, expression of a large RyR2 C-terminal construct in mammalian cells encompassing the pore-forming transmembrane domains exhibits rapamycin-sensitive binding specifically to FKBP12.6 but not to FKBP12. We also obtained some evidence for involvement of the RyR2 N-terminal, but not the central domain, in FKBP12.6 interaction. Our studies suggest that a novel interaction site for FKBP12.6 may be present at the RyR2 C terminus, proximal to the channel pore, a sterically appropriate location that would enable this protein to play a central role in the modulation of this critical ion channel.</dc:description><dc:language>en</dc:language><dc:publisher>American Society for Biochemistry and Molecular Biology</dc:publisher><dc:source>1083-351X</dc:source><dc:title>Interaction of FKBP12.6 with the cardiac ryanodine receptor C-terminal domain</dc:title><rioxxterms:author>Zissimopoulos, Spyros</rioxxterms:author><rioxxterms:author>Lai, Francis Anthony</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1074/jbc.M412954200</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:77
Date: 2016-03-19

RIOXX

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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:77</identifier>
      <datestamp>2016-03-19T22:00:17Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:language>en</dc:language><dc:source>15244539</dc:source><dc:title>Prognostic value of coronary vascular endothelial dysfunction</dc:title><rioxxterms:author>Halcox, Julian P. J.</rioxxterms:author><rioxxterms:author>Quyyumi, A. A.</rioxxterms:author><rioxxterms:author>Zalos, G.</rioxxterms:author><rioxxterms:author>Schenke, W. H.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1161/01.CIR.0000025404.78001.D8</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:78
Date: 2016-03-19

RIOXX

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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
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    <header>
      <identifier>oai:http://orca.cf.ac.uk:78</identifier>
      <datestamp>2016-03-19T22:00:17Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:language>en</dc:language><dc:source>15244571</dc:source><dc:title>Coronary vasodilation and improvement in endothelial dysfunction with endothelin ETA receptor blockade</dc:title><rioxxterms:author>Halcox, Julian P. J.</rioxxterms:author><rioxxterms:author>Quyyumi, A. A.</rioxxterms:author><rioxxterms:author>Zalos, G.</rioxxterms:author><rioxxterms:author>Nour, K.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1161/hh2301.100980</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:79
Date: 2016-03-19

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:79</identifier>
      <datestamp>2016-03-19T22:00:17Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5231</setSpec>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Background: Cardiovascular risk factors contribute to atherogenesis by inducing endothelial-cell injury and dysfunction. We hypothesized that endothelial progenitor cells derived from bone marrow have a role in ongoing endothelial repair and that impaired mobilization or depletion of these cells contributes to endothelial dysfunction and cardiovascular disease progression.&#13;
   &#13;
Methods: We measured the number of colony-forming units of endothelial progenitor cells in peripheral-blood samples from 45 men (mean [+/-SE] age, 50+/-2 years). The subjects had various degrees of cardiovascular risk but no history of cardiovascular disease. Endothelium-dependent and endothelium-independent function was assessed by high-resolution ultrasonography of the brachial artery.&#13;
   &#13;
Results: We observed a strong correlation between the number of circulating endothelial progenitor cells and the subjects' combined Framingham risk factor score (r=-0.47, P=0.001). Measurement of flow-mediated brachial-artery reactivity also revealed a significant relation between endothelial function and the number of progenitor cells (r=0.59, P&lt;0.001). Indeed, the levels of circulating endothelial progenitor cells were a better predictor of vascular reactivity than was the presence or absence of conventional risk factors. In addition, endothelial progenitor cells from subjects at high risk for cardiovascular events had higher rates of in vitro senescence than cells from subjects at low risk.&#13;
   &#13;
Conclusions: In healthy men, levels of endothelial progenitor cells may be a surrogate biologic marker for vascular function and cumulative cardiovascular risk. These findings suggest that endothelial injury in the absence of sufficient circulating progenitor cells may affect the progression of cardiovascular disease.</dc:description><dc:language>en</dc:language><dc:source>15334406</dc:source><dc:subject>R1</dc:subject><dc:title>Circulating endothelial progenitor cells, vascular function, and cardiovascular risk</dc:title><rioxxterms:author>Hill, Jonathan M.</rioxxterms:author><rioxxterms:author>Zalos, Gloria</rioxxterms:author><rioxxterms:author>Halcox, Julian P. J.</rioxxterms:author><rioxxterms:author>Schenke, William H.</rioxxterms:author><rioxxterms:author>Waclawiw, Myron A.</rioxxterms:author><rioxxterms:author>Quyyumi, Arshed A.</rioxxterms:author><rioxxterms:author>Finkel, Toren</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1056/NEJMoa022287</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:80
Date: 2016-03-19

RIOXX

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<record>
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      <identifier>oai:http://orca.cf.ac.uk:80</identifier>
      <datestamp>2016-03-19T22:00:17Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:language>en</dc:language><dc:source>07351097</dc:source><dc:title>Non-invasive assessment of endothelial function: which technique?</dc:title><rioxxterms:author>Halcox, Julian P. J.</rioxxterms:author><rioxxterms:author>Donald, A. E.</rioxxterms:author><rioxxterms:author>Charakida, M.</rioxxterms:author><rioxxterms:author>Cole, T. J.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/j.jacc.2006.07.039</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:81
Date: 2016-10-25

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:81</identifier>
      <datestamp>2016-10-25T01:30:19Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>OBJECTIVE: The purpose of this study was to compare chronic with acute mechanisms by which Type A might predict incident coronary heart disease (CHD). &#13;
&#13;
METHOD: The study included 2394 men aged 50 to 64 years who were assessed for CHD, Type A behavior, and CHD risk factors. Type A was assessed using the Jenkins Activity Survey (JAS), the Bortner scale, and the Framingham scale. Further examinations were completed at 5 and 9 years for incident CHD. &#13;
&#13;
RESULTS: After 9 years, there was no increased risk of CHD associated with any Type A score. Nevertheless, high Bortner scores were associated with increased risk of incident CHD at 5 years and high JAS and Bortner scores were associated with a decreased risk between 5 and 9 years. Further analysis of Type A scores on time to first coronary event found strong inverse associations for all type A scores (JAS = 205 -0.49 months to first event, 95% CI = -0.20, -0.78, p = .001) (Bortner = 176 -0.27 months; 95% CI = -0.10, -0.44; p = .002) (Framingham = 0.44 -0.0011 months; 95% CI = -0.0002, -0.0019; p = .01). &#13;
&#13;
CONCLUSIONS: The data show Type A is a strong predictor of when incident coronary heart disease (or coronary event) will occur rather than if it will occur. These findings suggest that Type A increases exposure to potential triggers, rather than materially affecting the process of atherosclerosis.</dc:description><dc:language>en</dc:language><dc:source>15347796</dc:source><dc:subject>R1</dc:subject><dc:title>Is type A behavior really a trigger for coronary heart disease events?</dc:title><rioxxterms:author>Gallacher, John Edward</rioxxterms:author><rioxxterms:author>Sweetnam, Peter M.</rioxxterms:author><rioxxterms:author>Yarnell, John W.G.</rioxxterms:author><rioxxterms:author>Elwood, Peter Creighton</rioxxterms:author><rioxxterms:author>Stansfeld, Stephen A.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1097/01.PSY.0000041608.55974.A8</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:82
Date: 2016-10-25

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:82</identifier>
      <datestamp>2016-10-25T01:30:19Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:language>en</dc:language><dc:source>15244628</dc:source><dc:title>Does psychological distress predict the risk of ischemic stroke and transient ischemic attach? The Caerphilly Study</dc:title><rioxxterms:author>Gallacher, John Edward</rioxxterms:author><rioxxterms:author>May, M.</rioxxterms:author><rioxxterms:author>McCarron, P.</rioxxterms:author><rioxxterms:author>Stansfeld, S.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1161/hs0102.100529</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:83
Date: 2016-10-25

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:83</identifier>
      <datestamp>2016-10-25T01:30:19Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5231</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><ali:free_to_read/><dc:description>Background. Studies have found associations between psychological distress (PD) and increased&#13;
risk of myocardial infarction (MI). However, it is not clear whether the relationship reflects the&#13;
subtle influence of pre-existing illness on both PD and MI. This study examines the association&#13;
between PD and MI in a prospective epidemiological study of 1864 middle-aged men to examine if&#13;
the association is explained by existing illness.&#13;
Method. This study was a prospective cohort study modelling the association between PD, measured&#13;
using the 30-item General Health Questionnaire (GHQ) and non-fatal myocardial infarction&#13;
(NFMI) and fatal/non-fatal myocardial infarction (FNFMI).The relationship was modelled in a&#13;
series of logistic regression models adjusted for age, then cigarette smoking, then social position,&#13;
and finally for all sociodemographic characteristics, coronary heart disease (CHD) risk factors, and&#13;
baseline CHD.&#13;
Results. PD was associated with a 70% and 68% increased risk of NFMI and FNFMI in fully&#13;
adjusted analysis. However, PD was not associated with an increased risk of NFMI and FNFMI in&#13;
analyses excluding those with baseline CHD. Further, being psychologically distressed and physically&#13;
ill was associated with a greater than twofold risk of NFMI and FNFMI, 2.37 (95% CI&#13;
1.33–4.20) and 2.33 (95% CI 1.32–4.12) respectively.&#13;
Conclusion. This study suggests that PD is a moderator of the increased risk of MI associated with&#13;
existing physical illness. PD in men who are physically ill is a marker of an underlying chronic&#13;
physical illness. The prospective association of PD with MI is not independent of baseline physical&#13;
illness.</dc:description><dc:format>application/pdf</dc:format><dc:identifier>http://orca.cf.ac.uk/83/1/GALLACHER__Orca83.pdf</dc:identifier><dc:language>en</dc:language><dc:source>14698978</dc:source><dc:subject>R1</dc:subject><dc:title>Psychological distress, physical illness and risk of myocardial infarction in the Caerphilly Study</dc:title><rioxxterms:author>Rasul, Farhat</rioxxterms:author><rioxxterms:author>Stansfeld, F. A.</rioxxterms:author><rioxxterms:author>Davey Smith, G.</rioxxterms:author><rioxxterms:author>Shlomo, Y. Ben</rioxxterms:author><rioxxterms:author>Gallacher, John Edward</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1017/S0033291707000402</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:84
Date: 2016-10-25

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:84</identifier>
      <datestamp>2016-10-25T01:30:19Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:language>en</dc:language><dc:publisher>BMJ Publishing Group</dc:publisher><dc:source>1351-0711</dc:source><dc:title>Health status as a potential effect modifier of the relation between noise annoyance and incidence of ischaemic heart disease</dc:title><rioxxterms:author>Gallacher, John Edward</rioxxterms:author><rioxxterms:author>Ising, H.</rioxxterms:author><rioxxterms:author>Babisch, W.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1136/oem.60.10.739</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:88
Date: 2016-02-12

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:88</identifier>
      <datestamp>2016-02-12T22:00:19Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5231</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Objectives: We sought to investigate the effects of short- and long-term vitaminC therapy on endothelial dysfunction in patients with homocystinuria.&#13;
&#13;
Background: Untreated homocystinuria due to cystathionine b-synthase deficiency is associated with premature atherothrombotic disease; 25% of untreated patients suffer a vascular event by the age of 16 years and 50% by 29 years. Treatment directed at reducing homocysteine accumulation significantly reduces this risk. However, despite ‘optimal’ treatment and compliance,&#13;
hyperhomocysteinaemia usually persists and individuals exhibit endothelial dysfunction indicative of an adverse cardiovascular prognosis. Additional intervention is therefore required to further reduce cardiovascular risk.&#13;
&#13;
Methods: We investigated the endothelial effects of acute (2 g single dose) and chronic (1 g/day for 6 months) administration of oral vitamin C in 5 patients with homocystinuria (mean age 26 years, 1 male) and 5 age- and sex-matched controls. Brachial artery endothelium-dependent £ow-mediated dilatation (FMD) and endothelium-independent responses to nitroglycerin (NTG) were measured using high-resolution ultrasonic vessel wall-tracking.&#13;
&#13;
Results: Baseline: Plasma total homocysteine was 100:8±61:6 and 9:2±1:9 µmol/L in the patient and control groups, respectively (p &lt; 0:001).&#13;
FMD responses were impaired in the patient group (20±40 µm) compared with the controls (116±30 µm) (p &lt; 0:001). Vitamin C administration: FMD responses in the patient group improved both acutely, 160±65 µm at 4h&#13;
(p &lt; 0:001), and chronically, 170±70 µm at 2 weeks (p &lt; 0:001) and 170±40 µm at 6 months (p &lt; 0:001). FMD responses in the control group were unaltered (p = 0:526). Within both groups, neither the vascular response to&#13;
NTG nor plasma homocysteine was altered (p &gt; 0:4).&#13;
&#13;
Conclusions: Vitamin C ameliorates endothelial dysfunction in patients with homocystinuria, independent of changes in homocysteine concentration and should therefore be considered as an additional adjunct to therapy to reduce&#13;
the potential long-term risk of atherothrombotic disease.</dc:description><dc:language>en</dc:language><dc:source>15732665</dc:source><dc:subject>R1</dc:subject><dc:title>Vitamin C therapy ameliorates vascular endothelial dysfunction in treated patients with homocystinuria</dc:title><rioxxterms:author>Pullin, C. H.</rioxxterms:author><rioxxterms:author>Bonham, James R.</rioxxterms:author><rioxxterms:author>McDowell, Ian Frederick</rioxxterms:author><rioxxterms:author>Lee, P. J.</rioxxterms:author><rioxxterms:author>Powers, H. J.</rioxxterms:author><rioxxterms:author>Wilson, John Fawcett</rioxxterms:author><rioxxterms:author>Lewis, Malcolm John</rioxxterms:author><rioxxterms:author>Moat, Stuart James</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1023/A:1015672625913</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:89
Date: 2016-11-21

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:89</identifier>
      <datestamp>2016-11-21T10:40:21Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5231</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>PURPOSE: Considerable uncertainty exists regarding relative effects of allogeneic peripheral blood stem cells transplantation (PBSCT) versus bone marrow transplantation (BMT) on outcomes of patients with hematologic malignancies.&#13;
&#13;
PATIENTS AND METHODS: To provide the totality of research evidence related to the effects of PBSCT versus BMT, we conducted an individual-patient data meta-analysis using data from nine randomized trials enrolling 1,111 adult patients.&#13;
&#13;
RESULTS: Compared with BMT, PBSCT led to faster neutrophil (odds ratio [OR] = 0.31; 95% CI, 0.25 to 0.38; P &lt; .00001) and platelet engraftment (OR = 0.52; 95% CI, 0.44 to 0.61; P &lt; .00001). PBSCT was associated with a significant increase in the development of grade 3-4 acute graft-versus-host disease (GVHD; OR = 1.39; 95% CI, 1.03 to 1.88) and extensive (47% v 31% at 3 years; OR = 1.89; 95% CI, 1.47 to 2.42; P &lt; .000001) and overall chronic GVHD (68% v 52% at 3 years; OR = 1.92; 95% CI, 1.47 to 2.49; P &lt; .000001), but not grade 2-4 acute GVHD (54% v 53%; P = .49). PBSCT was associated with a decrease in relapse (21% v 27% at 3 years; OR = 0.71; 95% CI, 0.54 to 0.93; P = .01) in both late-stage-(33% v 51% at 3 years; OR = 0.59; 95% CI, 0.38 to 0.93; P = .02) and early-stage-disease patients (16% v 20% at 3 years; OR = 0.69; 95% CI, 0.49 to 0.98; P = .04). Nonrelapse mortality was not different between groups. Overall and disease-free survival were only statistically significantly improved in patients with late-stage disease (overall survival: 46% v 31% at 3 years; OR = 0.64; 95% CI, 0.46 to 0.90; P = .01; disease-free survival: 41% v 27% at 3 years; OR = 0.63 95% CI, 0.45 to 0.87; P = .01).&#13;
&#13;
CONCLUSION: PBSCT is associated with a decreased relapse rate in hematologic malignancies and improvement in overall and disease-free survival in patients with late-stage disease. PBSCT is also associated with a significant risk of extensive chronic GVHD.</dc:description><dc:language>en</dc:language><dc:source>15277755</dc:source><dc:subject>R1</dc:subject><dc:title>Allogeneic peripheral blood stem-cell compared with bone marrow transplantation in the management of hematologic malignancies: an individual patient data meta-analysis of nine randomized trials</dc:title><rioxxterms:author>al-Jurf, Mahmoud</rioxxterms:author><rioxxterms:author>Aranha, Francisco</rioxxterms:author><rioxxterms:author>Annasetti, Claudio</rioxxterms:author><rioxxterms:author>Apperley, Jane F.</rioxxterms:author><rioxxterms:author>Baynes, Roy</rioxxterms:author><rioxxterms:author>Bensinger, William I.</rioxxterms:author><rioxxterms:author>Blaise, Didier</rioxxterms:author><rioxxterms:author>Chaudhary, M. Ashraf</rioxxterms:author><rioxxterms:author>Clarke, Mike</rioxxterms:author><rioxxterms:author>Cornelissen, Jan J</rioxxterms:author><rioxxterms:author>Couban, Stephen</rioxxterms:author><rioxxterms:author>Cutler, Corey</rioxxterms:author><rioxxterms:author>Djulbegovic, Benjamin</rioxxterms:author><rioxxterms:author>Gyger, Martin</rioxxterms:author><rioxxterms:author>Gratwohl, Alois</rioxxterms:author><rioxxterms:author>Heldal, Dag</rioxxterms:author><rioxxterms:author>Hills, Robert Kerrin</rioxxterms:author><rioxxterms:author>Stem Cell Trialists Collaborative Group</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1200/JCO.2005.09.020</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:91
Date: 2016-03-19

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:91</identifier>
      <datestamp>2016-03-19T22:00:18Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:language>en</dc:language><dc:source>15280020</dc:source><dc:title>RAS mutation in acute myeloid leukemia is associated with distinct cytogenetic subgroups but does not influence outcome in patients younger than 60 years</dc:title><rioxxterms:author>Bowen, David T.</rioxxterms:author><rioxxterms:author>Frew, Marion E.</rioxxterms:author><rioxxterms:author>Hills, Robert Kerrin</rioxxterms:author><rioxxterms:author>Gale, Rosemary E.</rioxxterms:author><rioxxterms:author>Wheatley, Keith</rioxxterms:author><rioxxterms:author>Groves, Michael J.</rioxxterms:author><rioxxterms:author>Langabeer, Stephen E.</rioxxterms:author><rioxxterms:author>Kottaridis, Panagiotis D.</rioxxterms:author><rioxxterms:author>Moorman, Anthony V.</rioxxterms:author><rioxxterms:author>Burnett, Alan Kenneth</rioxxterms:author><rioxxterms:author>Linch, David C.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1182/blood-2005-03-0867</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:92
Date: 2016-03-19

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:92</identifier>
      <datestamp>2016-03-19T22:00:18Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Polymerase chain reaction (PCR) assessment of clonal T-cell receptor (TCR) and immunoglobulin (Ig) gene rearrangements is an important diagnostic tool in mature T-cell neoplasms. However, lack of standardized primers and PCR protocols has hampered comparability of data in previous clonality studies. To obtain reference values for Ig/TCR rearrangement patterns, 19 European laboratories investigated 188 T-cell malignancies belonging to five World Health Organization-defined entities. The TCR/Ig spectrum of each sample was analyzed in duplicate in two different laboratories using the standardized BIOMED-2 PCR multiplex tubes accompanied by international pathology panel review. TCR clonality was detected in 99% (143/145) of all definite cases of T-cell prolymphocytic leukemia, T-cell large granular lymphocytic leukemia, peripheral T-cell lymphoma (unspecified) and angioimmunoblastic T-cell lymphoma (AILT), whereas nine of 43 anaplastic large cell lymphomas did not show clonal TCR rearrangements. Combined use of TCRB and TCRG genes revealed two or more clonal signals in 95% of all TCR clonal cases. Ig clonality was mostly restricted to AILT. Our study indicates that the BIOMED-2 multiplex PCR tubes provide a powerful strategy for clonality assessment in T-cell malignancies assisting the firm diagnosis of T-cell neoplasms. The detected TCR gene rearrangements can also be used as PCR targets for monitoring of minimal residual disease.</dc:description><dc:language>en</dc:language><dc:source>08876924</dc:source><dc:subject>R1</dc:subject><dc:title>Powerful strategy for polymerase chain reaction-based clonality assessment in T-cell malignancies Report of the BIOMED-2 Concerted Action BHM4 CT98-3936</dc:title><rioxxterms:author>Brüggemann, M.</rioxxterms:author><rioxxterms:author>White, H.</rioxxterms:author><rioxxterms:author>Gaulard, P.</rioxxterms:author><rioxxterms:author>Garcia-Sanz, R.</rioxxterms:author><rioxxterms:author>Gameiro, P.</rioxxterms:author><rioxxterms:author>Oeschger, S.</rioxxterms:author><rioxxterms:author>Jasani, Bharat</rioxxterms:author><rioxxterms:author>Ott, M.</rioxxterms:author><rioxxterms:author>Delsol, G.</rioxxterms:author><rioxxterms:author>Orfao, A.</rioxxterms:author><rioxxterms:author>Tiemann, M.</rioxxterms:author><rioxxterms:author>Herbst, H.</rioxxterms:author><rioxxterms:author>Langerak, A.W.</rioxxterms:author><rioxxterms:author>Spaargaren, M.</rioxxterms:author><rioxxterms:author>Moreau, E.</rioxxterms:author><rioxxterms:author>Groenen, P.J.T.A.</rioxxterms:author><rioxxterms:author>Sambade, C.</rioxxterms:author><rioxxterms:author>Foroni, L.</rioxxterms:author><rioxxterms:author>Carter, G.I.</rioxxterms:author><rioxxterms:author>Hummel, M.</rioxxterms:author><rioxxterms:author>Bastard, C.</rioxxterms:author><rioxxterms:author>Davi, F.</rioxxterms:author><rioxxterms:author>Delfau-Larue, M-H</rioxxterms:author><rioxxterms:author>Kneba, M.</rioxxterms:author><rioxxterms:author>Dongen, J.J.M. van</rioxxterms:author><rioxxterms:author>Beldjord, K.</rioxxterms:author><rioxxterms:author>Molina, T.J.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1038/sj.leu.2404481</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:93
Date: 2016-02-12

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      <identifier>oai:http://orca.cf.ac.uk:93</identifier>
      <datestamp>2016-02-12T22:00:19Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:language>en</dc:language><dc:source>1532-1827</dc:source><dc:title>Caveolin-1 overexpression predicts poor disease-free survival of patients with clinically confined renal cell carcinoma</dc:title><rioxxterms:author>Campbell, Lee</rioxxterms:author><rioxxterms:author>Gumbleton, Mark</rioxxterms:author><rioxxterms:author>Griffiths, David Francis Rees</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1038/sj.bjc.6601359</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:94
Date: 2016-02-12

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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
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    <header>
      <identifier>oai:http://orca.cf.ac.uk:94</identifier>
      <datestamp>2016-02-12T22:00:19Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>New facets to Knudson's [corrected] "two-hit" hypothesis have been proposed recently in relation to adenomatous polyposis coli (APC): protein inactivation may be selected weakly, and the two hits may be interdependent. We reviewed published data on 165 sporadic and 102 familial adenomatous polyposis-associated colorectal tumors with two characterized mutations. Using a Poisson model, we redefined the mutation cluster region (MCR) to residues 1281-1556 and confirmed that the locations of pairs of APC mutations are interdependent (P &lt; 0.0001). A mathematical model, based on the data for sporadic tumors, implied different growth advantages for different combinations of APC mutations: genotype I/I (I: mutation inside MCR) was 3.9 times more likely to be selected than IO or IL (O: mutation outside MCR, L: allelic loss), which were 27.8 times more likely to be selected than OO or OL.</dc:description><dc:language>en</dc:language><dc:publisher>American Association for Cancer Research</dc:publisher><dc:source>0008-5472</dc:source><dc:subject>R1</dc:subject><dc:title>Different combinations of biallelic APC mutation confer different growth advantages in colorectal tumours</dc:title><rioxxterms:author>Cheadle, Jeremy Peter</rioxxterms:author><rioxxterms:author>Krawczak, Michael</rioxxterms:author><rioxxterms:author>Thomas, Meinir W</rioxxterms:author><rioxxterms:author>Hodges, Angela Kaye</rioxxterms:author><rioxxterms:author>Al-Tassan, Nada</rioxxterms:author><rioxxterms:author>Fleming, Nick</rioxxterms:author><rioxxterms:author>Sampson, Julian Roy</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:96
Date: 2016-05-02

RIOXX

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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:96</identifier>
      <datestamp>2016-05-02T16:31:53Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Immunologic approaches are emerging as new treatment options in several types of cancer. However, whereas the ability of patients to develop potent CD8+ T-cell responses is crucial for efficient antitumor responses, immunocompetence and T-cell function are not tested routinely in patients entering immunotherapy. The objective of our study was to monitor T-cell function in advanced cancer and during chemotherapy. CD8+ T-cell function of 21 patients with advanced ovarian cancer (stages III-IV) was assessed by cytokine flow cytometry following stimulation of 42 PBMC samples with a panel of synthetic viral peptides in vitro, consisting of pan-Caucasian epitopes. CD8+ T-cell responses were significantly lower in patients with high levels (&gt;200 units/mL) of Ca125 (marker of tumor load and progression) than in those with low Ca125 levels (P = 0.0013). In longitudinal studies of nine patients, chemotherapy was associated with decreasing Ca125 levels in seven cases and also with improvement or maintenance of CD8+ T-cell function in seven cases. After the full course of chemotherapy, five of nine patients in remission displayed potent CD8+ T-cell responses, whereas four of nine patients in progression displayed low or decreasing T-cell responses, pointing toward a correlation between T-cell function and clinical response. Our results show for the first time that CD8+ T-cell function is not permanently suppressed in advanced cancer and successful chemotherapy is associated with improved antigen-specific T-cell reactivity. We suggest that functional assays determining T-cell immunocompetence can be valuable tools for optimizing cancer immunotherapy for improved clinical success.</dc:description><dc:language>en</dc:language><dc:source>15387445</dc:source><dc:subject>RC0254</dc:subject><dc:title>Recovery of CD8+ T-cell function during systemic chemotherapy in advanced ovarian cancer</dc:title><rioxxterms:author>Coleman, Sharon Louise</rioxxterms:author><rioxxterms:author>Clayton, Aled</rioxxterms:author><rioxxterms:author>Mason, Malcolm David</rioxxterms:author><rioxxterms:author>Jasani, Bharat</rioxxterms:author><rioxxterms:author>Adams, Malcolm</rioxxterms:author><rioxxterms:author>Tabi, Zsuzsanna</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1158/0008-5472.CAN-04-3792</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:99
Date: 2016-03-19

RIOXX

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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:99</identifier>
      <datestamp>2016-03-19T22:00:19Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:language>en</dc:language><dc:source>15280020</dc:source><dc:subject>R1</dc:subject><dc:title>No evidence that FLT3 status should be considered as an indicator for transplantation in acute myeloid leukemia (AML): an analysis of 1135 patients, excluding acute promyelocytic leukemia, from the UK MRC AML10 and 12 trials</dc:title><rioxxterms:author>Gale, Rosemary E.</rioxxterms:author><rioxxterms:author>Hills, Robert Kerrin</rioxxterms:author><rioxxterms:author>Kottaridis, Panagiotis D.</rioxxterms:author><rioxxterms:author>Srirangan, Sivatharsini</rioxxterms:author><rioxxterms:author>Wheatley, Keith</rioxxterms:author><rioxxterms:author>Burnett, Alan Kenneth</rioxxterms:author><rioxxterms:author>Linch, David C.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1182/blood-2005-03-1323</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:100
Date: 2016-03-19

RIOXX

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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:100</identifier>
      <datestamp>2016-03-19T22:00:19Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>In an attempt to improve induction chemotherapy for older patients with acute myeloid leukemia (AML),1314 patients were randomized to 1 of 3 induction treatments for 2 courses of DAT (daunorubicin, cytarabine, and thioguanine) 3 + 10, ADE (daunorubicin, cytarabine, and etoposide) 10 + 3 + 5, or MAC (mitoxantrone-cytarabine). The remission rate in the DAT arm was significantly better than ADE (62% vs 50%; P = .002) or MAC (62% vs 55%; P = .04). This benefit was seen in patients younger and older than 70 years. There were no differences between the induction schedules with respect to overall survival at 5 years (12% vs 8% vs 10%). A total of 226 patients were randomized to receive granulocyte colony-stimulating factor (G-CSF) or placebo as supportive care from day 8 after the end of treatment course 1. The remission rate or survival were not improved by G-CSF, although the median number of days to recover neutrophils to 1.0</dc:description><dc:language>en</dc:language><dc:source>15280020</dc:source><dc:subject>R1</dc:subject><dc:title>Attempts to improve treatment outcomes in acute myeloid leukemia (AML) in older patients: the results of the United Kingdom Medical Research Council AML11 trial</dc:title><rioxxterms:author>Goldstone, Anthony H.</rioxxterms:author><rioxxterms:author>Burnett, Alan Kenneth</rioxxterms:author><rioxxterms:author>Wheatley, Keith</rioxxterms:author><rioxxterms:author>Smith, Alastair G.</rioxxterms:author><rioxxterms:author>Hutchinson, R. Michael</rioxxterms:author><rioxxterms:author>Clark, Richard E.</rioxxterms:author><rioxxterms:author>Medical Research Council Adult Leukaemia Working Party</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1182/blood.V98.5.1302</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:101
Date: 2016-03-19

RIOXX

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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:101</identifier>
      <datestamp>2016-03-19T22:00:20Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>BACKGROUND: The role of sentinel lymph node biopsy (SLNB) in patients with a core needle-biopsy diagnosis of ductal carcinoma in situ (DCIS) has been intensely debated. Core needle-biopsy has an inherent sampling error leading to histologic underestimation of invasive disease. If SLNB is not performed at the time of the definitive operative procedure, patients found to have an invasive cancer, will require a second operative procedure. The study was designed to determine when the risk of finding invasive disease on final pathology in patients with an initial diagnosis of DCIS was sufficiently high to justify the use of SLNB. METHODS: We identified 587 women with an initial core needle-biopsy diagnosis of DCIS in the prospective Breast Test Wales (BTW) database from 1995 through 2005. A variety of clinical, mammographic and histologic features were identified and correlated with the presence of invasion at excision using univariate and multivariate analyses. RESULTS: Median age of patients at the time of diagnosis was 58 years (range 41 to 83 years). 201 patients (36%) were treated by mastectomy and 354 (64%) by breast conservation surgery. 220 of 587 patients (38%) were found to have invasive disease on final pathology. On univariate analysis, the rate of upstaging was related to the presence of a clinically palpable mass and size of the mass (both p&lt;0.0001, Mann-Whitney test); mammographic presence of a mass and size of the mass (both p&lt;0.0001, Mann-Whitney test). Multivariate logistic regression analysis revealed 2 independent predictors of invasive cancer on final pathology: mass on clinical examination (odds ratio [OR], 5.09; p&lt;0.0001) and mammographic mass (OR, 7.37; p&lt;0.0001). Age, grade of DCIS, microinvasion and presence of comedonecrosis did not help in distinguishing between patients with DCIS and those upstaged to invasive carcinoma at definitive surgery. Axillary nodal staging (four node sampling or clearance) was done at the time of surgery in 269 patients. Axillary nodal metastases were found in 35 of 269 patients (13%). All 35 patients had invasive carcinoma on final pathology. CONCLUSION: The indiscriminate use of SLNB in patients with DCIS seems excessive. Our study suggests that patients with a mass on clinical examination or mammogram have an increased risk of invasive disease at the time of definitive operative procedure and should undergo SLNB at the initial procedure. In addition, SLNB should be performed in patients undergoing mastectomy because mastectomy precludes SLNB if invasive disease is subsequently discovered.</dc:description><dc:language>en</dc:language><dc:publisher>Kluwer</dc:publisher><dc:source>1573-7217</dc:source><dc:title>Is there a role of sentinel lymph node biopsy in ductal carcinoma in situ?: analysis of 587 cases</dc:title><rioxxterms:author>Goyal, Amit</rioxxterms:author><rioxxterms:author>Douglas-Jones, Anthony Gordon</rioxxterms:author><rioxxterms:author>Monypenny, Ian</rioxxterms:author><rioxxterms:author>Sweetland, Helen Margaret</rioxxterms:author><rioxxterms:author>Stevens, Guy</rioxxterms:author><rioxxterms:author>Mansel, Robert Edward</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1007/s10549-006-9167-2</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:102
Date: 2016-12-13

RIOXX

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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
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      <datestamp>2016-12-13T02:32:05Z</datestamp>
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      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>BACKGROUND: Despite the widespread application of sentinel lymph node biopsy (SLNB) for early stage breast cancer, there is a wide variation in reported test performance characteristics. A major aim of this prospective multicentre validation study was to quantify detection and false-negative rates of SLNB and evaluate factors influencing them. METHODS: Eight-hundred and fourty-two patients with clinically node-negative breast cancer underwent SLNB according to a standardised protocol that used a combination of radiopharmaceutical 99mTc-albumin colloid and Patent Blue V dye. SLNB was followed by standard axillary treatment at the same operation in all patients. RESULTS: Sentinel lymph nodes (SLNs) were identified in 803 (96.1%) of 836 evaluable cases. The median number of SLNs removed per patient was 2 (range 1-9). There were 19 false negatives, resulting in a sensitivity of 263/282 (93.3%) and accuracy 782/803 (97.6%). SLNs were successfully identified by blue dye in 698 (85.6%), by isotope in 698 (85.6%), and by the combination of blue dye and isotope in 782 (96.0%) of 815 patients. Among 276 node positive patients, one or more positive SLNs were identified by blue dye in 251 (90.9%), by isotope in 246 (89.1%) and by the combination of blue dye and gamma probe in 258 (93.5%). Obesity, tumor location other than upper outer quadrant and non-visualisation of SLNs on the pre-operative lymphoscintiscan were significantly associated with failed localisation (p&lt;0.001, p=0.008, p&lt;0.001, respectively). The false-negative rate in patients with grade 3 tumors was 9.6%, compared with 4.7% in those with grade 2 tumors (p=0.022). The false-negative rate in patients who had one SLN harvested was 10.1%, compared with 1.1% in those who had multiple SLNs (three or more) removed (p=0.010). CONCLUSION: SLNB can accurately determine whether axillary metastases are present in patients with early stage breast cancer with clinically negative axillary nodes. Both success and accuracy of SLNB are optimised by the combined use of blue dye and isotope. SLNB success decreases with increasing body mass, tumor location other than the upper outer quadrant and non-visualisation of hot nodes on the pre-operative lymphoscintiscan. This study demonstrates reduction in the predictive value of a negative SLNB in grade 3 tumors.</dc:description><dc:language>en</dc:language><dc:publisher>Kluwer</dc:publisher><dc:source>1573-7217</dc:source><dc:title>Factors affecting failed localisation and false-negative rates of sentinel node biopsy in breast cancer--results of the ALMANAC validation phase</dc:title><rioxxterms:author>Goyal, Amit</rioxxterms:author><rioxxterms:author>Newcombe, Robert Gordon</rioxxterms:author><rioxxterms:author>Chhabra, Alok</rioxxterms:author><rioxxterms:author>Mansel, Robert Edward</rioxxterms:author><rioxxterms:author>ALMANAC Trialists Group</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1007/s10549-006-9192-1</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:104
Date: 2016-02-12

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:104</identifier>
      <datestamp>2016-02-12T22:00:21Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5231</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Critical functions of hamartin and tuberin, encoded by the TSC1 and TSC2 genes, are likely to be closely linked. The proteins interact directly with one another and mutations affecting either gene result in the tuberous sclerosis phenotype. However, the regions of hamartin and tuberin that interact have not been well defined, and the relationship between their interaction and the pathogenesis of tuberous sclerosis has not been explored. To address these issues a series of hamartin and tuberin constructs were used to assay for interaction in the yeast two-hybrid system. Hamartin (amino acids 302–430) and tuberin (amino acids 1–418) interacted strongly with one another. A region of tuberin encoding a putative coiled-coil (amino acids 346–371) was necessary but not sufficient to mediate the interaction with hamartin, as more N-terminal residues were also required. A region of hamartin (amino acids 719–998) predicted to encode coiled-coils was capable of oligermerization but was not important for the interaction with tuberin. Subtle, non-truncating mutations identified in patients with tuberous sclerosis and located within the putative binding regions of hamartin (N198_F199delinsI;593–595delACT) or tuberin (G294E and I365del), abolished or dramatically reduced interaction of the proteins as assessed by yeast two-hybrid assays and by co-immunoprecipitation of the full-length proteins from Cos7 cells. In contrast, three non-pathogenic missense polymorphisms of tuberin (R261W, M286V, R367Q) in the same region as the disease-causing TSC2 mutations did not. These results indicate a requirement for interaction in critical growth suppressing functions of hamartin and tuberin.</dc:description><dc:language>en</dc:language><dc:publisher>Oxford University Press</dc:publisher><dc:source>1460-2083</dc:source><dc:subject>R1</dc:subject><dc:title>Pathological mutations in TSC1 and TSC2 disrupt the interaction between hamartin and tuberin</dc:title><rioxxterms:author>Hodges, Angela K.</rioxxterms:author><rioxxterms:author>Li, Shaowei</rioxxterms:author><rioxxterms:author>Maynard, Julie Helen</rioxxterms:author><rioxxterms:author>Parry, Lee</rioxxterms:author><rioxxterms:author>Braverman, Richard</rioxxterms:author><rioxxterms:author>DeClue, Jeffrey E.</rioxxterms:author><rioxxterms:author>Cheadle, Jeremy Peter</rioxxterms:author><rioxxterms:author>Sampson, Julian Roy</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1093/hmg/10.25.2899</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:105
Date: 2016-02-12

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:105</identifier>
      <datestamp>2016-02-12T22:00:21Z</datestamp>
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      <setSpec>7375626A656374733D52:5231</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>PURPOSE: Hepatocyte growth factor/scatter factor (HGF/SF), via its receptor c-MET, has been implicated to play a pivotal role in breast cancer development and progression. This study examined a transgene-consisting of a combination of U1snRNA, hammerhead ribozyme, and antisense, designed to inhibit c-met expression-and its impact on the migration and in vitro invasion of breast cancer cells.&#13;
&#13;
EXPERIMENTAL DESIGN: A hammerhead ribozyme targeting human c-MET was cloned into a modified pZeoU1EcoSpe vector and transfected into breast cancer cells MDA MB 231 and MCF-7 by electroporation. Expression of MET mRNA and protein was determined. Migration and in vitro invasiveness of transfected cells were also analyzed.&#13;
&#13;
RESULTS: Breast cancer cells were transfected with the ribozyme-containing plasmids. Stable transfectants manifested an almost complete loss of MET mRNA and protein, as shown by reverse transcription-PCR, Northern blotting, and Western blotting, respectively, whereas the wild-type plasmid had no effects. Met-ribozyme transfected cells exhibited reduced migration and in vitro invasiveness through extracellular matrix (Matrigel), compared with the wild-type cells and cells transfected with empty plasmid.&#13;
&#13;
CONCLUSIONS: These data show that targeting c-MET by way of a hammerhead ribozyme encoding antisense to c-MET is an effective approach in reducing the invasiveness of breast cancer cells.</dc:description><dc:language>en</dc:language><dc:source>1078-0432</dc:source><dc:subject>R1</dc:subject><dc:title>A hammerhead ribozyme suppresses expression of hepatocyte growth factor/scatter factor receptor c-MET and reduces migration and invasiveness of breast cancer cells</dc:title><rioxxterms:author>Jiang, Wen Guo</rioxxterms:author><rioxxterms:author>Grimshaw, Alfred David</rioxxterms:author><rioxxterms:author>Lane, Jane</rioxxterms:author><rioxxterms:author>Martin, Tracey Amanda</rioxxterms:author><rioxxterms:author>Abounader, R.</rioxxterms:author><rioxxterms:author>Laterra, J.</rioxxterms:author><rioxxterms:author>Mansel, Robert Edward</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:106
Date: 2016-03-19

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:106</identifier>
      <datestamp>2016-03-19T22:00:21Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5231</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Purpose: Hepatocyte growth factor/scatter factor (HGF/SF) is known to increase the invasiveness and migration of cancer cells in vitro and induce angiogenesis. This study examined if inhibition of HGF/SF receptor expression by cancer cells and HGF/SF expression by stromal fibroblasts affects the growth of mammary cancer. &#13;
&#13;
Experimental Design: Transgenes encoding ribozymes to specifically target human HGF/SF receptor (pLXSN-MET) or HGF/SF (pLXSN-HGF) were constructed using a pLXSN retroviral vector. Human mammary cancer cells MDA MB 231 was transduced with pLXSN-MET (MDA+/+). A human fibroblast cell line MRC5, which produces bioactive HGF/SF, was transduced with pLXSN-HGF (MRC5+/+). These cells were used in a nude mice breast tumor model. &#13;
&#13;
Results: HGF receptor in MDA+/+ cells and HGF in MRC5+/+cells were successfully removed with respective ribozymes as shown by reverse transcription-PCR and Western blotting, respectively. MDA+/+ was found to have reduced invasiveness when stimulated with HGF/SF. MRC5+/+ exhibited a significant reduction in HGF/SF production. When injected into athymic nude mice, MDA+/+ exhibited a slower rate of growth, compared with the wild type (MDA?/?), and the cells transduced with control viral vector (MDA+/?). The growth of MDA?/? tumor was significantly enhanced when coimplanted with wild-type MRC5 (MRC5?/?), and the stimulatory effect was reduced when MRC5+/+ cells were coimplanted instead of MRC5?/?. The reduction of tumor growth was accompanied by reduction of angiogenesis, as demonstrated by the staining of VE-cadherin in primary tumor tissues. &#13;
&#13;
Conclusions: Retroviral ribozyme transgenes targeting HGF/SF in fibroblasts or its receptor cMET in mammary cancer cells can reduce the growth of mammary cancer and associated angiogenesis by inhibiting paracrine stromal–tumor cell interactions.</dc:description><dc:language>en</dc:language><dc:source>1078-0432</dc:source><dc:subject>R1</dc:subject><dc:title>Reduction of stromal fibroblast-induced mammary tumor growth, by retroviral ribozyme transgenes to hepatocyte growth factor/scatter factor and its receptor, c-MET</dc:title><rioxxterms:author>Jiang, Wen Guo</rioxxterms:author><rioxxterms:author>Grimshaw, Alfred David</rioxxterms:author><rioxxterms:author>Martin, Tracey Amanda</rioxxterms:author><rioxxterms:author>Davies, Gaynor</rioxxterms:author><rioxxterms:author>Parr, Christian</rioxxterms:author><rioxxterms:author>Watkins, Gareth</rioxxterms:author><rioxxterms:author>Lane, Jane</rioxxterms:author><rioxxterms:author>Abounader, Roger</rioxxterms:author><rioxxterms:author>Laterra, John</rioxxterms:author><rioxxterms:author>Mansel, Robert Edward</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:107
Date: 2016-10-25

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:107</identifier>
      <datestamp>2016-10-25T01:30:24Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Purpose: The aim of this study was to correlate the expression of pigment epithelium–derived factor (PEDF), a potent endogenous antiangiogenic molecule, with severity and prognosis in breast cancer. &#13;
&#13;
Experimental Design: To investigate the gene expression profile of PEDF in human breast cancer in relation to a patient's clinical variables, we examined human breast cancer tissue (n = 119), background breast tissue (n = 33), and a range of cell lines for mRNA and protein levels of PEDF by using reverse transcription PCR, real-time quantitative PCR, immunohistochemistry, and ELISA. &#13;
&#13;
Results: By using reverse transcription PCR, real-time quantitative PCR, immunohistochemistry, and ELISA, PEDF expression was found to be dramatically decreased in breast cancer. An overall outlook for the patients inversely correlated with PEDF mRNA levels. Exogenous PEDF inhibits endothelial tubule formation induced by breast cancer cell–conditioned medium, in vitro. &#13;
&#13;
Conclusion: These observations collectively support the hypothesis that a lack of PEDF expression is a potent factor for the enhancement of tumor growth and angiogenesis in breast cancer.</dc:description><dc:language>en</dc:language><dc:publisher>American Association for Cancer Research</dc:publisher><dc:source>1078-0432</dc:source><dc:title>Decreased pigment epithelium-derived factor expression in human breast cancer progression</dc:title><rioxxterms:author>Cai, Jun</rioxxterms:author><rioxxterms:author>Parr, Christian</rioxxterms:author><rioxxterms:author>Watkins, Gareth</rioxxterms:author><rioxxterms:author>Jiang, Wen Guo</rioxxterms:author><rioxxterms:author>Boulton, Michael Edwin</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1158/1078-0432.CCR-06-0094</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:108
Date: 2016-03-19

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:108</identifier>
      <datestamp>2016-03-19T22:00:22Z</datestamp>
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      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:language>en</dc:language><dc:source>08876924</dc:source><dc:title>Improved reliability of lymphoma diagnostics via PCR-based clonal testing: - Report of the BIOMED-2 Concerted Action BHM4-CT98-3936</dc:title><rioxxterms:author>Jasani, Bharat</rioxxterms:author><rioxxterms:author>Langerak, A. W.</rioxxterms:author><rioxxterms:author>Macintyre, E. A.</rioxxterms:author><rioxxterms:author>Kneba, M.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1038/sj.leu.2404467</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:109
Date: 2016-09-13

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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:109</identifier>
      <datestamp>2016-09-13T01:30:28Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5231</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>We performed a retrospective study of 90 consecutive cases with inoperable carcinoma of the oesophagus treated with definitive chemoradiation at a single cancer centre between 1995 and 2002. For the last 4 years, 73 patients have received therapy according to an agreed protocol. This outpatient-based regimen involves four cycles of chemotherapy, cycles 3 and 4 given concurrently with 50 Gy external beam radiotherapy (XRT) delivered in 25 fractions over 5 weeks. Cisplatin 60 mg m-2 day-1 is given every 3 weeks together with continuous infusional 5-fluorouracil 300 mg m-2 day-1, reduced to 225 mg m-2 day-1 during the XRT. In all, 45 (50%) patients suffered one or more WHO grade 3/4 toxicity, grade 3 in 93% cases. Patients received more than 90% of the planned chemoradiation schedule. The median overall survival was 26 (15, &gt;96) months, 51% (41, 64) and 26% (13, 52) surviving 2 and 5 years, respectively. Advanced stage, particularly T4 disease, was associated with a worse prognosis. Patients considered not suitable for surgery for reasons other than their disease, mainly co-morbidity, had a significantly better outcome, median survival 40 (26, &gt;96) months, 2- and 5-year survivals 67% (54, 84) and 32% (13, 79), respectively (P&lt;0.001). This schedule is a feasible, tolerable and effective treatment for patients with oesophageal cancer considered unsuitable for surgery.</dc:description><dc:language>en</dc:language><dc:source>15321827</dc:source><dc:subject>R1</dc:subject><dc:title>Definitive chemoradiation in patients with inoperable oesophageal carcinoma</dc:title><rioxxterms:author>Crosby, Thomas David Lewis</rioxxterms:author><rioxxterms:author>Brewster, A. E.</rioxxterms:author><rioxxterms:author>Borley, A.</rioxxterms:author><rioxxterms:author>Perschky, L.</rioxxterms:author><rioxxterms:author>Kehagioglou, Pinelopi</rioxxterms:author><rioxxterms:author>Court, J.</rioxxterms:author><rioxxterms:author>Maughan, Timothy Stanley</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1038/sj.bjc.6601461</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:110
Date: 2016-03-19

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:110</identifier>
      <datestamp>2016-03-19T22:00:22Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5231</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>The feasibility of combining gemtuzumab ozogamicin (GO) with intensive chemotherapy as first-line treatment of acute myeloid leukemia (AML) was assessed in 72 patients, aged 17 to 59 years, as a prelude to the United Kingdom Medical Research Council (MRC) AML15 trial. Sixty-four patients received induction chemotherapy (DAT [daunorubicin, ara-C, thioguanine], DA [daunorubicin, ara-C], or FLAG-Ida [fludarabine, ara-C, G-CSF, idarubicin]) with GO on day 1. It was possible to give GO 3 mg/m2 with course 1, but 6 mg/m2 with course 1 or GO in a dose of 3 mg/m2 with consecutive courses was not feasible because of hepatotoxicity and delayed hematopoietic recovery. Thirty-one patients who were treated in consolidation with MACE (amsacrine, ara-C, etoposide) or HidAC (HidAC) and GO (3 mg/m2), and 23 in induction and consolidation, tolerated GO (3 mg/m2) well. Grade 4 liver toxicity and sinusoidal obstructive syndrome was more common in thioguanine-containing schedules (P =.007). Remission with course 1 was seen in 86% of patients. DA or FLAG-Ida with GO in induction achieved complete remission in 91% of patients and 78% of these patients are in continuous complete remission at 8 months. GO given with induction (DA or FLAG-Ida) and consolidation (MACE or HidAC) was well tolerated. These schedules are now being compared in the MRC AML15 trial in patients younger than 60 years.</dc:description><dc:language>en</dc:language><dc:source>15280020</dc:source><dc:subject>R1</dc:subject><dc:title>A feasibility study of simultaneous administration of gemtuzumab ozogamicin with intensive chemotherapy in induction and consolidation in younger patients with acute myeloid leukemia</dc:title><rioxxterms:author>Kell, William Jonathan</rioxxterms:author><rioxxterms:author>Burnett, Alan Kenneth</rioxxterms:author><rioxxterms:author>Chopra, Raj</rioxxterms:author><rioxxterms:author>Yin, John A. L.</rioxxterms:author><rioxxterms:author>Clark, Richard E.</rioxxterms:author><rioxxterms:author>Rohatiner, Ama</rioxxterms:author><rioxxterms:author>Culligan, Dominic</rioxxterms:author><rioxxterms:author>Hunter, Ann</rioxxterms:author><rioxxterms:author>Prentice, Archie G.</rioxxterms:author><rioxxterms:author>Milligan, Donald W.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1182/blood-2003-05-1620</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:111
Date: 2016-03-19

RIOXX

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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:111</identifier>
      <datestamp>2016-03-19T22:00:23Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5231</setSpec>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Activating mutations of FMS-like tyrosine kinase 3 (FLT3) are present in approximately one third of patients with acute myeloid leukemia (AML) and are associated with adverse prognosis. The important role played by FLT3 in the survival and proliferation of blasts, and its overexpression in most patients with AML, make FLT3 an attractive therapeutic target. We undertook a phase 2 trial of the FLT3-selective tyrosine kinase inhibitor lestaurtinib (CEP701) used as monotherapy in untreated older patients with AML not considered fit for intensive chemotherapy, irrespective of FLT3 mutation status. Lestaurtinib was administered orally for 8 weeks, initially at a dose of 60 mg twice daily, escalating to 80 mg twice daily, and was generally well tolerated. Clinical activity, manifest as transient reductions in bone marrow and peripheral-blood blasts or longer periods of transfusion independence, was seen in 3 (60%) of 5 patients with mutated FLT3 and 5 (23%) of 22 evaluable wild-type FLT3 patients. Laboratory data demonstrated that clinical responses occurred where the presence of sustained FLT3-inhibitory drug levels were combined with in vitro cytotoxic sensitivity of blasts to lestaurtinib. Further evaluation of this compound, in combination with cytotoxic chemotherapy or other targeted agents, is warranted in both FLT3 mutant and wild-type patients.</dc:description><dc:language>en</dc:language><dc:source>15280020</dc:source><dc:subject>R1</dc:subject><dc:title>A phase 2 trial of the FLT3 inhibitor lestaurtinib (CEP701) as first-line treatment for older patients with acute myeloid leukemia not considered fit for intensive chemotherapy</dc:title><rioxxterms:author>Knapper, Steven</rioxxterms:author><rioxxterms:author>Burnett, Alan K.</rioxxterms:author><rioxxterms:author>Littlewood, Tim</rioxxterms:author><rioxxterms:author>Kell, William Jonathan</rioxxterms:author><rioxxterms:author>Agrawal, Sam</rioxxterms:author><rioxxterms:author>Chopra, Raj</rioxxterms:author><rioxxterms:author>Clark, Richard</rioxxterms:author><rioxxterms:author>Levis, Mark J.</rioxxterms:author><rioxxterms:author>Small, Donald</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1182/blood-2006-04-015560</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:112
Date: 2016-03-19

RIOXX

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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:112</identifier>
      <datestamp>2016-03-19T22:00:23Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5231</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>The receptor tyrosine kinase FLT3 is a promising molecular therapeutic target in acute myeloid leukemia (AML). Activating mutations of FLT3 are present in approximately one-third of patients, while many nonmutants show evidence of FLT3 activation, which appears to play a significant role in leukemogenesis. We studied the effects of lestaurtinib (CEP701) and PKC412, 2 small molecule inhibitors of FLT3, on 65 diagnostic AML blast samples. Both agents induced concentration-dependent cytotoxicity in most cases, although responses to PKC412 required higher drug concentrations. Cytotoxic responses were highly heterogeneous and were only weakly associated with FLT3 mutation status and FLT3 expression. Importantly, lestaurtinib induced cytotoxicity in a synergistic fashion with cytarabine, particularly in FLT3 mutant samples. Both lestaurtinib and PKC412 caused inhibition of FLT3 phosphorylation in all samples. Translation of FLT3 inhibition into cytotoxicity was influenced by the degree of residual FLT3 phosphorylation remaining and correlated with deactivation of STAT5 and MAP kinase. FLT3 mutant and wild-type cases both varied considerably in their dependence on FLT3 signaling for survival. These findings support the continued clinical assessment of FLT3 inhibitors in combination with cytotoxic chemotherapy: Entry to future clinical trials should include FLT3 wild-type patients and should remain unrestricted by FLT3 expression level.</dc:description><dc:language>en</dc:language><dc:source>15280020</dc:source><dc:subject>R1</dc:subject><dc:title>The effects of lestaurtinib (CEP701) and PKC412 on primary AML blasts: the induction of cytotoxicity varies with dependence on FLT3 signaling in both FLT3-mutated and wild-type cases</dc:title><rioxxterms:author>Knapper, Steven</rioxxterms:author><rioxxterms:author>Mills, Kenneth I.</rioxxterms:author><rioxxterms:author>Gilkes, Amanda F.</rioxxterms:author><rioxxterms:author>Austin, Steve J.</rioxxterms:author><rioxxterms:author>Walsh, Valerie</rioxxterms:author><rioxxterms:author>Burnett, Alan K.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1182/blood-2006-04-015487</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:116
Date: 2016-03-19

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:116</identifier>
      <datestamp>2016-03-19T22:00:23Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5231</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>The optimum chemotherapy schedule for reinduction of patients with high-risk acute myeloid leukemia (relapsed, resistant/refractory, or adverse genetic disease) is uncertain. The MRC AML (Medical Research Council Acute Myeloid Leukemia) Working Group designed a trial comparing fludarabine and high-dose cytosine (FLA) with standard chemotherapy comprising cytosine arabinoside, daunorubicin, and etoposide (ADE). Patients were also randomly assigned to receive filgrastim (G-CSF) from day 0 until neutrophil count was greater than 0.5 x 109/L (or for a maximum of 28 days) and all-trans retinoic acid (ATRA) for 90 days. Between 1998 and 2003, 405 patients were entered: 250 were randomly assigned between FLA and ADE; 356 to G-CSF versus no G-CSF; 362 to ATRA versus no ATRA. The complete remission rate was 61% with 4-year disease-free survival of 29%. There were no significant differences in the CR rate, deaths in CR, relapse rate, or DFS between ADE and FLA, although survival at 4 years was worse with FLA (16% versus 27%, P = .05). Neither the addition of ATRA nor G-CSF demonstrated any differences in the CR rate, relapse rate, DFS, or overall survival between the groups. In conclusion these findings indicate that FLA may be inferior to standard chemotherapy in high-risk AML and that the outcome is not improved with the addition of either G-CSF or ATRA.</dc:description><dc:language>en</dc:language><dc:source>15280020</dc:source><dc:subject>R1</dc:subject><dc:title>Fludarabine and cytosine are less effective than standard ADE chemotherapy in high-risk acute myeloid leukemia, and addition of G-CSF and ATRA are not beneficial: results of the MRC AML-HR randomized trial</dc:title><rioxxterms:author>Milligan, Donald W.</rioxxterms:author><rioxxterms:author>Wheatley, Keith</rioxxterms:author><rioxxterms:author>Littlewood, Timothy</rioxxterms:author><rioxxterms:author>Craig, Jenny I. O.</rioxxterms:author><rioxxterms:author>Burnett, Alan Kenneth</rioxxterms:author><rioxxterms:author>NCRI Haematological Oncology Clinical Studies Group</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1182/blood-2005-10-4202</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:118
Date: 2016-03-19

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:118</identifier>
      <datestamp>2016-03-19T22:00:24Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5231</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>EB1089, a novel vitamin D3 analog, has been shown to have cytotoxic and antiproliferative properties in a variety of malignant cells. However, its potential as a treatment for B-cell chronic lymphocytic leukemia (B-CLL) has not been evaluated. EB1089 induced apoptosis in all of the 102 B-CLL samples tested with a mean LD50 (the concentration of EB1089 required to kill 50% of cells) value (</dc:description><dc:language>en</dc:language><dc:relation>http://bloodjournal.hematologylibrary.org/cgi/reprint/101/7/2454</dc:relation><dc:source>15280020</dc:source><dc:subject>R1</dc:subject><dc:title>The vitamin D3 analog EB1089 induces apoptosis via a p53-independent mechanism involving p38 MAP kinase activation and suppression of ERK activity in B-cell chronic lymphocytic leukemia cells in vitro</dc:title><rioxxterms:author>Pepper, Christopher John</rioxxterms:author><rioxxterms:author>Thomas, Alun</rioxxterms:author><rioxxterms:author>Hoy, Terence George</rioxxterms:author><rioxxterms:author>Milligan, Donald</rioxxterms:author><rioxxterms:author>Bentley, Paul</rioxxterms:author><rioxxterms:author>Fegan, Christopher Daniel</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1182/blood-2002-07-1984</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:119
Date: 2016-03-19

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:119</identifier>
      <datestamp>2016-03-19T22:00:24Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5231</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Li Fraumeni syndrome (LFS) is characterised by a predisposition to the early onset of certain tumors and is associated with germline mutation of the anti-oncogene p53. In this study we analysed the in vitro responses of lymphocytes from two LFS patients to chemotherapeutic drugs in terms of apoptosis induction and the expression of key intracellular proteins that regulate this process. One of the LFS patients also suffered from B-cell chronic lymphocytic leukemia (B-CLL) and hence presented with a light-chain restricted B-cell lymphocytosis while the other patient had entirely normal blood counts. The&#13;
B-lymphocytes from both LFS patients showed a marked degree of resistance to chlorambucil and fludarabine when compared to age-matched controls but were remarkably sensitive&#13;
to the novel flavone, flavopiridol. Loss of function of p53 was demonstrated by a failure to induce Bax and p21 protein expression. In addition, altered basal expression patterns&#13;
of Bcl-2 and Bax, two key regulators of apoptosis, were found in the LFS lymphocytes when compared with controls. These results suggest that LFS lymphocytes carrying a p53&#13;
mutation show intrinsic resistance to conventional chemotherapeutic drugs and this is associated with dysregulation of Bcl-2 family proteins. Furthermore, The innate resistance profile was similar in leukemic and non-leukemic lymphocytes and was therefore independent&#13;
of genetic changes acquired during malignant transformation. Novel agents that induce p53-independent cell killing may be useful not only in the treatment of LFS-associated tumors but also drug resistant tumors in general where p53 and/or Bcl-2 family dysregulation is a feature.</dc:description><dc:language>en</dc:language><dc:source>1551-4005</dc:source><dc:subject>R1</dc:subject><dc:title>Leukemic and non-leukemic lymphocytes from patients with Li Fraumeni syndrome demonstrate loss of p53 function, Bcl-2 family dysregulation and intrinsic resistance to conventional chemotherapeutic drugs but not flavopiridol</dc:title><rioxxterms:author>Pepper, Christopher John</rioxxterms:author><rioxxterms:author>Thomas, Alun</rioxxterms:author><rioxxterms:author>Hoy, Terence George</rioxxterms:author><rioxxterms:author>Tighe, Jane</rioxxterms:author><rioxxterms:author>Culligan, Dominic</rioxxterms:author><rioxxterms:author>Fegan, Christopher Daniel</rioxxterms:author><rioxxterms:author>Bentley, Paul</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:122
Date: 2016-02-12

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:122</identifier>
      <datestamp>2016-02-12T22:00:23Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5243:524330323534</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Summary. Familial adenomatous polyposis (FAP) and attenuated FAP are autosomal dominant disorders characterised by multiple colorectal adenomas and cancers. Both are caused by inherited mutations in the APC gene, and management includes genetic testing, colonoscopic surveillance, and prophylactic surgery for the relatives of index cases. Among 614 families recorded in six regional registers of polyposis in the UK, we identified 111 with neither dominant transmission nor evidence of APC mutation. Molecular genetic analysis showed that 25 had biallelic mutations of the MYH gene. Since our data show that MYH polyposis can be transmitted as an autosomal recessive trait, a change in genetic counselling, testing, and surveillance is needed.</dc:description><dc:language>en</dc:language><dc:publisher>Elsevier</dc:publisher><dc:source>0140-6736</dc:source><dc:subject>RC0254</dc:subject><dc:title>Autosomal recessive colorectal adenomatous polyposis due to inherited mutations of MYH</dc:title><rioxxterms:author>Sampson, Julian Roy</rioxxterms:author><rioxxterms:author>Dolwani, Sunil</rioxxterms:author><rioxxterms:author>Jones, Sian</rioxxterms:author><rioxxterms:author>Eccles, Diana</rioxxterms:author><rioxxterms:author>Ellis, Anthony</rioxxterms:author><rioxxterms:author>Evans, D. Gareth</rioxxterms:author><rioxxterms:author>Frayling, Ian Martin</rioxxterms:author><rioxxterms:author>Jordan, Sheila</rioxxterms:author><rioxxterms:author>Maher, Eamonn R.</rioxxterms:author><rioxxterms:author>Mak, Tony</rioxxterms:author><rioxxterms:author>Maynard, Julie Helen</rioxxterms:author><rioxxterms:author>Pigatto, Francesca</rioxxterms:author><rioxxterms:author>Shaw, Joan</rioxxterms:author><rioxxterms:author>Cheadle, Jeremy Peter</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/S0140-6736(03)13805-6</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:123
Date: 2016-10-21

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    <header>
      <identifier>oai:http://orca.cf.ac.uk:123</identifier>
      <datestamp>2016-10-21T01:30:29Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:language>en</dc:language><dc:source>1476-5594</dc:source><dc:title>Apc deficiency predisposes to renal carcinoma in the mouse</dc:title><rioxxterms:author>Sansom, Owen J.</rioxxterms:author><rioxxterms:author>Griffiths, David Francis Rees</rioxxterms:author><rioxxterms:author>Reed, Karen Ruth</rioxxterms:author><rioxxterms:author>Winton, Douglas J.</rioxxterms:author><rioxxterms:author>Clarke, Alan Richard</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1038/sj.onc.1208956</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:128
Date: 2016-03-19

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:128</identifier>
      <datestamp>2016-03-19T22:00:25Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5231</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:language>en</dc:language><dc:source>15376605</dc:source><dc:subject>R1</dc:subject><dc:title>An absence of cutaneous neurofibromas associated with a 3-bp inframe deletion in exon 17 of the NF1 gene (c.2970-2972 delAAT): evidence of a clinically significant NF1 genotype-phenotype correlation</dc:title><rioxxterms:author>Upadhyaya, Meena</rioxxterms:author><rioxxterms:author>Huson, Susan M.</rioxxterms:author><rioxxterms:author>Davies, Mark</rioxxterms:author><rioxxterms:author>Thomas, Nicholas Stuart Tudor</rioxxterms:author><rioxxterms:author>Chuzhanova, Nadia</rioxxterms:author><rioxxterms:author>Giovannini, S.</rioxxterms:author><rioxxterms:author>Evans, D. Gareth</rioxxterms:author><rioxxterms:author>Howard, E.</rioxxterms:author><rioxxterms:author>Kerr, B.</rioxxterms:author><rioxxterms:author>Griffiths, S.</rioxxterms:author><rioxxterms:author>Consoli, Claudia</rioxxterms:author><rioxxterms:author>Side, L.</rioxxterms:author><rioxxterms:author>Adams, D.</rioxxterms:author><rioxxterms:author>Pierpont, M.</rioxxterms:author><rioxxterms:author>Hachen, R.</rioxxterms:author><rioxxterms:author>Barnicoat, A.</rioxxterms:author><rioxxterms:author>Liu, H.</rioxxterms:author><rioxxterms:author>Wallace, P.</rioxxterms:author><rioxxterms:author>Van Biervliet, J. P.</rioxxterms:author><rioxxterms:author>Stevenson, D.</rioxxterms:author><rioxxterms:author>Viskochil, D.</rioxxterms:author><rioxxterms:author>Baralle, D.</rioxxterms:author><rioxxterms:author>Haan, E.</rioxxterms:author><rioxxterms:author>Riccardi, V.</rioxxterms:author><rioxxterms:author>Turnpenny, P.</rioxxterms:author><rioxxterms:author>Lazaro, C.</rioxxterms:author><rioxxterms:author>Messiaen, Ludwine</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1086/510781</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:129
Date: 2016-03-19

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:129</identifier>
      <datestamp>2016-03-19T22:00:25Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Malignant peripheral nerve sheath tumours (MPNSTs) are a major cause of mortality in patients with neurofibromatosis 1 (NF1). We have analysed lymphocyte DNA samples from 30 NF1 patients with MPNSTs to determine their underlying constitutional NF1 gene mutations. Mutations were detected in 27/30 (90%) of these patients. NF1 mutations identified included nonsense, missense, frameshift, splice site mutation and single or multi-exonic deletions and with no obvious clustering of the mutations across the gene. Fourteen of the mutations represent novel gene changes. There did not appear to be any relationship between the mutation type and the level of clinical severity observed. Of the 20 patients with high grade MPNSTs, seven patients had small (&lt;20bp) and multi-exonic deletions and three had small insertions (&lt;20bp). Several studies have suggested that NF1 patients with a constitutional 1.5 Mb deletion of the NF1 gene have an increased risk of developing malignant peripheral nerve sheath tumours (MPNSTs). None of our patients had a 1.5 Mb deletion. Larger prospective studies are needed to ascertain whether there is a different spectrum of NF1 mutations in NF1 patients with high grade compared to low grade MPNSTs and of patients with the 1.5Mb deletion, in order to determine the true frequency of MPNST in this sub-group of NF1 patients. © 2006 Wiley-Liss, Inc.</dc:description><dc:language>en</dc:language><dc:publisher>Wiley-Blackwell</dc:publisher><dc:source>1098-1004</dc:source><dc:title>The heterogeneous nature of germline mutations in NF1 patients with malignant peripheral serve sheath tumours (MPNSTs)</dc:title><rioxxterms:author>Upadhyaya, Meena</rioxxterms:author><rioxxterms:author>Spurlock, Gillian</rioxxterms:author><rioxxterms:author>Majounie, Elisa</rioxxterms:author><rioxxterms:author>Griffiths, Sian</rioxxterms:author><rioxxterms:author>Forrester, Natalie</rioxxterms:author><rioxxterms:author>Baser, Mike</rioxxterms:author><rioxxterms:author>Huson, Susan M.</rioxxterms:author><rioxxterms:author>Evans, Gareth</rioxxterms:author><rioxxterms:author>Ferner, Rosalie</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1002/humu.9429</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:130
Date: 2016-03-19

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:130</identifier>
      <datestamp>2016-03-19T22:00:25Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Tuberous sclerosis complex (TSC) is an autosomal dominant disorder caused by mutations in either the TSC1 or the TSC2 genes and characterized by the development of benign hamartomatous growths in multiple organ systems. We have inactivated Tsc1 in the mouse germ line by gene targeting in ES cells and confirmed that the mutant allele (Tsc1−) has a recessive embryonic lethal phenotype. We found that a significant number (∼27%) of heterozygous (Tsc1+/−) mice on the C57BL/6 background died before weaning (P=0.014) and show that these mice die in the post-natal period (P=0.033), normally at 1–2 days, from unknown causes. Forty-four percent (7/16) of Tsc1+/− mice on a C3H background developed macroscopically visible renal lesions as early as 3–6 months, increasing to 95% (37/39) by 15–18 months. Renal lesions progressed from cysts through cystadenomas to solid carcinomas. Eighty percent (16/20) of Tsc1+/− mice on a Balb/c background exhibited solid renal cell carcinomas (RCC) by 15–18 months and in 41%, RCCs were ≥5 mm, resulting in grossly deformed kidneys. Some RCCs had a sarcomatoid morphology of spindle cells in whorled patterns and metastasized to the lungs. We detected loss of the wild-type Tsc1 allele and elevated levels of p-mTOR and p-S6 in lesions from Tsc1+/− mice. This new murine model of hamartin deficiency exhibits a more severe phenotype than existing models.</dc:description><dc:language>en</dc:language><dc:publisher>Oxford University Press</dc:publisher><dc:source>0964-6906</dc:source><dc:subject>R1</dc:subject><dc:title>A mouse model of tuberous sclerosis 1 showing background specific early post-natal mortality and metastatic renal cell carcinoma</dc:title><rioxxterms:author>Wilson, Catherine Helen</rioxxterms:author><rioxxterms:author>Idziaszczyk, Shelley Alexis</rioxxterms:author><rioxxterms:author>Parry, Lee</rioxxterms:author><rioxxterms:author>Guy, Carol</rioxxterms:author><rioxxterms:author>Griffiths, David Francis Rees</rioxxterms:author><rioxxterms:author>Lazda, Edgar Janis</rioxxterms:author><rioxxterms:author>Bayne, Rosemary A. L.</rioxxterms:author><rioxxterms:author>Smith, Andrew J. H.</rioxxterms:author><rioxxterms:author>Sampson, Julian Roy</rioxxterms:author><rioxxterms:author>Cheadle, Jeremy Peter</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1093/hmg/ddi190</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:131
Date: 2016-04-07

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    <header>
      <identifier>oai:http://orca.cf.ac.uk:131</identifier>
      <datestamp>2016-04-07T07:21:34Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Introduction: Matrilysin (MMP-7) is a metalloproteinase that is involved in the degradation of extracellular matrix, invasion, and tumor progression. The current study examined if targeting matrilysin using retroviral ribozyme transgenes may have an impact on breast cancer cells and may have clinical implications. &#13;
&#13;
Experimental Design: Retroviral hammerhead ribozyme transgenes were designed to specifically target human matrilysin mRNA. The breast cancer cell MDA-MB-231 was transfected with either a retroviral matrilysin transgene or a control retroviral transgene. Stably transfected cells were tested for their invasiveness and migratory properties in vitro. The cells were also used in creating a tumor model in athymic nude mice in which the growth of tumors and levels of matrilysin were assessed. In addition, levels of both protein and mRNA of matrilysin were investigated in a cohort of human breast tumors. &#13;
&#13;
Results: Expression of matrilysin in MDA-MB-231 was successfully eliminated by the retroviral hammerhead ribozyme transgene for matrilysin as revealed by reverse transcription-PCR. Matrilysin transgene–transduced cancer cells (MDA-MB-231?Matrilysin) exhibited a significantly lower degree of invasion (number of invading cells 16.0 ± 2.5) compared with wild type (MDA-MB-231WT; 26.2 ± 6.2, P &lt; 0.05) or control transgene-transduced cancer cells (MDA-MB-231pRevTRE; 25.3 ± 4.2, P &lt; 0.01). However, the rate of growth of the cells in vitro was not significantly affected. In the in vivo tumor model, MDA-MB-231?Matrilysin tumors, which had very low levels of immunoreactive matrilysin, grew at a significantly lower rate (0.24 ± 0.03 cm3, 4 weeks after inoculation) compared with the wild-type MDA-MB-231WT (1.46 ± 0.04 cm3) and MDA-MB-231pRevTRE (1.12 ± 1.0 cm3) tumors. In human breast tumors, breast cancer cells stained matrilysin at a significantly higher density, compared with normal mammary epithelium. The highest level of matrilysin was seen in high-grade tumors and that from patients with moderate and poor prognosis. Finally, high levels of matrilysin were significantly linked with a poor long-term survival (P = 0.0143). &#13;
&#13;
Conclusion: Matrilysin, which is aberrantly expressed in human breast tumors, can be effectively eliminated from breast cancer cells by way of hammerhead ribozyme transgene. Elimination of matrilysin is associated with low invasiveness and slow tumor growth. Taken together, the study suggests that targeting matrilysin may have important therapeutic implications.</dc:description><dc:language>en</dc:language><dc:source>1557-3265</dc:source><dc:subject>R1</dc:subject><dc:title>Targeting matrilysin and its impact on tumor growth in vivo: the potential implications in breast cancer therapy</dc:title><rioxxterms:author>Jiang, Wen Guo</rioxxterms:author><rioxxterms:author>Davies, Gaynor</rioxxterms:author><rioxxterms:author>Martin, Tracey Amanda</rioxxterms:author><rioxxterms:author>Parr, Christian</rioxxterms:author><rioxxterms:author>Watkins, Gareth</rioxxterms:author><rioxxterms:author>Mason, Malcolm David</rioxxterms:author><rioxxterms:author>Mokbel, Kefah</rioxxterms:author><rioxxterms:author>Mansel, Robert Edward</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1158/1078-0432.CCR-05-0275</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:133
Date: 2016-03-19

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    <header>
      <identifier>oai:http://orca.cf.ac.uk:133</identifier>
      <datestamp>2016-03-19T22:00:26Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Diffuse malignant pleural mesothelioma (MPM) is the third most common lung malignancy showing rising incidence with 250,000 deaths expected from it in Western Europe over the next 35 year. The tumour is generally resistant to conventional treatment and there is urgent need for novel preventative and therapeutic measures to combat this growing public threat. Finding of SV40 DNA sequences in a high proportion (40–90%) of several series of MPM cases, and suggestion of its potential co-carcinogen role provide a rationale for the development of novel anti-MPM vaccines incorporating SV40 gene sequences or antigenic determinants. As a prelude to adopting this approach, general T cell function was examined in relatively early cases of MPM presenting for biopsy or debulking surgery. CD8+ T cell responses were studied using antigenic epitopes of common viral antigens covering a broad range of haplotypes. 74.1% (20/27) of MPM patients and 80% (8/10) of the control subjects showed T cell responsiveness to the viral peptides mix, whilst a small proportion showed SV40 specific recall immunity.</dc:description><dc:language>en</dc:language><dc:source>0264-410X</dc:source><dc:subject>R1</dc:subject><dc:title>Assessment of immunological competence and SV40 specific recall immunity in malignant pleural mesothelioma</dc:title><rioxxterms:author>Jasani, Bharat</rioxxterms:author><rioxxterms:author>Coleman, Sharon Louise</rioxxterms:author><rioxxterms:author>Butchart, Eric</rioxxterms:author><rioxxterms:author>Evans, Eve M.L.</rioxxterms:author><rioxxterms:author>Adams, Malcolm</rioxxterms:author><rioxxterms:author>Mason, Malcolm David</rioxxterms:author><rioxxterms:author>Gibbs, Allen</rioxxterms:author><rioxxterms:author>Tabi, Zsuzsanna</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/j.vaccine.2005.01.019</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:137
Date: 2016-03-19

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      <identifier>oai:http://orca.cf.ac.uk:137</identifier>
      <datestamp>2016-03-19T22:00:26Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:language>en</dc:language><dc:publisher>Oxford University Press</dc:publisher><dc:source>1460-2083</dc:source><dc:title>Biallelic germline mutations in MYH predispose to multiple colorectal ademona and somatic G:C to T:A mutations</dc:title><rioxxterms:author>Jones, Sian</rioxxterms:author><rioxxterms:author>Emmerson, Paul</rioxxterms:author><rioxxterms:author>Maynard, Julie Helen</rioxxterms:author><rioxxterms:author>Best, Jacqueline M.</rioxxterms:author><rioxxterms:author>Jordan, Sheila</rioxxterms:author><rioxxterms:author>Williams, Geraint Trefor</rioxxterms:author><rioxxterms:author>Sampson, Julian Roy</rioxxterms:author><rioxxterms:author>Cheadle, Jeremy Peter</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1093/hmg/11.23.2961</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:138
Date: 2016-03-19

RIOXX

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      <identifier>oai:http://orca.cf.ac.uk:138</identifier>
      <datestamp>2016-03-19T22:00:27Z</datestamp>
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      <setSpec>7375626A656374733D52:5231</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Late-onset erythropoietic protoporphyria (EPP) is a rare complication of myelodysplastic syndrome (MDS) but has not been described in association with a myeloproliferative disorder (MPD). EPP is normally an inherited disorder characterized by photosensitivity that starts in early childhood and results from overproduction of protoporphyrin secondary to ferrochelatase (FECH) deficiency. Severe liver disease occurs in 1% to 2% of patients. Here we report that severe photosensitivity and cholestatic liver disease in a patient with a myeloproliferative disorder was caused by excess protoporphyrin production from a clone of hematopoietic cells in which one FECH allele had been deleted. Our observations suggest that the usual explanation for the association of late-onset EPP with MPD and MDS is acquired somatic mutation of one FECH allele in bone marrow and show for the first time that the consequent overproduction of protoporphyrin may be severe enough to cause acute liver damage.</dc:description><dc:language>en</dc:language><dc:source>1528-0020</dc:source><dc:subject>R1</dc:subject><dc:title>Photosensitivity and acute liver injury in myeloproliferative disorder secondary to late-onset protoporphyria caused by deletion of a ferrochelastase gene in hematopoietic cells</dc:title><rioxxterms:author>Goodwin, Richard G.</rioxxterms:author><rioxxterms:author>Kell, William Jonathan</rioxxterms:author><rioxxterms:author>Laidler, Peter</rioxxterms:author><rioxxterms:author>Long, C. Colin</rioxxterms:author><rioxxterms:author>Whatley, Sharon D.</rioxxterms:author><rioxxterms:author>McKinley, Mark</rioxxterms:author><rioxxterms:author>Badminton, Michael Norman</rioxxterms:author><rioxxterms:author>Burnett, Alan Kenneth</rioxxterms:author><rioxxterms:author>Williams, Geraint Trefor</rioxxterms:author><rioxxterms:author>Elder, George Hill</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1182/blood-2004-12-4939</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:140
Date: 2016-02-12

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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
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ali:license_refMinimum of 1 value(s) required for ali:license_ref - found 0 values
<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:140</identifier>
      <datestamp>2016-02-12T22:00:25Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5231</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Biallelic inherited mutations of the MYH gene (also known as MutYH or human MutY homologue) are associated with multiple colorectal adenomas and a high risk of colorectal cancer that approaches 100%.1,2 This recessive disorder has become known as MYH-associated polyposis (MAP) to distinguish it from dominantly inherited familial adenomatous polyposis. The risk of colorectal cancer in heterozygotes seems to be only marginally increased, if at all.2 During a review of the Wales Polyposis Register we noted that although only 4 of the 115 recorded families were of Asian origin, all four had MAP. This was in contrast to the 111 indigenous families, only 12 of which had MAP. All affected members of three unrelated British Indian families were homozygous for the mutation E466X and one patient of Pakistani descent was homozygous for Y90X.3 These mutations have not been observed in other ethnic groups. As the overall incidence of colorectal cancer among Asians living in England and Wales is markedly below that of the general population,4 we postulated that MYH mutations might contribute more significantly to colorectal cancer among British Asians than among indigenous northern Europeans. We conducted a retrospective study to assess the contribution of MYH mutations to colorectal cancer among British Asians.</dc:description><dc:language>en</dc:language><dc:publisher>BMJ Publishing Group Ltd</dc:publisher><dc:relation>http://gut.bmj.com/content/56/4/593.1.full.pdf+html</dc:relation><dc:source>0017-5749</dc:source><dc:subject>R1</dc:subject><dc:title>Analysis of inherited MYH (MUTYH) mutations in British Asian patients with colorectal cancer [Letter]</dc:title><rioxxterms:author>Dolwani, Sunil</rioxxterms:author><rioxxterms:author>Williams, Geraint Trefor</rioxxterms:author><rioxxterms:author>West, K.P.</rioxxterms:author><rioxxterms:author>Newman, J.</rioxxterms:author><rioxxterms:author>Stock, D.</rioxxterms:author><rioxxterms:author>Williams, A.P.</rioxxterms:author><rioxxterms:author>Best, J.</rioxxterms:author><rioxxterms:author>Cheadle, Jeremy Peter</rioxxterms:author><rioxxterms:author>Sampson, Julian Roy</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1136/gut.2006.094532</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:141
Date: 2016-12-13

RIOXX

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RCUK-RIOXX

RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
This is not a valid RCUK-RIOXX record
PropertyError
rioxxterms:projectMinimum of 1 value(s) required for rioxxterms:project - found 0 values
dcterms:dateAcceptedMinimum of 1 value(s) required for dcterms:dateAccepted - found 0 values
dc:identifierMinimum of 1 value(s) required for dc:identifier - found 0 values
ali:license_refMinimum of 1 value(s) required for ali:license_ref - found 0 values
<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:141</identifier>
      <datestamp>2016-12-13T02:32:10Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>BACKGROUND: Sentinel lymph node biopsy in women with operable breast cancer is routinely used in some countries for staging the axilla despite limited data from randomized trials on morbidity and mortality outcomes. We conducted a multicenter randomized trial to compare quality-of-life outcomes between patients with clinically node-negative invasive breast cancer who received sentinel lymph node biopsy and patients who received standard axillary treatment. METHODS: The primary outcome measures were arm and shoulder morbidity and quality of life. From November 1999 to October 2003, 1031 patients were randomly assigned to undergo sentinel lymph node biopsy (n = 515) or standard axillary surgery (n = 516). Patients with sentinel lymph node metastases proceeded to delayed axillary clearance or received axillary radiotherapy (depending on the protocol at the treating institution). Intention-to-treat analyses of data at 1, 3, 6, and 12 months after surgery are presented. All statistical tests were two-sided. RESULTS: The relative risks of any lymphedema and sensory loss for the sentinel lymph node biopsy group compared with the standard axillary treatment group at 12 months were 0.37 (95% confidence interval [CI] = 0.23 to 0.60; absolute rates: 5% versus 13%) and 0.37 (95% CI = 0.27 to 0.50; absolute rates: 11% versus 31%), respectively. Drain usage, length of hospital stay, and time to resumption of normal day-to-day activities after surgery were statistically significantly lower in the sentinel lymph node biopsy group (all P &lt; .001), and axillary operative time was reduced (P = .055). Overall patient-recorded quality of life and arm functioning scores were statistically significantly better in the sentinel lymph node biopsy group throughout (all P &lt; or = .003). These benefits were seen with no increase in anxiety levels in the sentinel lymph node biopsy group (P &gt; .05). CONCLUSION: Sentinel lymph node biopsy is associated with reduced arm morbidity and better quality of life than standard axillary treatment and should be the treatment of choice for patients who have early-stage breast cancer with clinically negative nodes.</dc:description><dc:language>en</dc:language><dc:publisher>Oxford University Press</dc:publisher><dc:source>1460-2105</dc:source><dc:title>Randomized multicentre trial of sentinal node biopsy versus standard axillary treatment in operable breast cancer:  The ALMANAC Trial</dc:title><rioxxterms:author>Mansel, Robert Edward</rioxxterms:author><rioxxterms:author>Fallowfield, Lesley</rioxxterms:author><rioxxterms:author>Kissin, Mark</rioxxterms:author><rioxxterms:author>Goyal, Amit</rioxxterms:author><rioxxterms:author>Newcombe, Robert Gordon</rioxxterms:author><rioxxterms:author>Dixon, J. Michael</rioxxterms:author><rioxxterms:author>Yiangou, Constantinos</rioxxterms:author><rioxxterms:author>Horgan, Kieran</rioxxterms:author><rioxxterms:author>Bundred, Nigel</rioxxterms:author><rioxxterms:author>Monypenny, Ian</rioxxterms:author><rioxxterms:author>England, David</rioxxterms:author><rioxxterms:author>Sibbering, Mark</rioxxterms:author><rioxxterms:author>Abdullah, Tholkifl I.</rioxxterms:author><rioxxterms:author>Barr, Lester</rioxxterms:author><rioxxterms:author>Chetty, Utheshtra</rioxxterms:author><rioxxterms:author>Sinnett, Dudley H.</rioxxterms:author><rioxxterms:author>Fleissig, Anne</rioxxterms:author><rioxxterms:author>Clarke, Dayalan</rioxxterms:author><rioxxterms:author>Ell, Peter J.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1093/jnci/djj158</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:142
Date: 2016-03-19

RIOXX

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This is not a valid RIOXX record
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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
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rioxxterms:projectMinimum of 1 value(s) required for rioxxterms:project - found 0 values
dcterms:dateAcceptedMinimum of 1 value(s) required for dcterms:dateAccepted - found 0 values
dc:identifierMinimum of 1 value(s) required for dc:identifier - found 0 values
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:142</identifier>
      <datestamp>2016-03-19T22:00:27Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5231</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Hepatocyte growth factor/scatter factor (HGF/SF) is a cytokine primarily produced by stromal fibroblasts and is a known angiogenic and invasion-inducing factor. It is increased in patients with breast cancer. This study examined the effect of NK4, a newly described HGF/SF antagonist, on HGF/SF-promoted growth of a human breast cancer. Both in vitro (invasion and migration assays) and in vivo (murine tumour model) methods were used to ascertain the effect of NK4 on HGF/SF from two sources: human fibroblast-derived HGF/SF and recombinant HGF/SF. In the in vitro invasion assay and migration assay, both HGF/SF and human fibroblasts, which secrete bioactive HGF/SF, increased the invasiveness and migration of the breast cancer cells (MDA MB 231). NK4 significantly reduced this invasiveness and motility. In the animal model, tumour volume and weight was significantly reduced with addition of NK4. It also suppressed HGF/SF-induced growth and markedly retarded tumour growth induced by fibroblasts (MRC5), secreting bioactive HGF/SF. Tumour angiogenesis was assessed by immunohistochemical staining of primary tissue sections using VE-cadherin (an endothelial cell specific cell–cell adhesion molecule). Again, NK4 reduced the effects of both HGF/SF and fibroblasts. We conclude that NK4 has a significant effect on the growth of human breast tumours in nude mice, particularly when stimulated by HGF/SF or fibroblasts. This may occur by decreasing angiogenesis. This gives a clear indication of the therapeutic worth of NK4.</dc:description><dc:language>en</dc:language><dc:source>1460-2180</dc:source><dc:subject>R1</dc:subject><dc:title>Growth and angiogenesis of human breast cancer in a nude mouse tumour model is reduced by NK4, a HGF/SF antagonist</dc:title><rioxxterms:author>Martin, Tracey Amanda</rioxxterms:author><rioxxterms:author>Parr, Christian</rioxxterms:author><rioxxterms:author>Davies, Gaynor</rioxxterms:author><rioxxterms:author>Watkins, Gareth</rioxxterms:author><rioxxterms:author>Lane, Jane</rioxxterms:author><rioxxterms:author>Matsumoto, Kunio</rioxxterms:author><rioxxterms:author>Nakamura, T.</rioxxterms:author><rioxxterms:author>Mansel, Robert Edward</rioxxterms:author><rioxxterms:author>Jiang, Wen Guo</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1093/carcin/bgg072</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:143
Date: 2016-03-19

RIOXX

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RCUK-RIOXX

RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
This is not a valid RCUK-RIOXX record
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rioxxterms:projectMinimum of 1 value(s) required for rioxxterms:project - found 0 values
dcterms:dateAcceptedMinimum of 1 value(s) required for dcterms:dateAccepted - found 0 values
dc:identifierMinimum of 1 value(s) required for dc:identifier - found 0 values
ali:license_refMinimum of 1 value(s) required for ali:license_ref - found 0 values
<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:143</identifier>
      <datestamp>2016-03-19T22:00:28Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5231</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>In this study, the effect of a prior UV irradiation on the removal of cyclobutane pyrimidine dimers (CPDs) from the transcribed strand (TS) and non-transcribed strand (NTS) of the MFA2 gene in haploid Saccharomyces cerevisiae (S. cerevisiae) cells was investigated. In NER competent cells, the pre-irradiation with a dose of 20 J/m2 enhances the removal of CPDs induced by a second UV dose of 100 J/m2 in the TS and the NTS of MFA2 gene except for the CPDs in the region +258 to +298 in the NTS, where the enhanced repair was absent. No inducible repair was observed in rad9, rad24, rad16 and rad26 cells, indicating two checkpoint genes RAD9 and RAD24, the global repair gene RAD16 and the transcription coupled repair gene RAD26 are essential for inducible NER.</dc:description><dc:language>en</dc:language><dc:source>0921-8777</dc:source><dc:subject>R1</dc:subject><dc:title>RAD9, RAD24, RAD16 and RAD26 are required for the inducible nucleotide excision repair of UV-induced cyclobutane pyrimidine dimmers from the transcribed and non-transcribed regions of the Sacchoromyces cerevisiae MFA2 gene</dc:title><rioxxterms:author>Yu, Shirong</rioxxterms:author><rioxxterms:author>Teng, Yumin</rioxxterms:author><rioxxterms:author>Lowndes, Noel F.</rioxxterms:author><rioxxterms:author>Waters, Raymond</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/S0921-8777(01)00061-1</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:146
Date: 2016-03-19

RIOXX

Base RIOXX scheme designed for low-level interoperability
This is not a valid RIOXX record
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dc:identifierMinimum of 1 value(s) required for dc:identifier - found 0 values

RCUK-RIOXX

RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
This is not a valid RCUK-RIOXX record
PropertyError
rioxxterms:projectMinimum of 1 value(s) required for rioxxterms:project - found 0 values
dcterms:dateAcceptedMinimum of 1 value(s) required for dcterms:dateAccepted - found 0 values
dc:identifierMinimum of 1 value(s) required for dc:identifier - found 0 values
ali:license_refMinimum of 1 value(s) required for ali:license_ref - found 0 values
<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:146</identifier>
      <datestamp>2016-03-19T22:00:28Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>7375626A656374733D52:5231</setSpec>
      <setSpec>74797065733D6D6F6E6F6772617068</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>In yeast, global genome nucleotide-excision repair (GG-NER) requires a protein complex containing Rad7 and Rad16. Rad16 is a member of the switch/sucrose nonfermentable superfamily, and it is presumed that chromatin remodelling is its primary function during repair. We show that RAD16 is required for ultraviolet-dependent hyperacetylation of histone H3 (Lys 9 and Lys 14) at the MFA2 promoter and throughout the genome. The yeast repressor complex Ssn6-Tup1 represses many genes including MFA2. TUP1 deletion results in constitutive hyperacetylation of histone H3, nucleosome disruption and derepression of gene transcription in Tup1-regulated genes. GG-NER in the MFA2 promoter proceeds more rapidly in tup1Delta alpha-cells compared with wild type, even when transcription is inhibited. We show that elevated histone H3 acetylation levels in the MFA2 promoter in tup1Delta alpha-cells result in Rad7- and Rad16-independent GG-NER, and that Rad16 mediates the ultraviolet-induced acetylation of histone H3, necessary for efficient GG-NER.</dc:description><dc:language>en</dc:language><dc:publisher>EMBO Reports</dc:publisher><dc:source>1469-221X</dc:source><dc:subject>R1</dc:subject><dc:title>Saccharomyces cerevisiae Rad16 mediates UV dependent histone H3 acetylation required for efficient global genome nucleotide excision repair</dc:title><rioxxterms:author>Teng, Yumin</rioxxterms:author><rioxxterms:author>Liu, Hairong</rioxxterms:author><rioxxterms:author>Gill, Hefin</rioxxterms:author><rioxxterms:author>Yu, Yachuan</rioxxterms:author><rioxxterms:author>Waters, Raymond</rioxxterms:author><rioxxterms:author>Reed, Simon Huw</rioxxterms:author><rioxxterms:type>Monograph</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>

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