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Base URL:  http://orca.cf.ac.uk/cgi/oai2
Sample date:  2017-10-05
Sample size:  100 records harvested

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ID: oai:http://orca.cf.ac.uk:100
Date: 2017-06-25

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:100</identifier>
      <datestamp>2017-06-25T01:30:52Z</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>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:99
Date: 2017-06-25

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:99</identifier>
      <datestamp>2017-06-25T01:30:51Z</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: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:98
Date: 2017-06-04

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:98</identifier>
      <datestamp>2017-06-04T01:30:41Z</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>Purpose: The origin licensing factors minichromosome maintenance 2 (Mcm2) and Geminin have recently been identified as critical regulators of growth and differentiation. Here we have investigated the regulation of these licensing factors together with Ki67 to further elucidate the cell cycle kinetics of renal cell carcinoma (RCC). Furthermore, we have examined the role of Ki67, Mcm2, and Geminin in disease-free survival after nephrectomy in patients with localized RCC. &#13;
&#13;
Experimental Design: Tissue sections from 176 radical nephrectomy specimens were immunohistochemically stained with Mcm2, Geminin, and Ki67 antibodies. Labeling indices (LI) for these markers were compared with clinicopathologic parameters (median follow-up 44 months). &#13;
&#13;
Results: In RCC, Mcm2 is expressed at much higher levels than Ki-67 and Geminin, respectively [medians 41.6%, 7.3%, and 3.5% (P &lt; 0.001)] and was most closely linked to tumor grade (P &lt; 0.001). For each marker, Kaplan-Meier survival curves provided strong evidence that increased expression is associated with reduced disease-free survival time (P &lt; 0.001). Additionally, an Mcm2 – Ki67 LI identified a unique licensed but nonproliferating population of tumor cells that increased significantly with tumor grade (P = 0.004) and was also of prognostic value (P = 0.01). On multivariate analysis, grade, vascular invasion, capsular invasion, Ki67 LI &gt;12%, and age were found to be independent prognostic markers. &#13;
&#13;
Conclusions: Although Ki67 is identified as an independent prognostic marker, semiquantitative assessment is difficult due to the very low proliferative fraction identified by this marker. In contrast, Mcm2 identifies an increased growth fraction that is closely linked to grade, provides prognostic information, and is amenable to semiquantitative analysis in routine pathologic assessment.</dc:description><dc:language>en</dc:language><dc:source>15573265</dc:source><dc:title>Mcm2, Geminin, and KI67 define proliferative state and are prognostic markers in renal cell carcinoma</dc:title><rioxxterms:author>Dudderidge, Tim J.</rioxxterms:author><rioxxterms:author>Stoeber, Kai</rioxxterms:author><rioxxterms:author>Loddo, Marco</rioxxterms:author><rioxxterms:author>Atkinson, Geraldine</rioxxterms:author><rioxxterms:author>Fanshawe, Thomas</rioxxterms:author><rioxxterms:author>Griffiths, David Francis Rees</rioxxterms:author><rioxxterms:author>Williams, Gareth H.</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-04-1776</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:97
Date: 2017-06-04

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:97</identifier>
      <datestamp>2017-06-04T01:30:41Z</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>14602105</dc:source><dc:title>A double-blind, placebo-controlled, randomized trial of oral sodium clodronate for metastatic prostate cancer (MRC PR05 Trial)</dc:title><rioxxterms:author>Dearnaley, David P.</rioxxterms:author><rioxxterms:author>Sydes, Matthew R.</rioxxterms:author><rioxxterms:author>Mason, Malcolm David</rioxxterms:author><rioxxterms:author>Stott, Mark</rioxxterms:author><rioxxterms:author>Powell, Christopher S.</rioxxterms:author><rioxxterms:author>Robinson, Anne C. R.</rioxxterms:author><rioxxterms:author>Thompson, Peter M.</rioxxterms:author><rioxxterms:author>Moffat, Leslie E.</rioxxterms:author><rioxxterms:author>Naylor, Sharon L.</rioxxterms:author><rioxxterms:author>Parmar, Mahesh K. B.</rioxxterms:author><rioxxterms:author>MRC PR05 Collaborators</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/djg038</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:96
Date: 2017-06-04

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
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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:96</identifier>
      <datestamp>2017-06-04T01:30:41Z</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:95
Date: 2017-06-04

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:95</identifier>
      <datestamp>2017-06-04T01:30:41Z</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>Purpose: Despite a high cure rate in patients with testicular cancer, there remain patients in the poor prognosis group who have a less favorable outcome. Intensive induction chemotherapy using a regimen consisting of carboplatin, bleomycin, vincristine, and cisplatin, followed by bleomycin, etoposide, and cisplatin (CBOP/BEP), developed at the Royal Marsden Hospital, is designed to overcome the rapid proliferation seen in germ cell tumors. This study assesses the outcome of patients with poor-prognosis nonseminomatous germ cell tumors (NSGCT) treated with CBOP/BEP. &#13;
&#13;
Patients and Methods: Patients with NSGCT from three centers, classified as poor prognosis according to International Germ Cell Classification Consensus Group criteria, were treated with CBOP/BEP regimen during the period from 1989 to 2000. Data on treatment toxicity, relapse-free survival (RFS), and overall survival (OS) were collected prospectively on a hospital database. &#13;
&#13;
Results: Fifty-four male patients with poor prognosis NSGCT were treated with CBOP/BEP. The RFS at 3 and 5 years for all patients was 83.2% (95% confidence interval [CI], 68.8% to 91.3%). After a median follow-up of 4 years, the OS of the 54 patients was 91.5% (95% CI, 78.6% to 96.8%) at 3 years and 87.6% (95% CI, 71.3% to 94.9%) at 5 years. Three-year OS in patients with a primary mediastinal germ cell tumor was 77.1% (95% CI, 34.5% to 93.9%) compared with 95.4% (95% CI, 82.8% to 98.8%) in patients with a testicular primary tumor (P = .24). &#13;
&#13;
Conclusion: The results reported here compare favorably with the historical results of alternative regimens used in the management of poor-prognosis NSGCT. We suggest a phase III trial to confirm our findings.</dc:description><dc:language>en</dc:language><dc:source>15277755</dc:source><dc:subject>R1</dc:subject><dc:title>Intensive induction chemotherapy with CBOP/BEP in patients with poor prognosis germ cell tumors</dc:title><rioxxterms:author>Christian, J. A.</rioxxterms:author><rioxxterms:author>Huddart, R. A.</rioxxterms:author><rioxxterms:author>Norman, A.</rioxxterms:author><rioxxterms:author>Mason, Malcolm David</rioxxterms:author><rioxxterms:author>Fossa, S.</rioxxterms:author><rioxxterms:author>Aass, N.</rioxxterms:author><rioxxterms:author>Nicholl, E. J.</rioxxterms:author><rioxxterms:author>Dearnaley, David P.</rioxxterms:author><rioxxterms:author>Horwich, A.</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.2003.05.155</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:94
Date: 2017-06-04

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:94</identifier>
      <datestamp>2017-06-04T01:30:41Z</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>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:93
Date: 2017-06-04

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
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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:93</identifier>
      <datestamp>2017-06-04T01:30:40Z</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>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: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>
      <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>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:91
Date: 2017-06-25

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:91</identifier>
      <datestamp>2017-06-25T01:30:49Z</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>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:90
Date: 2017-06-04

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:90</identifier>
      <datestamp>2017-06-04T01:30:40Z</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>15280020</dc:source><dc:title>Genetic variation in XPD predicts treatment outcome and risk of acute myeloid leukemia following chemotherapy</dc:title><rioxxterms:author>Allan, James M.</rioxxterms:author><rioxxterms:author>Smith, Alexandra G.</rioxxterms:author><rioxxterms:author>Wheatley, Keith</rioxxterms:author><rioxxterms:author>Hills, Robert Kerrin</rioxxterms:author><rioxxterms:author>Travis, Lois B.</rioxxterms:author><rioxxterms:author>Hill, Deirdre A.</rioxxterms:author><rioxxterms:author>Swirsky, David M.</rioxxterms:author><rioxxterms:author>Morgan, Gareth J.</rioxxterms:author><rioxxterms:author>Wild, Christopher P.</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-2004-06-2161</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:89
Date: 2017-06-04

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:89</identifier>
      <datestamp>2017-06-04T01:30:40Z</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:88
Date: 2017-06-04

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:88</identifier>
      <datestamp>2017-06-04T01:30:40Z</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:87
Date: 2017-06-04

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:87</identifier>
      <datestamp>2017-06-04T01:30:40Z</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 molecular basis of cystathionine ß-synthase (CBS) deficiency has been studied in 536 patient alleles with 130 different mutations described. To date, no study has reported on the incidence of any of the reported mutations in patients from the UK and the US. We developed a new antisense oligonucleotide (ASO) PCR/hybridization method to screen for 12 of the most frequent CBS mutations in 14 unrelated patients from the UK and 38 unrelated patients from the US, a total of 104 independent alleles. We determined 16/28 (57%) and 28/76 (37%) of the affected alleles in the UK and US patients, respectively. Four different mutations were identified in the UK patients (c.374G&gt;A, R125Q; c.430G&gt;A, E144K; c.833T&gt;C, I278T; c.919G&gt;A, G307S) and 8 mutations identified in the patients from the US (c.341C&gt;T, A114V; c.374G&gt;A, R125Q; c.785C&gt;T, T262M; c.797G&gt;A, R266K; c.833T&gt;C, I278T; c.919G&gt;A, G307S; g.13217A&gt;C (del ex 12); c.1330G&gt;A, D444N). The I278T was the predominant mutation in both populations, present in 8 (29%) of 28 independent alleles from the UK and in 14 (18%) of 76 independent alleles from the US. The incidence of the G307S mutation was 21% in the UK patients and 8% in the US patients. The spectrum of mutations observed in the patients from the UK and US is closer to that which is observed in Northern Europe and bears less resemblance to that observed in Ireland.</dc:description><dc:language>en</dc:language><dc:source>10981004</dc:source><dc:title>The molecular basis of cystathionine beta-synthase (CBS) deficiency in UK and US patients with homocystinuria</dc:title><rioxxterms:author>Moat, Stuart James</rioxxterms:author><rioxxterms:author>Bao, Liming</rioxxterms:author><rioxxterms:author>Fowler, Brian</rioxxterms:author><rioxxterms:author>Bonham, James R.</rioxxterms:author><rioxxterms:author>Walter, John H.</rioxxterms:author><rioxxterms:author>Kraus, Jan P.</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.9214</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:86
Date: 2017-06-04

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:86</identifier>
      <datestamp>2017-06-04T01:30:39Z</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>The nuclear-encoded Krebs cycle enzymes, fumarate hydratase (FH) and succinate dehydrogenase (SDHB, -C and -D), act as tumour suppressors. Germline mutations in FH predispose individuals to leiomyomas and renal cell cancer (HLRCC), whereas mutations in SDH cause paragangliomas and phaeochromocytomas (HPGL). In this study, we have shown that FH-deficient cells and tumours accumulate fumarate and, to a lesser extent, succinate. SDH-deficient tumours principally accumulate succinate. In situ analyses showed that these tumours also have over-expression of hypoxia-inducible factor 1? (HIF1?), activation of HIF1? targets (such as vascular endothelial growth factor) and high microvessel density. We found no evidence of increased reactive oxygen species in our cells. Our data provide in vivo evidence to support the hypothesis that increased succinate and/or fumarate causes stabilization of HIF1? a plausible mechanism, inhibition of HIF prolyl hydroxylases, has previously been suggested by in vitro studies. The basic mechanism of tumorigenesis in HPGL and HLRCC is likely to be pseudo-hypoxic drive, just as it is in von Hippel–Lindau syndrome.</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>Accumulation of Krebs cycle intermediates and over-expression of HIF1 alpha in tumours which result from germline FH and SDH mutations</dc:title><rioxxterms:author>Pollard, P. J.</rioxxterms:author><rioxxterms:author>Briere, J. J.</rioxxterms:author><rioxxterms:author>Alam, N. A.</rioxxterms:author><rioxxterms:author>Barwell, J.</rioxxterms:author><rioxxterms:author>Barclay, E.</rioxxterms:author><rioxxterms:author>Wortham, N. C.</rioxxterms:author><rioxxterms:author>Hunt, T.</rioxxterms:author><rioxxterms:author>Mitchell, M.</rioxxterms:author><rioxxterms:author>Olpin, S.</rioxxterms:author><rioxxterms:author>Moat, Stuart James</rioxxterms:author><rioxxterms:author>Hargreaves, I. P.</rioxxterms:author><rioxxterms:author>Heales, S. J.</rioxxterms:author><rioxxterms:author>Chung, Y. L.</rioxxterms:author><rioxxterms:author>Griffiths, J. R.</rioxxterms:author><rioxxterms:author>Dalgleish, A.</rioxxterms:author><rioxxterms:author>McGrath, J. A.</rioxxterms:author><rioxxterms:author>Gleeson, M. J.</rioxxterms:author><rioxxterms:author>Hodgson, S. V.</rioxxterms:author><rioxxterms:author>Poulsom, R.</rioxxterms:author><rioxxterms:author>Rustin, P.</rioxxterms:author><rioxxterms:author>Tomlinson, I. P. M.</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/ddi227</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:85
Date: 2017-06-04

RIOXX

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RCUK-RIOXX

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:85</identifier>
      <datestamp>2017-06-04T01:30:39Z</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>Global improvement of vascular function and redox state with low-dose folic acid: implications for folate therapy in patients with coronary artery disease</dc:title><rioxxterms:author>Shirodaria, Cheerag</rioxxterms:author><rioxxterms:author>Antoniades, Charalambos</rioxxterms:author><rioxxterms:author>Lee, Justin</rioxxterms:author><rioxxterms:author>Jackson, Clare E.</rioxxterms:author><rioxxterms:author>Robson, Matthew D.</rioxxterms:author><rioxxterms:author>Francis, Jane M.</rioxxterms:author><rioxxterms:author>Moat, Stuart James</rioxxterms:author><rioxxterms:author>Ratnatunga, Chandi</rioxxterms:author><rioxxterms:author>Pillai, Ravi</rioxxterms:author><rioxxterms:author>Refsum, Helga</rioxxterms:author><rioxxterms:author>Neubauer, Stefan</rioxxterms:author><rioxxterms:author>Channon, Keith M.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1161/CIRCULATIONAHA.106.679084</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:84
Date: 2016-10-25

RIOXX

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RCUK-RIOXX

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: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:83
Date: 2016-10-25

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:83</identifier>
      <datestamp>2016-10-25T01:30:19Z</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"><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:82
Date: 2016-10-25

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
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rioxxterms:projectMinimum of 1 value(s) required for rioxxterms:project - found 0 values
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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:82</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: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:81
Date: 2017-06-04

RIOXX

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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
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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:81</identifier>
      <datestamp>2017-06-04T01:30:39Z</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: 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:80
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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ali:license_refMinimum of 1 value(s) required for ali:license_ref - found 0 values
<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:80</identifier>
      <datestamp>2016-03-19T22:00:17Z</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>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:79
Date: 2016-03-19

RIOXX

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rioxxterms:projectMinimum of 1 value(s) required for rioxxterms:project - found 0 values
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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:79</identifier>
      <datestamp>2016-03-19T22:00:17Z</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: 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:78
Date: 2016-03-19

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      <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:77
Date: 2016-03-19

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      <identifier>oai:http://orca.cf.ac.uk:77</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: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:76
Date: 2017-06-04

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:76</identifier>
      <datestamp>2017-06-04T01:30:38Z</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-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:75
Date: 2017-06-04

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    <header>
      <identifier>oai:http://orca.cf.ac.uk:75</identifier>
      <datestamp>2017-06-04T01:30:38Z</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:74
Date: 2017-06-04

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:74</identifier>
      <datestamp>2017-06-04T01:30:38Z</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:73
Date: 2017-06-04

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:73</identifier>
      <datestamp>2017-06-04T01:30:38Z</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) 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:72
Date: 2017-06-04

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<record>
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      <identifier>oai:http://orca.cf.ac.uk:72</identifier>
      <datestamp>2017-06-04T01:30:38Z</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:71
Date: 2017-06-04

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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:70
Date: 2017-06-04

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:70</identifier>
      <datestamp>2017-06-04T01:30:36Z</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>10958657</dc:source><dc:title>Two-dimensional crystallization of the ryanodine receptor Ca2+ release channel on lipid membranes</dc:title><rioxxterms:author>Lai, Francis Anthony</rioxxterms:author><rioxxterms:author>Yin, C. C.</rioxxterms:author><rioxxterms:author>Han, H.</rioxxterms:author><rioxxterms:author>Wei, R.</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.jsb.2004.10.008</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:69
Date: 2017-06-30

RIOXX

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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
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PropertyError
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:69</identifier>
      <datestamp>2017-06-30T01:30:23Z</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>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:68
Date: 2017-06-04

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
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PropertyError
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:68</identifier>
      <datestamp>2017-06-04T01:30:35Z</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>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:67
Date: 2017-06-04

RIOXX

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This is not a valid RIOXX record
PropertyError
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RCUK-RIOXX

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:67</identifier>
      <datestamp>2017-06-04T01:30:35Z</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— Arterial stiffness is an important determinant of cardiovascular risk. Several lines of evidence support a role for the endothelium in regulating arterial stiffness by release of vasoactive mediators. We hypothesized that nitric oxide (NO) acting locally regulates arterial stiffness in vivo, and the aim of this experiment was to test this hypothesis in an ovine hind-limb preparation. &#13;
&#13;
Methods and Results— All studies were conducted in anesthetized sheep. Pulse wave velocity (PWV) was calculated by the foot-to-foot methodology from 2 pressure waveforms recorded simultaneously with a high-fidelity dual pressure-sensing catheter placed in the common iliac artery. Intra-arterial infusion of NG-monomethyl-L-arginine (L-NMMA) increased iliac PWV significantly, by 3±2% (P&lt;0.01). Infusion of acetylcholine and glyceryl trinitrate reduced PWV significantly, by 6±4% (P=0.03) and 5±2% (P&lt;0.01), respectively. Only the effect of acetylcholine, however, was significantly inhibited during coinfusion of L-NMMA (P=0.03). There was no change in systemic arterial pressure throughout the studies. Importantly, infusion of L-NMMA or acetylcholine distal to the common iliac artery (via the sheath) did not affect PWV. &#13;
&#13;
Conclusions— These results demonstrate, for the first time, that basal NO production influences large-artery distensibility. In addition, exogenous acetylcholine and glyceryl trinitrate both increase arterial distensibility, the former mainly through NO production. This may help explain why conditions that exhibit endothelial dysfunction are also associated with increased arterial stiffness. Therefore, reversal of endothelial dysfunction or drugs that are large-artery vasorelaxants may be effective in reducing large-artery stiffness in humans, and thus cardiovascular risk.</dc:description><dc:language>en</dc:language><dc:source>1524-4539</dc:source><dc:subject>R1</dc:subject><dc:title>Nitric oxide regulates local arterial distensibility in vivo</dc:title><rioxxterms:author>Wilkinson, Ian B.</rioxxterms:author><rioxxterms:author>Qasem, Ahmed</rioxxterms:author><rioxxterms:author>McEniery, Carmel M.</rioxxterms:author><rioxxterms:author>Webb, David J.</rioxxterms:author><rioxxterms:author>Avolio, Albert P.</rioxxterms:author><rioxxterms:author>Cockcroft, John Ronald</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1161/hc0202.101970</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:66
Date: 2017-06-04

RIOXX

Base RIOXX scheme designed for low-level interoperability
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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
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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:66</identifier>
      <datestamp>2017-06-04T01:30:35Z</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>07351097</dc:source><dc:title>Increased central pulse pressure and augmentation index in subjects with hypercholesterolemia</dc:title><rioxxterms:author>Wilkinson, Ian B.</rioxxterms:author><rioxxterms:author>Prasad, Krishna</rioxxterms:author><rioxxterms:author>Hall, Ian R.</rioxxterms:author><rioxxterms:author>Thomas, Anne Gwenllian</rioxxterms:author><rioxxterms:author>MacCallum, Helen</rioxxterms:author><rioxxterms:author>Webb, David J.</rioxxterms:author><rioxxterms:author>Frenneaux, Michael Paul</rioxxterms:author><rioxxterms:author>Cockcroft, John Ronald</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(02)01723-0</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:65
Date: 2017-06-04

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
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rioxxterms:projectMinimum of 1 value(s) required for rioxxterms:project - found 0 values
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:65</identifier>
      <datestamp>2017-06-04T01:30:35Z</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>15244563</dc:source><dc:title>Pressure amplification explains why pulse pressure is unrelated to risk in young subjects</dc:title><rioxxterms:author>Wilkinson, Ian B.</rioxxterms:author><rioxxterms:author>Franklin, Stanley S.</rioxxterms:author><rioxxterms:author>Hall, Ian R.</rioxxterms:author><rioxxterms:author>Tyrrell, Sian</rioxxterms:author><rioxxterms:author>Cockcroft, John Ronald</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1161/hy1201.097723</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:64
Date: 2017-06-04

RIOXX

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

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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
rioxxterms:projectMinimum of 1 value(s) required for rioxxterms:project - found 0 values
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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:64</identifier>
      <datestamp>2017-06-04T01:30:35Z</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>Using the bacterial K+ channel KcsA as a template, we constructed models of the pore region of the cardiac ryanodine receptor channel (RyR2) monomer and tetramer. Physicochemical characteristics of the RyR2 model monomer were compared with the template, including homology, predicted secondary structure, surface area, hydrophobicity, and electrostatic potential. Values were comparable with those of KcsA. Monomers of the RyR2 model were minimized and assembled into a tetramer that was, in turn, minimized. The assembled tetramer adopts a structure equivalent to that of KcsA with a central pore. Characteristics of the RyR2 model tetramer were compared with the KcsA template, including average empirical energy, strain energy, solvation free energy, solvent accessibility, and hydrophobic, polar, acid, and base moments. Again, values for the model and template were comparable. The pores of KcsA and RyR2 have a common motif with a hydrophobic channel that becomes polar at both entrances. Quantitative comparisons indicate that the assembled structure provides a plausible model for the pore of RyR2. Movement of Ca2+, K+, and tetraethylammonium (TEA+) through the model RyR2 pore were simulated with explicit solvation. These simulations suggest that the model RyR2 pore is permeable to Ca2+ and K+ with rates of translocation greater for K+. In contrast, simulations indicate that tetraethylammonium blocks movement of metal cations.</dc:description><dc:format>application/pdf</dc:format><dc:identifier>http://orca.cf.ac.uk/64/1/modelofputativepore.pdf</dc:identifier><dc:language>en</dc:language><dc:source>1542-0086</dc:source><dc:subject>R1</dc:subject><dc:title>A model of the putative pore region of the cardiac ryanodine receptor channel</dc:title><rioxxterms:author>Welch, William</rioxxterms:author><rioxxterms:author>Rheault, Shana</rioxxterms:author><rioxxterms:author>West, Duncan J.</rioxxterms:author><rioxxterms:author>Williams, Alan John</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.104.044180</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:63
Date: 2017-06-04

RIOXX

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

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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
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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:63</identifier>
      <datestamp>2017-06-04T01:30:35Z</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>OBJECTIVE: Although C-reactive protein (CRP) is increasingly recognized as an independent risk factor for acute myocardial events, recent evidence suggests that it can directly induce vasorelaxation. This study aimed to investigate the mechanism of this CRP-induced response. METHODS AND RESULTS: Isometric tension recordings were used to measure endothelium-dependent and endothelium-independent vascular smooth muscle relaxation in isolated rabbit aortic rings. CRP generated in-house by genetic engineering and expressed in Chinese hamster ovary cells, CRP purified from ascites, and CRP obtained from commercial sources were assessed for vasorelaxing properties. Only the commercial CRP preparation induced vasorelaxation; more than half maximal relaxation was observed at 0.025 microg/mL and maximum relaxation attained at 0.25 microg/mL. Commercial CRP contains high levels of sodium azide, a well-known vasorelaxant. Removal of this agent by dialysis abolished the vasodilatory effect of commercial CRP. Sodium azide alone at concentrations equivalent to that present in the commercial CRP produced a near-identical relaxation pattern to the undialyzed commercial product. CONCLUSIONS: CRP has no vasorelaxant properties per se, and the reported vasorelaxant ability of CRP is an artifact caused by sodium azide present in commercial preparations of this agent.</dc:description><dc:language>en</dc:language><dc:source>1524-4636</dc:source><dc:title>C-reactive protein-induced in vitro vasorelaxation is an artefact caused by the presence of sodium azide in commercial preparations</dc:title><rioxxterms:author>Van Den Berg, Carmen Wilma</rioxxterms:author><rioxxterms:author>Taylor, Karolina E.</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/10.1161/01.ATV.0000142807.92781.d9</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:62
Date: 2017-06-04

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:62</identifier>
      <datestamp>2017-06-04T01:30:35Z</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>1538-7933</dc:source><dc:title>Loxosceles spider venom induces the release of thrombomodulin and Endothelial Protein C Receptor: implications for the pathogenesis of intravascular coagulation as observed in loxoscelism</dc:title><rioxxterms:author>Van Den Berg, Carmen Wilma</rioxxterms:author><rioxxterms:author>Tambourgi, D. V.</rioxxterms:author><rioxxterms:author>Magnoli, F. C.</rioxxterms:author><rioxxterms:author>Goncalves-de-Andrade, R. M.</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.1538-7836.2007.02382.x</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:61
Date: 2017-06-04

RIOXX

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This is not a valid RIOXX record
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RCUK-RIOXX

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:61</identifier>
      <datestamp>2017-06-04T01:30:35Z</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>10181172</dc:source><dc:title>Modulation of gap-junction-dependent arterial relaxation by ascorbic acid</dc:title><rioxxterms:author>Edwards, David Hughes</rioxxterms:author><rioxxterms:author>Chaytor, Andrew Thomas</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/10.1159/000104254</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:60
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:60</identifier>
      <datestamp>2016-03-19T22:00:14Z</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>Essential role of Gap junctions in NO- and prostanoid-independent relaxations evoked by acetylcholine in rabbit intracerebral arteries</dc:title><rioxxterms:author>Ujiie, Hiroshi</rioxxterms:author><rioxxterms:author>Chaytor, Andrew Thomas</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/10.1161/01.STR.0000054158.72610.EC</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:59
Date: 2017-06-04

RIOXX

Base RIOXX scheme designed for low-level interoperability
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PropertyError
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:59</identifier>
      <datestamp>2017-06-04T01:30:34Z</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:format>application/pdf</dc:format><dc:identifier>http://orca.cf.ac.uk/59/1/Connexin_Hemichannels_and_Gap_Junction.pdf</dc:identifier><dc:language>en</dc:language><dc:source>10591524</dc:source><dc:title>Connexin hemichannels and gap junction channels are differentially influenced by lipopolysaccharide and basic fibroblast growth factor</dc:title><rioxxterms:author>Evans, William Howard</rioxxterms:author><rioxxterms:author>Vuyst, E. De</rioxxterms:author><rioxxterms:author>Decrock, E.</rioxxterms:author><rioxxterms:author>Bock, M. De</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.E06-03-0182</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:58
Date: 2017-06-04

RIOXX

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RCUK-RIOXX

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:58</identifier>
      <datestamp>2017-06-04T01:30:34Z</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:57
Date: 2017-06-04

RIOXX

Base RIOXX scheme designed for low-level interoperability
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PropertyError
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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:57</identifier>
      <datestamp>2017-06-04T01:30:34Z</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>Objectives: Point mutations in the cardiac ryanodine receptor (RyR2) mediate abnormal intracellular Ca2+ release and are associated with stress-induced ventricular tachycardia (VT), leading to sudden cardiac death (SCD). Although the precise molecular basis of RyR2 dysfunction in SCD remains controversial, there is consensus that the mutations characterised to date all exhibit gain-of-function Ca2+ release properties following cell stimulation. We investigated the functional impact of a distinct set of SCD-linked RyR2 mutations (L433P, N2386I, R176Q/T2504M) on intracellular Ca2+ handling. Methods: We expressed full-length recombinant human wild-type (WT) and SCD-linked RyR2 mutations in human embryonic kidney (HEK) cells, and profiled the spatial and amplitude characteristics of caffeine-evoked Ca2+ release through homo-tetrameric channels in living cells using rapid confocal laser scanning microscopy. Results: Analysis of the precise mode of Ca2+ release in HEK cells expressing RyR2 mutants demonstrated profound differences when compared with WT channels. The SCD-linked RyR2 mutations characterised in this study exhibited heterogeneous Ca2+ release profiles, including the novel observation that one of the mutants, (L433P), exhibited a marked reduction in sensitivity to channel activation. However, all SCD-linked RyR2 mutations characterised in this study resulted in an increased duration of elevated cytoplasmic Ca2+ levels following channel activation. Conclusions: Our live cell-based data demonstrates functional heterogeneity of Ca2+ release through SCD-linked RyR2 mutants, suggesting that the mechanistic basis of RyR2 dysfunction in SCD may be more complex than previously anticipated. These findings may have profound consequences for the therapeutic modulation of RyR2 in stress-induced VT and SCD.</dc:description><dc:language>en</dc:language><dc:publisher>Elsevier</dc:publisher><dc:source>0008-6363</dc:source><dc:title>Functional heterogeneity of ryanodine receptor mutations associated with sudden cardiac death</dc:title><rioxxterms:author>Thomas, Nia Lowri</rioxxterms:author><rioxxterms:author>George, Christopher</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.cardiores.2004.06.009</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:56
Date: 2017-06-04

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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ali:license_refMinimum of 1 value(s) required for ali:license_ref - found 0 values
<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:56</identifier>
      <datestamp>2017-06-04T01:30:33Z</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:55
Date: 2017-06-04

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:55</identifier>
      <datestamp>2017-06-04T01:30:33Z</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>15407748</dc:source><dc:title>An anionic ryanoid, 10-O-succinoylryanodol, provides insights into the mechanisms governing the interaction of ryanoids and the subsequent altered function of ryanodine-receptor channels</dc:title><rioxxterms:author>Williams, Alan John</rioxxterms:author><rioxxterms:author>Tanna, B.</rioxxterms:author><rioxxterms:author>Ruest, L.</rioxxterms:author><rioxxterms:author>Welch, W.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1085/jgp.200208753</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:54
Date: 2017-06-04

RIOXX

Base RIOXX scheme designed for low-level interoperability
This is 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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    <header>
      <identifier>oai:http://orca.cf.ac.uk:54</identifier>
      <datestamp>2017-06-04T01:30:33Z</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"><ali:free_to_read/><dc:description>Background: Induction of anaesthesia can precipitate catecholamine release from an undiscovered pheochromocytoma and induce a hypertensive crisis. However, it is assumed that catecholamine and metabolite values resulting from the effects of surgery per se in the early postoperative period would overlap with the values generated by a tumour, and it is not known how soon after biochemical investigations can be carried out. &#13;
&#13;
Aim: To study patterns of urinary catecholamine excretion and the feasibility of biochemical screening for phaeochromocytomas in the immediate postoperative period in otherwise healthy subjects undergoing a single type of major surgical procedure. &#13;
&#13;
Methods: Catecholamines and metabolites were measured for each mole of creatinine in single voided urine on one preoperative and four postoperative days in five subjects who underwent elective coronary artery bypass graft surgery with an uncomplicated postoperative course. Reference ranges were established from 33 healthy normotensive volunteers. &#13;
&#13;
Results: Excretion of adrenaline, noradrenaline, dopamine, vanillylmandelic acid, and metadrenaline was within normal limits. Normetadrenaline excretion was mildly raised in four patients, but did not exceed 1.5 times the upper reference limit, and returned to normality by the fourth postoperative day. &#13;
&#13;
Conclusion: It is feasible to perform simple urinary screening for possible phaeochromocytoma in the immediate postoperative period.</dc:description><dc:format>application/pdf</dc:format><dc:identifier>http://orca.cf.ac.uk/54/1/Urinary_catecholamines.pdf</dc:identifier><dc:language>en</dc:language><dc:source>00219746</dc:source><dc:subject>R1</dc:subject><dc:title>Urinary catecholamines and metabolites in the immediate postoperative period following major surgery</dc:title><rioxxterms:author>Syed, A. A.</rioxxterms:author><rioxxterms:author>Wheatley, H. A.</rioxxterms:author><rioxxterms:author>Badminton, Michael Norman</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/10.1136/jcp.2003.013201</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:53
Date: 2017-06-04

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:53</identifier>
      <datestamp>2017-06-04T01:30:33Z</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>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:52
Date: 2017-06-04

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:52</identifier>
      <datestamp>2017-06-04T01:30:32Z</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>The specific, high-affinity interaction of the plant toxin ryanodine with its molecular target the ryanodine receptor channel (RyR) has been instrumental in RyR research. Alanine scanning of putative pore regions of mouse RyR2 has highlighted the amino acid Gln4863, predicted to lie within trans-membrane helix TM10, as an important determinant of ryanodine binding. We have investigated the effects of several ryanodine derivatives, guanidinopropionylryanodine, 21-p-nitrobenzoylamino-9?-hydroxyryanodine, 8?-amino-9?-hydroxyryanodine, and 21-amino-9?-hydroxyryanodine, with the mouse Q4863A RyR2 mutant at the single-channel level. Our results demonstrate that the rate of dissociation of all ryanoids investigated is increased by the mutation. The modification of channel function after ryanoid binding is qualitatively similar for wild-type and mutant, but in several cases, single-channel conductances were increased with Q4863A. These novel findings have been interpreted within the framework of existing comparative molecular field analysis studies on ryanoids. We suggest that replacement of a glutamine by an alanine residue at position 4863 causes RyR2 to simultaneously alter interactions with both ends of the ryanoid molecule.</dc:description><dc:language>en</dc:language><dc:source>0026-895X</dc:source><dc:subject>R1</dc:subject><dc:title>The Gln4863Ala mutation within a putative, pore-lining trans-membrane helix of the cardiac ryanodine receptor channel alters both the kinetics of ryanoid interaction and the subsequent fractional conductance</dc:title><rioxxterms:author>Ranatunga, Kishani M.</rioxxterms:author><rioxxterms:author>Moreno-King, Tracy M.</rioxxterms:author><rioxxterms:author>Tanna, Bhavna</rioxxterms:author><rioxxterms:author>Wang, Ruiwu</rioxxterms:author><rioxxterms:author>Chen, S. R. Wayne</rioxxterms:author><rioxxterms:author>Ruest, Luc</rioxxterms:author><rioxxterms:author>Welch, William</rioxxterms:author><rioxxterms:author>Williams, Alan John</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1124/mol.105.012807</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:51
Date: 2017-06-30

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:51</identifier>
      <datestamp>2017-06-30T01:30:21Z</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>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:50
Date: 2017-06-04

RIOXX

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    <header>
      <identifier>oai:http://orca.cf.ac.uk:50</identifier>
      <datestamp>2017-06-04T01:30:32Z</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:49
Date: 2017-06-04

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:49</identifier>
      <datestamp>2017-06-04T01:30:32Z</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:48
Date: 2017-06-04

RIOXX

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    <header>
      <identifier>oai:http://orca.cf.ac.uk:48</identifier>
      <datestamp>2017-06-04T01:30:31Z</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>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:47
Date: 2017-06-04

RIOXX

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This is a valid RIOXX record

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:47</identifier>
      <datestamp>2017-06-04T01:30:31Z</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>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:46
Date: 2017-06-04

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:46</identifier>
      <datestamp>2017-06-04T01:30:31Z</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>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:45
Date: 2017-06-30

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:45</identifier>
      <datestamp>2017-06-30T01:30:20Z</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: 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:44
Date: 2016-03-19

RIOXX

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    <header>
      <identifier>oai:http://orca.cf.ac.uk:44</identifier>
      <datestamp>2016-03-19T22:00:11Z</datestamp>
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      <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>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:43
Date: 2017-06-04

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    <header>
      <identifier>oai:http://orca.cf.ac.uk:43</identifier>
      <datestamp>2017-06-04T01:30:30Z</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:format>application/pdf</dc:format><dc:identifier>http://orca.cf.ac.uk/43/1/Electrostatic_Mechanisms_Underlie_Neomycin.pdf</dc:identifier><dc:language>en</dc:language><dc:source>15420086</dc:source><dc:title>Electrostatic mechanisms underlie neomycin block of the cardiac ryanodine receptor channel (RyR2)</dc:title><rioxxterms:author>Williams, Alan John</rioxxterms:author><rioxxterms:author>Mead, F.</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.104.049338</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:42
Date: 2017-06-04

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    <header>
      <identifier>oai:http://orca.cf.ac.uk:42</identifier>
      <datestamp>2017-06-04T01:30:30Z</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>Normal vascular aging: differential effects on wave reflection and aortic pulse wave velocity: the Anglo-Cardiff Collaborative Trial (ACCT)</dc:title><rioxxterms:author>McEniery, Carmel M.</rioxxterms:author><rioxxterms:author>Yasmin, </rioxxterms:author><rioxxterms:author>Hall, Ian R.</rioxxterms:author><rioxxterms:author>Qasem, Ahmad</rioxxterms:author><rioxxterms:author>Cockcroft, John Ronald</rioxxterms:author><rioxxterms:author>Wilkinson, Ian B.</rioxxterms:author><rioxxterms:author>Anglo-Cardiff Collaboration Trial (ACCT) Investigators</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.2005.07.037</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:41
Date: 2017-06-04

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:41</identifier>
      <datestamp>2017-06-04T01:30:30Z</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>15229645</dc:source><dc:title>Non-invasive diagnosis of coronary artery disease by quantitative stress echocardiography: optimal diagnostic models using off-line tissue Doppler in the MYDISE study</dc:title><rioxxterms:author>Madler, Christoph Friedrich</rioxxterms:author><rioxxterms:author>Payne, Nichola</rioxxterms:author><rioxxterms:author>Wilkenshoff, Ursula</rioxxterms:author><rioxxterms:author>Cohen, Ariel</rioxxterms:author><rioxxterms:author>Derumeaux, Genevieve A.</rioxxterms:author><rioxxterms:author>Pierard, Luc A.</rioxxterms:author><rioxxterms:author>Engvall, Jan</rioxxterms:author><rioxxterms:author>Brodin, Lars-Ake</rioxxterms:author><rioxxterms:author>Sutherland, George R.</rioxxterms:author><rioxxterms:author>Fraser, Alan Gordon</rioxxterms:author><rioxxterms:author>MYDISE Study Investigators (Myocardial Doppler in Stress Echocardiography)</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/S0195-668X(03)00099-X</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:40
Date: 2017-06-04

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:40</identifier>
      <datestamp>2017-06-04T01:30:30Z</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— Chronic heart failure (CHF) is a major cause of morbidity and mortality that requires a novel approach to therapy. Perhexiline is an antianginal drug that augments glucose metabolism by blocking muscle mitochondrial free fatty acid uptake, thereby increasing metabolic efficiency. We assessed the effects of perhexiline treatment in CHF patients. &#13;
&#13;
Methods and Results— In a double-blind fashion, we randomly assigned patients with optimally medicated CHF to either perhexiline (n=28) or placebo (n=28). The primary end point was peak exercise oxygen consumption (O2max), an important prognostic marker. In addition, the effect of perhexiline on myocardial function and quality of life was assessed. Quantitative stress echocardiography with tissue Doppler measurements was used to assess regional myocardial function in patients with ischemic CHF. 31P magnetic resonance spectroscopy was used to assess the effect of perhexiline on skeletal muscle energetics in patients with nonischemic CHF. Treatment with perhexiline led to significant improvements in O2max (16.1±0.6 to 18.8±1.1 mL · kg–1 · min–1; P&lt;0.001), quality of life (Minnesota score reduction from 45±5 to 34±5; P=0.04), and left ventricular ejection fraction (24±1% to 34±2%; P&lt;0.001). Perhexiline treatment also increased resting and peak dobutamine stress regional myocardial function (by 15% and 24%, respectively) and normalized skeletal muscle phosphocreatine recovery after exercise. There were no adverse effects during the treatment period. &#13;
&#13;
Conclusions— In patients with CHF, metabolic modulation with perhexiline improved O2max, left ventricular ejection fraction, symptoms, resting and peak stress myocardial function, and skeletal muscle energetics. Perhexiline may therefore represent a novel treatment for CHF with a good safety profile, provided that the dosage is adjusted according to plasma levels.</dc:description><dc:language>en</dc:language><dc:source>15244539</dc:source><dc:subject>R1</dc:subject><dc:title>Metabolic modulation with perhexiline in chronic heart failure: a randomized, controlled trial of short-term use of a novel treatment</dc:title><rioxxterms:author>Lee, Leong</rioxxterms:author><rioxxterms:author>Campbell, Ross</rioxxterms:author><rioxxterms:author>Scheuermann-Freestone, Michaela</rioxxterms:author><rioxxterms:author>Taylor, Rachel</rioxxterms:author><rioxxterms:author>Gunaruwan, Prasad</rioxxterms:author><rioxxterms:author>Williams, Lynne</rioxxterms:author><rioxxterms:author>Ashrafian, Houman</rioxxterms:author><rioxxterms:author>Horowitz, John</rioxxterms:author><rioxxterms:author>Fraser, Alan Gordon</rioxxterms:author><rioxxterms:author>Clarke, Kieran</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/CIRCULATIONAHA.105.551457</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:39
Date: 2017-06-30

RIOXX

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RCUK-RIOXX

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:39</identifier>
      <datestamp>2017-06-30T01:30:19Z</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>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:38
Date: 2017-06-30

RIOXX

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This is not a valid RIOXX record
PropertyError
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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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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:38</identifier>
      <datestamp>2017-06-30T01:30:19Z</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>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:37
Date: 2017-06-17

RIOXX

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RCUK-RIOXX

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>2017-06-17T01:30:32Z</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:36
Date: 2017-06-04

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
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rioxxterms:projectMinimum of 1 value(s) required for rioxxterms:project - found 0 values
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:36</identifier>
      <datestamp>2017-06-04T01:30:29Z</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: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:35
Date: 2017-06-04

RIOXX

Base RIOXX scheme designed for low-level interoperability
This is not a valid RIOXX record
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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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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:35</identifier>
      <datestamp>2017-06-04T01:30:28Z</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>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:34
Date: 2017-06-04

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
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PropertyError
rioxxterms:projectMinimum of 1 value(s) required for rioxxterms:project - found 0 values
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:34</identifier>
      <datestamp>2017-06-04T01:30:27Z</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>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:33
Date: 2017-06-04

RIOXX

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RCUK RIOXX scheme for reporting of open access publications funded through UK Research Council grants
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PropertyError
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:33</identifier>
      <datestamp>2017-06-04T01:30:27Z</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>The ryanodine receptor complex (RyR), a large oligomeric assembly that functions as a Ca2+-release channel in the sarcoplasmic reticulum (SR)/endoplasmic reticulum (ER), comprises four RyR subunits and four FK506-binding proteins (FKBP). The precise mode of interaction and modulation of the cardiac RyR (RyR2) channel by FKBP12/FKBP12.6 remains to be fully defined. We have generated a series of Chinese-hamster ovary (CHO) cell lines stably expressing discrete levels of recombinant human RyR2 (hRyR2) (CHOhRyR2). Confocal microscopy of CHOhRyR2 cells co-expressing either FKBP12 or FKBP12.6 demonstrated that FKBP12.6 was sequestered from the cytoplasm to ER membranes as the cellular levels of hRyR2 increased. There was negligible hRyR2-induced subcellular redistribution of FKBP12. The magnitude of Ca2+ release in CHOhRyR2 cells in response to stimulation by 4-chloro-m-cresol was in direct proportion to the expression levels of hRyR2. However, in CHOhRyR2 cells co-expressing FKBP12.6, Ca2+ release triggered by the addition of 4-chloro-m-cresol was markedly decreased. In contrast, co-expression of FKBP12 did not affect agonist-induced Ca2+ release in CHOhRyR2 cells. Resting cytoplasmic [Ca2+] in CHOhRyR2 remained unaltered after co-expression of FKBP12 or FKBP12.6, but estimation of the ER Ca2+ load status showed that co-expression of FKBP12.6, but not FKBP12, promoted superfilling of the ER Ca2+ store which could not be released by RyR2 after agonist activation. The effects of FKBP12.6 on hRyR2-mediated intracellular Ca2+ handling could be antagonized using rapamycin (5µM). These results suggest that FKBP12.6 associates with hRyR2 in situ to modulate precisely the functionality of hRyR2 Ca2+-release channel.</dc:description><dc:language>en</dc:language><dc:publisher>Biochemical Society</dc:publisher><dc:source>0264-6021</dc:source><dc:title>In situ modulation of the human cardiac ryanodine receptor (hRyR2) by FKBP12.6</dc:title><rioxxterms:author>George, Christopher</rioxxterms:author><rioxxterms:author>Sorathia, Rina</rioxxterms:author><rioxxterms:author>Bertrand, Benedicte M. A.</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/10.1042/BJ20021433</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:32
Date: 2017-06-04

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
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:32</identifier>
      <datestamp>2017-06-04T01:30:27Z</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>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:31
Date: 2017-06-04

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:31</identifier>
      <datestamp>2017-06-04T01:30:27Z</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>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:30
Date: 2017-06-04

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:30</identifier>
      <datestamp>2017-06-04T01:30:27Z</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>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:29
Date: 2017-06-04

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:29</identifier>
      <datestamp>2017-06-04T01:30:26Z</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>00219150</dc:source><dc:title>Downregulation of the ERK 1 and 2 mitogen activated protein kinases using antisense oligonucleotides inhibits proliferation of porcine vascular smooth muscle cells</dc:title><rioxxterms:author>Fisher, M.</rioxxterms:author><rioxxterms:author>Liu, B.</rioxxterms:author><rioxxterms:author>Glennon, P. E.</rioxxterms:author><rioxxterms:author>Southgate, K. M.</rioxxterms:author><rioxxterms:author>Sale, E. M.</rioxxterms:author><rioxxterms:author>Sale, G. J.</rioxxterms:author><rioxxterms:author>Lewis, Malcolm John</rioxxterms:author><rioxxterms:author>Groves, P. H.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/S0021-9150(00)00656-0</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:28
Date: 2017-06-04

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:28</identifier>
      <datestamp>2017-06-04T01:30:24Z</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"><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:27
Date: 2017-06-30

RIOXX

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rioxxterms:projectMinimum of 1 value(s) required for rioxxterms:project - found 0 values
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:27</identifier>
      <datestamp>2017-06-30T01:30:18Z</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>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:26
Date: 2017-06-30

RIOXX

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rioxxterms:projectMinimum of 1 value(s) required for rioxxterms:project - found 0 values
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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:26</identifier>
      <datestamp>2017-06-30T01:30:18Z</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>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:25
Date: 2017-06-04

RIOXX

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rioxxterms:projectMinimum of 1 value(s) required for rioxxterms:project - found 0 values
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:25</identifier>
      <datestamp>2017-06-04T01:30:23Z</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>14602075</dc:source><dc:title>Intracellular calcium changes trigger connexin 32 hemichannel opening</dc:title><rioxxterms:author>Evans, William Howard</rioxxterms:author><rioxxterms:author>Decrock, E.</rioxxterms:author><rioxxterms:author>Dubyak, G. R.</rioxxterms:author><rioxxterms:author>Cabooter, L.</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.emboj.7600908</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:24
Date: 2017-06-04

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:24</identifier>
      <datestamp>2017-06-04T01:30:23Z</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:23
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: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:22
Date: 2017-06-04

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:22</identifier>
      <datestamp>2017-06-04T01:30:22Z</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>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:21
Date: 2017-06-04

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:21</identifier>
      <datestamp>2017-06-04T01:30:22Z</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>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:20
Date: 2017-06-04

RIOXX

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:20</identifier>
      <datestamp>2017-06-04T01:30:22Z</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>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:19
Date: 2017-06-04

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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:19</identifier>
      <datestamp>2017-06-04T01:30:22Z</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>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:18
Date: 2017-06-04

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rioxxterms:projectMinimum of 1 value(s) required for rioxxterms:project - found 0 values
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<record>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:18</identifier>
      <datestamp>2017-06-04T01:30:22Z</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:17
Date: 2017-06-04

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ID: oai:http://orca.cf.ac.uk:16
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ID: oai:http://orca.cf.ac.uk:15
Date: 2017-06-04

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ID: oai:http://orca.cf.ac.uk:14
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ID: oai:http://orca.cf.ac.uk:13
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ID: oai:http://orca.cf.ac.uk:12
Date: 2017-06-04

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ID: oai:http://orca.cf.ac.uk:11
Date: 2017-06-04

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ID: oai:http://orca.cf.ac.uk:10
Date: 2017-06-04

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ID: oai:http://orca.cf.ac.uk:9
Date: 2017-06-04

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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 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:8
Date: 2017-06-04

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>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:8</identifier>
      <datestamp>2017-06-04T01:30:20Z</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:7
Date: 2017-06-04

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:7</identifier>
      <datestamp>2017-06-04T01:30:20Z</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>Altered gap junction coupling of cardiac myocytes during ischemia may contribute to development of lethal arrhythmias. The phosphoprotein connexin 43 (Cx43) is the major constituent of gap junctions. Dephosphorylation of Cx43 and uncoupling of gap junctions occur during ischemia, but the significance of Cx43 phosphorylation in this setting is unknown. Here we show that Cx43 dephosphorylation in synchronously contracting myocytes during ischemia is reversible, independent of hypoxia, and closely associated with cellular ATP levels. Cx43 became profoundly dephosphorylated during hypoxia only when glucose supplies were limited and was completely rephosphorylated within 30 minutes of reoxygenation. Similarly, direct reduction of ATP by various combinations of metabolic inhibitors and by ouabain was closely paralleled by loss of phosphoCx43 and recovery of phosphoCx43 accompanied restoration of ATP. Dephosphorylation of Cx43 could not be attributed to hypoxia, acid pH or secreted metabolites, or to AMP-activated protein kinase; moreover, the process was selective for Cx43 because levels of phospho-extracellular signal regulated kinase (ERK)1/2 were increased throughout. Rephosphorylation of Cx43 was not dependent on new protein synthesis, or on activation of protein kinases A or G, ERK1/2, p38 mitogen-activated protein kinase, or Jun kinase; however, broad-spectrum protein kinase C inhibitors prevented Cx43 rephosphorylation while also sensitizing myocytes to reoxygenation-mediated cell death. We conclude that Cx43 is reversibly dephosphorylated and rephosphorylated during hypoxia and reoxygenation by a novel mechanism that is sensitive to nonlethal fluctuations in cellular ATP. The role of this regulated phosphorylation in the adaptation to ischemia remains to be determined.</dc:description><dc:format>application/pdf</dc:format><dc:identifier>http://orca.cf.ac.uk/7/1/Turner%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=15358666</dc:relation><dc:source>0009-7330</dc:source><dc:title>Reversible connexin 43 dephosphorylation during hypoxia and reoxygenation is linked to cellular ATP levels</dc:title><rioxxterms:author>Turner, Mark Stephen</rioxxterms:author><rioxxterms:author>Haywood, Guy A.</rioxxterms:author><rioxxterms:author>Andreka, Peter</rioxxterms:author><rioxxterms:author>You, Lijing</rioxxterms:author><rioxxterms:author>Martin, Patricia Esther Mary</rioxxterms:author><rioxxterms:author>Evans, William Howard</rioxxterms:author><rioxxterms:author>Webster, Keith A.</rioxxterms:author><rioxxterms:author>Bishopric, Nanette H.</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.0000144805.11519.1e</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:http://orca.cf.ac.uk:6
Date: 2017-06-04

RIOXX

Base RIOXX scheme designed for low-level interoperability
This is not a valid RIOXX record
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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>
    <header>
      <identifier>oai:http://orca.cf.ac.uk:6</identifier>
      <datestamp>2017-06-04T01:30:20Z</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:5
Date: 2017-06-04

RIOXX

Base RIOXX scheme designed for low-level interoperability
This is not a valid RIOXX record
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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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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>2017-06-04T01:30:20Z</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:4
Date: 2017-06-30

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
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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:4</identifier>
      <datestamp>2017-06-30T01:30:15Z</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>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:3
Date: 2017-06-04

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
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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:3</identifier>
      <datestamp>2017-06-04T01:30:19Z</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>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:2
Date: 2017-06-04

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>2017-06-04T01:30:19Z</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: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:1
Date: 2017-06-30

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
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rioxxterms:projectMinimum of 1 value(s) required for rioxxterms:project - found 0 values
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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:1</identifier>
      <datestamp>2017-06-30T01:30:15Z</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: 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>

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