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ID: oai:publications.aston.ac.uk:146
Date: 2017-08-22

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<record>
    <header>
      <identifier>oai:publications.aston.ac.uk:146</identifier>
      <datestamp>2017-08-22T11:55:56Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>The oxidative base lesion 8-oxo-deoxyguanosine (8-oxo-dG) has been identified in DNA isolated from normal tissue and may occur at elevated levels during disease. However, the use of phenol during DNA extraction may artificially elevate the detected levels of this lesion. Herein, we have performed a comparative methodological study using both pronase E and phenol extraction techniques; native or oxidatively stressed DNA was isolated to determine the validity of each extraction technique for the subsequent determination of 8-oxo-dG. Whilst the yields of DNA were comparable, after pronase E extraction there was no detectable induction of 8-oxo-dG in reextracted naked DNA or peripheral blood mononuclear cell DNA that had been oxidatively stressed. However, phenol extraction enhanced the basal levels of 8-oxo-dG detected, and also induced a significant increase in levels of the modified base after exposure to oxidative stress. The latter was dependent on the presence of foetal calf serum in the extracellular medium. We have confirmed that phenol extraction sensitises native DNA to subsequent oxidative damage. In addition, this work shows that the extent of sensitisation occurring during phenol extraction varies with the degree of oxidative damage already incurred and infers that labile guanine sites generated during oxidative stress may be detected as 8-oxo-dG residues after phenol extraction.</dc:description><dc:language>en</dc:language><dc:source>1873-4596</dc:source><dc:title>Evidence for sensitisation of DNA to oxidative damage during isolation</dc:title><rioxxterms:author>Finnegan, M.T.</rioxxterms:author><rioxxterms:author>Herbert, Karl E.</rioxxterms:author><rioxxterms:author>Evans, Mark D.</rioxxterms:author><rioxxterms:author>Griffiths, Helen R.</rioxxterms:author><rioxxterms:author>Lunec, Joseph</rioxxterms:author><rioxxterms:publication_date>1996-05-26</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/0891-5849(95)02003-9</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:145
Date: 2017-08-22

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
dcterms:dateAcceptedMinimum of 1 value(s) required for dcterms:dateAccepted - found 0 values
dc:identifierMinimum of 1 value(s) required for dc:identifier - found 0 values
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<record>
    <header>
      <identifier>oai:publications.aston.ac.uk:145</identifier>
      <datestamp>2017-08-22T11:55:56Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>IgG can be denatured in vitro by reactive oxygen species (ROS). Native IgG activates the complement cascade through C1q. Using a modified ELISA, C1q binding activity of rheumatoid IgG has been compared to IgG denatured by neutrophil-derived ROS. The C1q binding activity of rheumatoid synovial fluid IgG is greater than the corresponding serum IgG (P &lt; 0.01). Denaturation of IgG by activated polymorphs or the Fenton reaction decreased its C1q binding activity (P &lt; 0.01). In vitro exposure of IgG to OH. and ROO. increased its interaction with C1q (P &lt; 0.01). Hypochlorous acid had no effect. ROS-induced alteration to IgG-C1q binding activity may promote the inflammatory response in rheumatoid arthritis.</dc:description><dc:language>en</dc:language><dc:source>1873-3468</dc:source><dc:title>The C1q binding activity of IgG is modified in vitro by reactive oxygen species: implications for rheumatoid arthritis</dc:title><rioxxterms:author>Griffiths, Helen R.</rioxxterms:author><rioxxterms:author>Lunec, Joseph</rioxxterms:author><rioxxterms:publication_date>1996-06-17</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/0014-5793(96)00542-X</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:144
Date: 2017-09-21

RIOXX

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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
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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:publications.aston.ac.uk:144</identifier>
      <datestamp>2017-09-21T07:00:56Z</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>Vitamin C is marketed as a dietary supplement, partly because of its 'antioxidant' properties. However, we report here that vitamin C administered as a dietary supplement to healthy humans exhibits a pro-oxidant, as well as an antioxidant, effect in vivo.</dc:description><dc:language>en</dc:language><dc:source>1476-4687</dc:source><dc:title>Vitamin C exhibits pro-oxidant properties</dc:title><rioxxterms:author>Podmore, Ian D.</rioxxterms:author><rioxxterms:author>Griffiths, Helen R.</rioxxterms:author><rioxxterms:author>Herbert, Karl E.</rioxxterms:author><rioxxterms:author>Mistry, Nalini</rioxxterms:author><rioxxterms:author>Mistry, Pratibha</rioxxterms:author><rioxxterms:author>Lunec, Joseph</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1038/33308</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:143
Date: 2017-08-28

RIOXX

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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:publications.aston.ac.uk:143</identifier>
      <datestamp>2017-08-28T07:01:36Z</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:description>Exposure to the solar ultraviolet spectrum that penetrates the Earth's stratosphere (UVA and UVB) causes cellular DNA damage within skin cells. This damage is elicited directly through absorption of energy (UVB), and indirectly through intermediates such as sensitizer radicals and reactive oxygen species (UVA). DNA damage is detected as strand breaks or as base lesions, the most common lesions being 8-hydroxydeoxyguanosine (8OHdG) from UVA exposure and cyclobutane pyrimidine dimers from UVB exposure. The presence of these products in the genome may cause misreading and misreplication. Cells are protected by free radical scavengers that remove potentially mutagenic radical intermediates. In addition, the glutathione-S-transferase family can catalyze the removal of epoxides and peroxides. An extensive repair capacity exists for removing (1) strand breaks, (2) small base modifications (8OHdG), and (3) bulky lesions (cyclobutane pyrimidine dimers). UV also stimulates the cell to produce early response genes that activate a cascade of signaling molecules (e.g., protein kinases) and protective enzymes (e.g., haem oxygenase). The cell cycle is restricted via p53-dependent and -independent pathways to facilitate repair processes prior to replication and division. Failure to rescue the cell from replication block will ultimately lead to cell death, and apoptosis may be induced. The implications for UV-induced genotoxicity in disease are considered.</dc:description><dc:language>en</dc:language><dc:relation>http://www.scopus.com/inward/record.url?scp=0031825295&amp;partnerID=8YFLogxK</dc:relation><dc:source>1549-781X</dc:source><dc:title>Molecular and cellular effects of ultraviolet light-induced genotoxicity</dc:title><rioxxterms:author>Griffiths, Helen R.</rioxxterms:author><rioxxterms:author>Mistry, Pratibha</rioxxterms:author><rioxxterms:author>Herbert, Karl E.</rioxxterms:author><rioxxterms:author>Lunec, Joseph</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1080/10408369891234192</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:142
Date: 2017-08-22

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:publications.aston.ac.uk:142</identifier>
      <datestamp>2017-08-22T11:55:56Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
      <setSpec>74797065733D61727469636C65</setSpec></header>
    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>There appears to be a paucity of data examining the effect of dietary antioxidants on levels of oxidative DNA damage in vivo, limiting evidence-based assessment of antioxidant efficacy, mechanisms and recommendation for optimal intake. We have examined levels of 8-oxo-2'-deoxyguanosine (8-oxodG) in mononuclear cell DNA, serum and urine from subjects undergoing supplementation with 500 mg/day vitamin C. Significant decreases in DNA levels of 8-oxodG were seen, correlating strongly with increases in plasma vitamin C concentration. Furthermore we established a timecourse for sequential, significant increases in serum and urinary 8-oxodG levels. These results illustrate, for the first time in humans, the kinetics of 8-oxodG removal and processing in vivo, suggesting a role for vitamin C in the regulation of DNA repair enzymes and thereby demonstrating a non-scavenging antioxidant effect.</dc:description><dc:language>en</dc:language><dc:source>1873-3468</dc:source><dc:title>Novel repair action of vitamin C upon in vivo oxidative DNA damage</dc:title><rioxxterms:author>Cooke, Marcus S.</rioxxterms:author><rioxxterms:author>Evans, Mark D.</rioxxterms:author><rioxxterms:author>Podmore, Ian D.</rioxxterms:author><rioxxterms:author>Herbert, Karl E.</rioxxterms:author><rioxxterms:author>Mistry, Nalini</rioxxterms:author><rioxxterms:author>Mistry, Pratibha</rioxxterms:author><rioxxterms:author>Hickenbotham, Peter T.</rioxxterms:author><rioxxterms:author>Hussieni, Amina</rioxxterms:author><rioxxterms:author>Griffiths, Helen R.</rioxxterms:author><rioxxterms:author>Lunec, Joseph</rioxxterms:author><rioxxterms:publication_date>1998-11-20</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/S0014-5793(98)01403-3</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:141
Date: 2017-08-22

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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rioxxterms:projectMinimum of 1 value(s) required for rioxxterms:project - found 0 values
dcterms:dateAcceptedMinimum of 1 value(s) required for dcterms:dateAccepted - found 0 values
dc:identifierMinimum of 1 value(s) required for dc:identifier - found 0 values
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<record>
    <header>
      <identifier>oai:publications.aston.ac.uk:141</identifier>
      <datestamp>2017-08-22T11:55:55Z</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 relevance of reactive oxygen species (ROS) in the pathogenesis of inflammatory diseases is widely documented. Immunochemical detection of ROS DNA adducts has been developed, however, recognition of glyoxal-DNA adducts has not previously been described. We have generated a polyclonal antibody that has shown increased antibody binding to ROS-modified DNA in comparison to native DNA. In addition, dose-dependent antibody binding to DNA modified with ascorbate alone was shown, with significant inhibition by desferrioxamine, catalase, and ethanol. Minimal inhibition was observed with uric acid, 1,10-phenanthroline and DMSO. However, antibody binding in the presence of EDTA increased 3500-fold. The involvement of hydrogen peroxide and hydroxyl radical in ascorbate-mediated DNA damage is consistent with ascorbate acting as a reducing agent for DNA-bound metal ions. Glyoxal is known to be formed during oxidation of ascorbate. Glyoxylated DNA, that previously had been proposed as a marker of oxidative damage, was recognised in a dose dependent manner using the antibody. We describe the potential use of our anti-ROS DNA antibody, that detects predominantly Fenton-type mediated damage to DNA and report on its specificity for the recognition of glyoxal-DNA adducts.</dc:description><dc:language>en</dc:language><dc:source>1873-4596</dc:source><dc:title>Immunochemical detection of glyoxal DNA damage</dc:title><rioxxterms:author>Mistry, Nalini</rioxxterms:author><rioxxterms:author>Evans, Mark D.</rioxxterms:author><rioxxterms:author>Griffiths, Helen R.</rioxxterms:author><rioxxterms:author>Kasai, H.</rioxxterms:author><rioxxterms:author>Herbert, Karl E.</rioxxterms:author><rioxxterms:author>Lunec, Joseph</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/S0891-5849(98)00326-8</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:140
Date: 2017-09-06

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
This is not a valid RCUK-RIOXX record
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ali:license_refMinimum of 1 value(s) required for ali:license_ref - found 0 values
<record>
    <header>
      <identifier>oai:publications.aston.ac.uk:140</identifier>
      <datestamp>2017-09-06T11:30:05Z</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>During inflammation, many cell types release reactive oxygen species (ROS) via the respiratory burst. These ROS are potent oxidants of LDL and its major protein, apolipoprotein B. Whilst native LDL is taken up by endothelial cells via a feedback controlled receptor-regulated process, oxidative modification of LDL renders it a ligand for many scavenger receptors. Scavenger receptors include CD-36, LOX-1 and the prototypic macrophage SR A I/II, all of which are variably expressed. Uncontrolled uptake of oxidised LDL is implicated in the pathogenesis of atherosclerosis. In addition, oxidised LDL increases CCR2 protein and mRNA expression on monocytes, and thus may contribute to monocyte retention and perpetuation in inflammatory, unstable atherosclerotic lesions. However, little data are available on the effects of specific minor modifications to apolipoprotein B. In order to identify the sequence specificity and nature of oxidative modifications which confer altered properties on LDL, we have investigated the effects of modified peptides (which correspond to the putative LDLR binding domain) on LDL uptake by HUVECs and U937 monocytes.</dc:description><dc:language>en</dc:language><dc:source>1743-2928</dc:source><dc:title>Oxidative modification of a specific apolipoprotein B lysine residue confers altered receptor specificity on LDL</dc:title><rioxxterms:author>Griffiths, Helen R.</rioxxterms:author><rioxxterms:author>Wright, J.</rioxxterms:author><rioxxterms:author>Bevan, Ruth J.</rioxxterms:author><rioxxterms:author>Lunec, Joseph</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1179/135100099101535089</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:139
Date: 2017-08-14

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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ali:license_refMinimum of 1 value(s) required for ali:license_ref - found 0 values
<record>
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      <identifier>oai:publications.aston.ac.uk:139</identifier>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>We have investigated vitamin C supplementation effects on immunoglobulin oxidation (carbonyls) and total plasma protein sulfhydryls in healthy human volunteers. After receiving placebo, plasma ascorbate and oxidation markers were unchanged. Following 5 weeks supplementation with vitamin C (400 mg/day), plasma ascorbate increased but no significant effect on protein oxidation was observed. At 10 and 15 weeks supplementation, carbonyl levels were significantly reduced (P &lt; 0.01) in subjects with low baseline ascorbate (29.51 ± 5.3 μM) but not in those with normal baseline ascorbate (51.81 ± 2.3 μM). To eliminate any effect from seasonal variation in dietary antioxidant intake, a second phase was undertaken. Subjects on vitamin C for 15 weeks were randomly assigned to receive either placebo or vitamin C. No difference in plasma sulfhydryl content was observed. Subjects withdrawn from supplementation showed an increase in immunoglobulin carbonyl content (P &lt; 0.01). This demonstrates that dietary vitamin C supplementation can reduce certain types of oxidative protein damage in subjects with low basal antioxidant. (C) 2000 Academic Press.</dc:description><dc:language>en</dc:language><dc:relation>http://www.scopus.com/inward/record.url?scp=0033873751&amp;partnerID=8YFLogxK</dc:relation><dc:source>1090-2104</dc:source><dc:title>The effects of vitamin C supplementation on protein oxidation in healthy volunteers</dc:title><rioxxterms:author>Carty, Julie L.</rioxxterms:author><rioxxterms:author>Bevan, Ruth J.</rioxxterms:author><rioxxterms:author>Waller, Helen</rioxxterms:author><rioxxterms:author>Mistry, Nalini</rioxxterms:author><rioxxterms:author>Cooke, Marcus S.</rioxxterms:author><rioxxterms:author>Lunec, Joseph</rioxxterms:author><rioxxterms:author>Griffiths, Helen R.</rioxxterms:author><rioxxterms:publication_date>2000-07-05</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1006/bbrc.2000.3014</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:138
Date: 2017-08-13

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      <identifier>oai:publications.aston.ac.uk:138</identifier>
      <datestamp>2017-08-13T11:04:27Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><ali:free_to_read/><dc:description>Proteins are susceptible to oxidation by reactive oxygen species, where the type of damage induced is characteristic of the denaturing species. The induction of protein carbonyls is a widely applied biomarker, arising from primary oxidative insult. However, when applied to complex biological and pathological conditions it can be subject to interference from lipid, carbohydrate and DNA oxidation products. More recently, interest has focused on the analysis of specific protein bound oxidised amino acids. Of the 22 amino acids, aromatic and sulphydryl containing residues have been regarded as being particularly susceptible to oxidative modification, with L-DOPA from tyrosine, ortho-tyrosine from phenylalanine; sulphoxides and disulphides from methionine and cysteine respectively; and kynurenines from tryptophan. Latterly, the identification of valine and leucine hydroxides, reduced from hydroperoxide intermediates, has been described and applied. In order to examine the nature of oxidative damage and protective efficacy of antioxidants the markers must be thoroughly evaluated for dosimetry in vitro following damage by specific radical species. Antioxidant protection against formation of the biomarker should be demonstrated in vitro. Quantification of biomarkers in proteins from normal subjects should be within the limits of detection of any analytical procedure. Further to this, the techniques for isolation and hydrolysis of specific proteins should demonstrate that in vitro oxidation is minimised. There is a need for the development of standards for quality assurance material to standardise procedures between laboratories. At present, antioxidant effects on protein oxidation in vivo are limited to animal studies, where dietary antioxidants have been reported to reduce dityrosine formation during rat exercise training. Two studies on humans have been reported last year. The further application of these methods to human studies is indicated, where the quality of the determinations will be enhanced through inter-laboratory validation.</dc:description><dc:format>application/pdf</dc:format><dc:identifier>http://publications.aston.ac.uk/138/1/Antioxidants_and_protein_oxidationi.pdf</dc:identifier><dc:language>en</dc:language><dc:source>1029-2470</dc:source><dc:title>Antioxidants and protein oxidation</dc:title><rioxxterms:author>Griffiths, Helen R.</rioxxterms:author><rioxxterms:publication_date>2000-11</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://www.scopus.com/inward/record.url?scp=0034527069&amp;partnerID=8YFLogxK</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:137
Date: 2017-08-22

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      <identifier>oai:publications.aston.ac.uk:137</identifier>
      <datestamp>2017-08-22T11:55:55Z</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>Monocyte recruitment and retention in the vasculature is influenced by oxidative stress and is involved in cardiovascular disease (CVD). Individuals with low plasma ascorbate are at elevated risk of CVD. It is unknown whether vitamin C supplementation affects monocyte adhesion to endothelial cells (ECs) in healthy non-smokers. In a randomised double-blind crossover study the effect of vitamin C supplementation (six weeks, 250 mg/day) was determined in subjects with normal (HIC) and below average (LOC) plasma vitamin C concentration at baseline (mean = 67μM, n = 20, mean = 32μM, n = 20, respectively). LOC subjects showed 30% greater monocyte adhesion to ECs. This was significantly reduced by 37% (P &lt; 0.02) following vitamin C supplementation to levels of HIC monocyte adhesion. No differences in plasma malondialdehyde concentrations were observed between groups or after supplementation. In conclusion, vitamin C supplementation normalises monocyte adhesion in subjects with low plasma vitamin C (LOC). This process may be related to a direct effect on monocytes, independent of lipid peroxidation. © 2002 Elsevier Science (USA). All rights reserved.</dc:description><dc:language>en</dc:language><dc:source>1090-2104</dc:source><dc:title>Effects of oral vitamin C on monocyte:Endothelial cell adhesion in healthy subjects</dc:title><rioxxterms:author>Woollard, Kevin J.</rioxxterms:author><rioxxterms:author>Loryman, Chris J.</rioxxterms:author><rioxxterms:author>Meredith, Elizabeth</rioxxterms:author><rioxxterms:author>Bevan, Ruth J.</rioxxterms:author><rioxxterms:author>Shaw, Jacqui A.</rioxxterms:author><rioxxterms:author>Lunec, Joe</rioxxterms:author><rioxxterms:author>Griffiths, Helen 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/S0006-291X(02)00603-4</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:136
Date: 2017-10-02

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    <header>
      <identifier>oai:publications.aston.ac.uk:136</identifier>
      <datestamp>2017-10-02T07:01:45Z</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>Introduction – Why do we need ‘biomarkers? Biomarkers of protein oxidation Introduction Major issues/questions Protein carbonyl biomarkers Biochemistry Methods of measurement Storage, stability and limitations in use Protein thiol biomarkers Biochemistry Methods of measurement Storage, stability and limitations on use Aliphatic amino acid biomarkers Biochemistry Methods of measurement Storage, stability and limitations on use Oxidised Tryptophan Biomarkers Biochemistry Method of measurement Storage, stability and limitations on use Oxidised tyrosine biomarkers Biochemistry Methods of measurement Storage, stability and limitations on use Formation of neoepitopes on oxidised proteins Validation of assays for protein oxidation biomarkers Relationship of protein oxidation to disease Modulation of protein oxidation biomarkers by antioxidants Future perspectives Introduction to lipid peroxidation biomarkers Introduction: biochemistry of lipid peroxidation Malondialdehyde Methods of measurement Storage, stability and limitations on use Conjugated dienes Method of measurement Storage, stability and limitations of use LDL lag phase Method of measurement Storage, stability and limitations of use Hydrocarbon gases Biochemistry Method of measurement Storage, stability and limitations on use Lipofuscin Biochemistry Method of measurement Storage, stability and limitation on use Lipid peroxides Biochemistry Method of measurement Storage, stability and limitations on use Isoprostanes Biochemistry Method of measurement Storage, stability and limitations on use Possible new biomarkers of lipid oxidation Relationship of lipid peroxidation to disease Modulation of lipid peroxidation biomarkers by antioxidants Functional consequences of lipid peroxidation Contribution of dietary intake to lipid peroxidation products Biomarkers of DNA oxidation Introduction Confounding factors Units and terminology Nuclear and mitochondrial DNA damage Lymphocytes as surrogate tissues Measurement of DNA damage with the comet assay Practical details Storage, stability, and limitations of the assay Measurement of DNA base oxidation by HPLC Practical details Storage, stability and limitations of the method Measurement of DNA base oxidation by GC–MS Biochemistry of 8-oxoguanine, adenine and fapy derivatives Methods of measurement Storage, stability and limitations of the method Analysis of guanine oxidation products in urine Method of measurement Limitations and criticisms Immunochemical methods Methods of measurement Storage, stability, and limitations of the assay 32P post-labelling Method of measurement Limitations and criticisms Validation of assays for DNA oxidation Oxo-dGuo in lymphocyte DNA Urinary measurements DNA–aldehyde adducts Biochemistry Method of measurement Products of reactive nitrogen species Endpoints arising from oxidative DNA damage Mutations Chromosome aberrations Micronuclei Site-specific DNA damage Relationship of DNA oxidation to disease Modulation of DNA oxidation biomarkers by antioxidants Direct and indirect effects of oxidative stress: measures of total oxidant/antioxidant levels Visualisation of cellular oxidants Biochemistry: histochemical detection of ROS Method of measurement Limitations, storage and stability Measurement of hydrogen peroxide Biochemistry Methods of measurement Storage, stability and limitations on use Measurement of the ratio of antioxidant/oxidised antioxidant Biochemistry Method of measurement Storage, stability and limitations on use Total antioxidant capacity Biochemistry Terminology Methods of measurement Storage, stability and limitations on use Validation of assays for direct oxidant and antioxidant biomarkers Relationship of oxidant/antioxidant measurement to disease Modulation of oxidant/antioxidant biomarkers by dietary antioxidants Induction of genes in response to oxidative stress Background Measurement of antioxidant responsive genes and proteins Effects of antioxidant intake on the activity of antioxidant enzymes</dc:description><dc:language>en</dc:language><dc:relation>http://www.scopus.com/inward/record.url?scp=3042656269&amp;partnerID=8YFLogxK</dc:relation><dc:source>1872-9452</dc:source><dc:title>Biomarkers</dc:title><rioxxterms:author>Griffiths, Helen R.</rioxxterms:author><rioxxterms:author>Møller, Lennart</rioxxterms:author><rioxxterms:author>Bartosz, Grzegorz</rioxxterms:author><rioxxterms:author>Bast, Aalt</rioxxterms:author><rioxxterms:author>Bertoni-Freddari, Carlo</rioxxterms:author><rioxxterms:author>Collins, Andrew</rioxxterms:author><rioxxterms:author>Cooke, Marcus</rioxxterms:author><rioxxterms:author>Coolen, Stefan</rioxxterms:author><rioxxterms:author>Haenen, Guido</rioxxterms:author><rioxxterms:author>Hoberg, Anne Mette</rioxxterms:author><rioxxterms:author>Loft, Steffen</rioxxterms:author><rioxxterms:author>Lunec, Joe</rioxxterms:author><rioxxterms:author>Olinski, Ryszard</rioxxterms:author><rioxxterms:author>Parry, James</rioxxterms:author><rioxxterms:author>Pompella, Alfonso</rioxxterms:author><rioxxterms:author>Poulsen, Henrik</rioxxterms:author><rioxxterms:author>Verhagen, Hans</rioxxterms:author><rioxxterms:author>Astley, Siân B.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/S0098-2997(02)00017-1</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:135
Date: 2017-08-31

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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>Redox-sensitive cell signalling Thiol groups and the regulation of gene expression Redox-sensitive signal transduction pathways Protein kinases Protein phosphatases Lipids and phospholipases Antioxidant (electrophile) response element Intracellular calcium signalling Transcription factors NF-?B AP-1 p53 Cellular responses to oxidative stress Cellular responses to change in redox state Proliferation Cell death Immune cell function Reactive oxygen and nitrogen species – good or bad? Reactive oxygen species and cell death Reactive oxygen species and inflammation Are specific reactive oxygen species and antioxidants involved in modulating cellular responses? Specific effects of dietary antioxidants in cell regulation Carotenoids Vitamin E Flavonoids Inducers of phase II enzymes Disease states affected Oxidants, antioxidants and mitochondria Introduction Mitochondrial generation of reactive oxygen and nitrogen species Mitochondria and apoptosis Mitochondria and antioxidant defences Key role of mitochondrial GSH in the defence against oxidative damage Mitochondrial oxidative damage Direct oxidative damage to the mitochondrial electron transport chain Nitric oxide and damage to mitochondria Effects of nutrients on mitochondria Caloric restriction and antioxidants Lipids Antioxidants Techniques and approaches Mitochondrial techniques cDNA microarray approaches Proteomics approaches Transgenic mice as tools in antioxidant research Gene knockout and over expression Transgenic reporter mice Conclusions Future research needs</dc:description><dc:language>en</dc:language><dc:relation>http://www.scopus.com/inward/record.url?scp=0036088349&amp;partnerID=8YFLogxK</dc:relation><dc:source>1872-9452</dc:source><dc:title>Antioxidants, reactive oxygen and nitrogen species, gene induction and mitochondrial function</dc:title><rioxxterms:author>Jackson, Malcolm J.</rioxxterms:author><rioxxterms:author>Papa, Sergio</rioxxterms:author><rioxxterms:author>Bolaños, Juan</rioxxterms:author><rioxxterms:author>Bruckdorfer, Richard</rioxxterms:author><rioxxterms:author>Carlsen, Harald</rioxxterms:author><rioxxterms:author>Elliott, Ruan M</rioxxterms:author><rioxxterms:author>Flier, Jacoba</rioxxterms:author><rioxxterms:author>Griffiths, Helen R.</rioxxterms:author><rioxxterms:author>Heales, Simon</rioxxterms:author><rioxxterms:author>Holst, Birgit</rioxxterms:author><rioxxterms:author>Lorusso, Michele</rioxxterms:author><rioxxterms:author>Lund, Elizabeth</rioxxterms:author><rioxxterms:author>Øivind Moskaug, Jan</rioxxterms:author><rioxxterms:author>Moser, Ulrich</rioxxterms:author><rioxxterms:author>Di Paola, Marco</rioxxterms:author><rioxxterms:author>Polidori, M Cristina</rioxxterms:author><rioxxterms:author>Signorile, Anna</rioxxterms:author><rioxxterms:author>Stahl, Wilhelm</rioxxterms:author><rioxxterms:author>Viña-Ribes, José</rioxxterms:author><rioxxterms:author>Astley, Siân B.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/S0098-2997(02)00018-3</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:134
Date: 2017-09-05

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      <identifier>oai:publications.aston.ac.uk:134</identifier>
      <datestamp>2017-09-05T07:02:03Z</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>DNA is susceptible to damage by reactive oxygen species (ROS). ROS are produced during normal and pathophysiological processes in addition to ionizing radiation, environmental mutagens, and carcinogens. 8-oxo-2′-deoxyguanosine (8-oxodG) is probably one of the most abundant DNA lesion formed during oxidative stress. This potentially mutagenic lesion causes G → T transversions and is therefore an important candidate lesion for repair, particularly in mammalian cells. Several pathways exist for the removal, or repair, of this lesion from mammalian DNA. The most established is via the base excision repair enzyme, human 8-oxoguanine glycosylase (hOgg1), which acts in combination with the human apurinic endonuclease (hApe). The latter is known to respond to regulation by redox reactions and may act in combination with hOgg1. We discuss evidence in this review article concerning alternative pathways in humans, such as nucleotide excision repair (NER), which could possibly remove the 8-oxodG lesion. We also propose that redox-active components of the diet, such as vitamin C, may promote such repair, affecting NER specifically. © 2002 Elsevier Science Inc.</dc:description><dc:language>en</dc:language><dc:relation>http://www.scopus.com/inward/record.url?scp=0036801252&amp;partnerID=8YFLogxK</dc:relation><dc:source>1873-4596</dc:source><dc:title>Urinary 8-oxo-2′-deoxyguanosine:Redox regulation of DNA repair in vivo?</dc:title><rioxxterms:author>Lunec, Joseph</rioxxterms:author><rioxxterms:author>Holloway, Karen A.</rioxxterms:author><rioxxterms:author>Cooke, Marcus S.</rioxxterms:author><rioxxterms:author>Faux, Steve</rioxxterms:author><rioxxterms:author>Griffiths, Helen R.</rioxxterms:author><rioxxterms:author>Evans, Mark D.</rioxxterms:author><rioxxterms:publication_date>2002-10</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/S0891-5849(02)00882-1</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:128
Date: 2017-08-13

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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>Cellular thiols are critical moieties in signal transduction, regulation of gene expression, and ultimately are determinants of specific protein activity. Whilst protein bound thiols are the critical effector molecules, low molecular weight thiols, such as glutathione, play a central role in cytoprotection through (1) direct consumption of oxidants, (2) regeneration of protein thiols and (3) export of glutathione containing mixed disulphides. The brain is particularly vulnerable to oxidative stress, as it consumes 20% of oxygen load, contains high concentrations of polyunsaturated fatty acids and iron in certain regions, and expresses low concentrations of enzymic antioxidants. There is substantial evidence for a role for oxidative stress in neurodegenerative disease, where excitotoxic, redox cycling and mitochondrial dysfunction have been postulated to contribute to the enhanced oxidative load. Others have suggested that loss of important trophic factors may underlie neurodegeneration. However, the two are not mutually exclusive; using cell based model systems, low molecular weight antioxidants have been shown to play an important neuroprotective role in vitro, where neurotrophic factors have been suggested to modulate glutathione levels. Glutathione levels are regulated by substrate availability, synthetic enzyme and metabolic enzyme activity, and by the presence of other antioxidants, which according to the redox potential, consume or regenerate GSH from its oxidised partner. Therefore we have investigated the hypothesis that amyloid beta neurotoxicity is mediated by reactive oxygen species, where trophic factor cytoprotection against oxidative stress is achieved through regulation of glutathione levels. Using PC12 cells as a model system, amyloid beta 25-35 caused a shift in DCF fluorescence after four hours in culture. This fluorescence shift was attenuated by both desferioxamine and NGF. After four hours, cellular glutathione levels were depleted by as much as 75%, however, 24 hours following oxidant exposure, glutathione concentration was restored to twice the concentration seen in controls. NGF prevented both the loss of viability seen after 24 hours amyloid beta treatment and also protected glutathione levels. NGF decreased the total cellular glutathione concentration but did not affect expression of GCS. In conclusion, loss of glutathione precedes cell death in PC12 cells. However, at sublethal doses the surviving fraction respond to oxidative stress by increasing glutathione levels, where this is achieved, at least in part, at the gene level through upregulation of GCS. Whilst NGF does protect against oxidative toxicity, this is not achieved through upregulation of GCS or glutathione.</dc:description><dc:format>application/pdf</dc:format><dc:identifier>http://publications.aston.ac.uk/128/1/pisa_paper2.pdf</dc:identifier><dc:language>en</dc:language><dc:source>1872-8081</dc:source><dc:title>Is glutathione an important neuroprotective effector molecule against amyloid beta toxicity?</dc:title><rioxxterms:author>Barber, Vicki S.</rioxxterms:author><rioxxterms:author>Griffiths, Helen R.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>VoR</rioxxterms:version><rioxxterms:version_of_record>http://www.scopus.com/inward/record.url?scp=0142107442&amp;partnerID=8YFLogxK</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:125
Date: 2017-08-22

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      <identifier>oai:publications.aston.ac.uk:125</identifier>
      <datestamp>2017-08-22T11:55:54Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>The application of an antiserum to ultraviolet radiation (UVR)-damaged DNA is presented. A novel experimental system was employed to ascertain the limits of detection for this antiserum. Using a DNA standard containing a known amount of dimer, the limits of detection were found to be 0.9 fmol of dimer. This was compared to a limit of 20-50 fmol dimer using gas chromatography-mass spectrometry (GC-MS). Induction of thymine dimers in DNA following UVR exposure, as assessed using this antiserum in an enzyme-linked immunosorbent assay (ELISA), was compared with GC-MS measurements. The ELISA method successfully demonstrated the induction of lesions in DNA irradiated either with UVC or UVB, although despite high sensitivity, no discernible binding was seen to UVA-irradiated DNA. The antiserum was also shown to be applicable to immunocytochemistry, localising damage in the nuclei of UVR exposed keratinocytes in culture. The ability of the antiserum to detect DNA damage in skin biopsies of individuals exposed to sub-erythemal doses of UVR was also demonstrated. Moreover, the subsequent removal of this damage, as evidenced by a reduction in antiserum staining, was noted in sections of biopsies taken in the hours following irradiation. © 2003 Elsevier B.V. All rights reserved.</dc:description><dc:language>en</dc:language><dc:source>1872-7905</dc:source><dc:title>Immunochemical detection of UV-induced DNA damage and repair</dc:title><rioxxterms:author>Cooke, Marcus S.</rioxxterms:author><rioxxterms:author>Podmore, Ian D.</rioxxterms:author><rioxxterms:author>Mistry, Nalini</rioxxterms:author><rioxxterms:author>Evans, Mark D.</rioxxterms:author><rioxxterms:author>Herbert, Karl E.</rioxxterms:author><rioxxterms:author>Griffiths, Helen R.</rioxxterms:author><rioxxterms:author>Lunec, Joseph</rioxxterms:author><rioxxterms:publication_date>2003-09</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/S0022-1759(03)00269-2</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:123
Date: 2017-08-22

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    <header>
      <identifier>oai:publications.aston.ac.uk:123</identifier>
      <datestamp>2017-08-22T11:55:54Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>A model system is presented using human umbilical vein endothelial cells (HUVECs) to investigate the role of homocysteine (Hcy) in atherosclerosis. HUVECs are shown to export Hcy at a rate determined by the flux through the methionine/Hcy pathway. Additional methionine increases intracellular methionine, decreases intracellular folate, and increases Hcy export, whereas additional folate inhibits export. An inverse relationship exists between intracellular folate and Hcy export. Hcy export may be regulated by intracellular S-adenosyl methionine rather than by Hcy. Human LDLs exposed to HUVECs exporting Hcy undergo time-related lipid oxidation, a process inhibited by the thiol trap dithionitrobenzoate. This is likely to be related to the generation of hydroxyl radicals, which we show are associated with Hcy export. Although Hcy is the major oxidant, cysteine also contributes, as shown by the effect of glutamate. Finally, the LDL oxidized in this system showed a time-dependent increase in uptake by human macrophages, implying an upregulation of the scavenger receptor. These results suggest that continuous export of Hcy from endothelial cells contributes to the generation of extracellular hydroxyl radicals, with associated oxidative modification of LDL and incorporation into macrophages, a key step in atherosclerosis. Factors that regulate intracellular Hcy metabolism modulate these effects. Copyright © 2005 by the American Society for Biochemistry and Molecular Biology, Inc.</dc:description><dc:language>en</dc:language><dc:source>1539-7262</dc:source><dc:title>Downstream effects on human low density lipoprotein of homocysteine exported from endothelial cells in an in vitro system</dc:title><rioxxterms:author>Nakano, E.</rioxxterms:author><rioxxterms:author>Taiwo, F.A.</rioxxterms:author><rioxxterms:author>Nugent, D.</rioxxterms:author><rioxxterms:author>Griffiths, Helen R.</rioxxterms:author><rioxxterms:author>Aldred, S.</rioxxterms:author><rioxxterms:author>Paisi, M.</rioxxterms:author><rioxxterms:author>Kwok, M.</rioxxterms:author><rioxxterms:author>Bhatt, P.</rioxxterms:author><rioxxterms:author>Hill, M.H.E</rioxxterms:author><rioxxterms:author>Moat, S.</rioxxterms:author><rioxxterms:author>Powers, H.J.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1194/jlr.M400339-JLR200</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:116
Date: 2017-08-22

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    <header>
      <identifier>oai:publications.aston.ac.uk:116</identifier>
      <datestamp>2017-08-22T11:55:54Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>We recently reported that methionine-loaded human umbilical vein endothelial cells (HUVECs) exported homocysteine (Hcy) and were associated with hydroxyl radical generation and oxidation of lipids in LDL. Herein we have analysed the Hcy-induced posttranslational modifications (PTMs) of LDL protein. PTMs have been characterised using electrophoretic mobility shift, protein carbonyl ELISA, HPLC with electrochemical detection and Western blotting of 3-nitrotyrosine, and LDL uptake by scavenger receptors on monocyte/macrophages. We have also analysed PTMs in LDL isolated from rheumatoid (RA) and osteo-(OA) arthritis patients with cardiovascular disease (CVD). While reagent Hcy (&lt;50 μM) promoted copper-catalysed LDL protein oxidation, Hcy released from methionine-loaded HUVECs promoted LDL protein nitration. In addition, LDL nitration was associated with enhanced monocyte/macrophage uptake when compared with LDL oxidation. LDL protein nitration and uptake by monocytes, but not carbonyl formation, was elevated in both RA and OA patients with CVD compared with disease-matched patients that had no evidence of CVD. Moreover, a direct correlation between plasma total Hcy (tHcy) and LDL uptake was observed. The present studies suggest that elevated plasma tHcy may promote LDL nitration and increased scavenger receptor uptake, providing a molecular mechanism that may contribute to the clinical link between CVD and elevated plasma tHcy. © 2005 Elsevier Inc. All rights reserved.</dc:description><dc:language>en</dc:language><dc:source>1873-4596</dc:source><dc:title>Homocysteine from endothelial cells promotes LDL nitration and scavenger receptor uptake</dc:title><rioxxterms:author>Griffiths, Helen R.</rioxxterms:author><rioxxterms:author>Aldred, Sarah</rioxxterms:author><rioxxterms:author>Dale, Chloe</rioxxterms:author><rioxxterms:author>Nakano, Emi</rioxxterms:author><rioxxterms:author>Kitas, George D.</rioxxterms:author><rioxxterms:author>Grant, Melissa G.</rioxxterms:author><rioxxterms:author>Nugent, Desmond</rioxxterms:author><rioxxterms:author>Taiwo, Fatai A.</rioxxterms:author><rioxxterms:author>Li, Li</rioxxterms:author><rioxxterms:author>Powers, Hilary 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.freeradbiomed.2005.08.039</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:113
Date: 2017-08-22

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<record>
    <header>
      <identifier>oai:publications.aston.ac.uk:113</identifier>
      <datestamp>2017-08-22T11:55:53Z</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>Oxidised LDL accumulates in macrophages following scavenger receptor (SR) uptake. The expression of the SR, CD36, is increased by oxidised LDL. The signalling molecule, ceramide, can modulate intracellular peroxides and increase lipid peroxidation. Ceramide also accumulates in atherosclerotic plaques. Thus, we have examined whether ceramide can modulate CD36 expression and function in human monocyte/macrophages. Addition of synthetic short chain ceramides or the action of sphingomyelinase to generate physiological long chain ceramides in situ caused significant reductions in CD36 expression by monocytes/macrophages which was not due to inhibition of mRNA expression. Inhibition of proteasomal degradation using lactacystin had no effect on CD36 expression, however, flow cytometric analysis of permeabilised cells suggested an intracellular trafficking blockade. Ceramide treated monocytes/macrophages showed dose dependent reduction in oxidised LDL uptake. Taken together, it is suggested that ceramide blocks the transport of CD36 to the membrane of monocytes/macrophages, thereby preventing uptake of oxidised LDL. © 2006 Elsevier Inc. All rights reserved.</dc:description><dc:language>en</dc:language><dc:source>1096-0384</dc:source><dc:title>Ceramides reduce CD36 cell surface expression and oxidised LDL uptake by monocytes and macrophages</dc:title><rioxxterms:author>Luan, Yingjun</rioxxterms:author><rioxxterms:author>Griffiths, Helen 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.abb.2006.03.016</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:105
Date: 2017-10-03

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    <header>
      <identifier>oai:publications.aston.ac.uk:105</identifier>
      <datestamp>2017-10-03T07:02:20Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><ali:free_to_read/><dc:description>Biomolecules are susceptible to many different post-translational modifications that have important effects on their function and stability, including glycosylation, glycation, phosphorylation and oxidation chemistries. Specific conversion of aspartic acid to its isoaspartyl derivative or arginine to citrulline leads to autoantibody production in models of rheumatoid disease, and ensuing autoantibodies cross-react with native antigens. Autoimmune conditions associate with increased activation of immune effector cells and production of free radical species via NADPH oxidases and nitric oxide synthases. Generation of neo-antigenic determinants by reactive oxygen and nitrogen species ROS and RNS) may contribute to epitope spreading in autoimmunity. The oxidation of amino acids by peroxynitrite, hypochlorous acid and other reactive oxygen species (ROS) increases the antigenicity of DNA, LDL and IgG, generating ligands for which autoantibodies show higher avidity. This review focuses on the evidence for ROS and RNS in promoting the autoimmune responses observed in diseases rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). It considers the evidence for ROS/RNS-induced antigenicity arising as a consequence of failure to remove or repair ROS/RNS damaged biomolecules and suggests that an associated defect, probably in T cell signal processing or/or antigen presentation, is required for the development of disease.</dc:description><dc:format>application/pdf</dc:format><dc:identifier>http://publications.aston.ac.uk/105/1/autoimmunity_reviews.pdf</dc:identifier><dc:language>en</dc:language><dc:relation>http://www.scopus.com/inward/record.url?scp=50949105388&amp;partnerID=8YFLogxK</dc:relation><dc:source>1873-0183</dc:source><dc:title>Is the generation of neo-antigenic determinants by free radicals central to the development of autoimmune rheumatoid disease?</dc:title><rioxxterms:author>Griffiths, Helen R.</rioxxterms:author><rioxxterms:publication_date>2008-07</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/j.autrev.2008.04.013</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:104
Date: 2017-09-28

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    <header>
      <identifier>oai:publications.aston.ac.uk:104</identifier>
      <datestamp>2017-09-28T07:03:33Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><ali:free_to_read/><dc:description>Ascorbate can act as both a reducing and oxidising agent in vitro depending on its environment. It can modulate the intracellular redox environment of cells and therefore is predicted to modulate thiol-dependent cell signalling and gene expression pathways. Using proteomic analysis of vitamin C-treated T cells in vitro, we have previously reported changes in expression of five functional protein groups associated with signalling, carbohydrate metabolism, apoptosis, transcription and immune function. The increased expression of the signalling molecule phosphatidylinositol transfer protein (PITP) was also confirmed using Western blotting. Herein, we have compared protein changes elicited by ascorbate in vitro, with the effect of ascorbate on plasma potassium levels, on peripheral blood mononuclear cell (PBMC) apoptosis and PITP expression, in patients supplemented with vitamin C (0-2 g/d) for up to 10 weeks to investigate whether in vitro model systems are predictive of in vivo effects. PITP varied in expression widely between subjects at all time-points analysed but was increased by supplementation with 2 g ascorbate/d after 5 and 10 weeks. No effects on plasma potassium levels were observed in supplemented subjects despite a reduction of K+ channel proteins in ascorbate-treated T cells in vitro. Similarly, no effect of vitamin C supplementation on PBMC apoptosis was observed, whilst ascorbate decreased expression of caspase 3 recruitment domain protein in vitro. These data provide one of the first demonstrations that proteomics may be valuable in developing predictive markers of nutrient effects in vivo and may identify novel pathways for studying mechanisms of action in vivo.</dc:description><dc:format>application/pdf</dc:format><dc:identifier>http://publications.aston.ac.uk/104/1/BJN2009PITPvitC.pdf</dc:identifier><dc:language>en</dc:language><dc:relation>http://www.scopus.com/inward/record.url?scp=67649443915&amp;partnerID=8YFLogxK</dc:relation><dc:source>1475-2662</dc:source><dc:title>In vivo vitamin C supplementation increases phosphoinositol transfer protein expression in peripheral blood mononuclear cells from healthy individuals</dc:title><rioxxterms:author>Griffiths, Helen R.</rioxxterms:author><rioxxterms:author>Willetts, Rachel S.</rioxxterms:author><rioxxterms:author>Grant, Melissa M.</rioxxterms:author><rioxxterms:author>Mistry, Nalini</rioxxterms:author><rioxxterms:author>Lunec, Joseph</rioxxterms:author><rioxxterms:author>Bevan, Ruth J.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1017/S0007114508079646</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:97
Date: 2017-08-21

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      <identifier>oai:publications.aston.ac.uk:97</identifier>
      <datestamp>2017-08-21T07:28:24Z</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>Yorick Wilks is a central figure in the fields of Natural Language Processing and Artificial Intelligence. His influence extends to many areas and includes contributions to Machines Translation, word sense disambiguation, dialogue modeling and Information Extraction. This book celebrates the work of Yorick Wilks in the form of a selection of his papers which are intended to reflect the range and depth of his work. The volume accompanies a Festschrift which celebrates his contribution to the fields of Computational Linguistics and Artificial Intelligence. The papers include early work carried out at Cambridge University, descriptions of groundbreaking work on Machine Translation and Preference Semantics as well as more recent works on belief modeling and computational semantics. The selected papers reflect Yorick’s contribution to both practical and theoretical aspects of automatic language processing.</dc:description><dc:language>en</dc:language><dc:publisher>Springer</dc:publisher><dc:source>978-1-4020-5285-9</dc:source><dc:title>Words and intelligence I:selected papers by Yorick Wilks</dc:title><rioxxterms:contributor>Ahmad, Khurshid</rioxxterms:contributor><rioxxterms:contributor>Brewster, Christopher</rioxxterms:contributor><rioxxterms:contributor>Stevenson, Mark</rioxxterms:contributor><rioxxterms:type>Book</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1007/1-4020-5285-5</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:95
Date: 2017-08-14

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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>Automatic Term Recognition (ATR) is a fundamental processing step preceding more complex tasks such as semantic search and ontology learning. From a large number of methodologies available in the literature only a few are able to handle both single and multi-word terms. In this paper we present a comparison of five such algorithms and propose a combined approach using a voting mechanism. We evaluated the six approaches using two different corpora and show how the voting algorithm performs best on one corpus (a collection of texts from Wikipedia) and less well using the Genia corpus (a standard life science corpus). This indicates that choice and design of corpus has a major impact on the evaluation of term recognition algorithms. Our experiments also showed that single-word terms can be equally important and occupy a fairly large proportion in certain domains. As a result, algorithms that ignore single-word terms may cause problems to tasks built on top of ATR. Effective ATR systems also need to take into account both the unstructured text and the structured aspects and this means information extraction techniques need to be integrated into the term recognition process.</dc:description><dc:language>en</dc:language><dc:source>Proceedings of the Sixth International Conference on Language Resources and Evaluation (LREC08)</dc:source><dc:title>A comparative evaluation of term recognition algorithms</dc:title><rioxxterms:author>Zhang, Ziqi</rioxxterms:author><rioxxterms:author>Iria, José</rioxxterms:author><rioxxterms:author>Brewster, Christopher</rioxxterms:author><rioxxterms:author>Ciravegna, Fabio</rioxxterms:author><rioxxterms:type>Book chapter</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:94
Date: 2017-08-23

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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 main argument of this paper is that Natural Language Processing (NLP) does, and will continue to, underlie the Semantic Web (SW), including its initial construction from unstructured sources like the World Wide Web (WWW), whether its advocates realise this or not. Chiefly, we argue, such NLP activity is the only way up to a defensible notion of meaning at conceptual levels (in the original SW diagram) based on lower level empirical computations over usage. Our aim is definitely not to claim logic-bad, NLP-good in any simple-minded way, but to argue that the SW will be a fascinating interaction of these two methodologies, again like the WWW (which has been basically a field for statistical NLP research) but with deeper content. Only NLP technologies (and chiefly information extraction) will be able to provide the requisite RDF knowledge stores for the SW from existing unstructured text databases in the WWW, and in the vast quantities needed. There is no alternative at this point, since a wholly or mostly hand-crafted SW is also unthinkable, as is a SW built from scratch and without reference to the WWW. We also assume that, whatever the limitations on current SW representational power we have drawn attention to here, the SW will continue to grow in a distributed manner so as to serve the needs of scientists, even if it is not perfect. The WWW has already shown how an imperfect artefact can become indispensable.</dc:description><dc:language>en</dc:language><dc:source>1555-0788</dc:source><dc:title>Natural language processing as a foundation of the semantic Web</dc:title><rioxxterms:author>Wilks, Yorick</rioxxterms:author><rioxxterms:author>Brewster, Christopher</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1561/1800000002</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:93
Date: 2017-09-01

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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>This paper describes part of the corpus collection efforts underway in the EC funded Companions project. The Companions project is collecting substantial quantities of dialogue a large part of which focus on reminiscing about photographs. The texts are in English and Czech. We describe the context and objectives for which this dialogue corpus is being collected, the methodology being used and make observations on the resulting data. The corpora will be made available to the wider research community through the Companions Project web site.</dc:description><dc:language>en</dc:language><dc:source>Proceedings of the Sixth International Conference on Language Resources and Evaluation (LREC08)</dc:source><dc:title>Dialogue, speech and images:the companions project data set</dc:title><rioxxterms:author>Wilks, Yorick</rioxxterms:author><rioxxterms:author>Benyon, David</rioxxterms:author><rioxxterms:author>Brewster, Christopher</rioxxterms:author><rioxxterms:author>Ircing, Pavel</rioxxterms:author><rioxxterms:author>Mival, Oli</rioxxterms:author><rioxxterms:publication_date>2008-06</rioxxterms:publication_date><rioxxterms:type>Book chapter</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:92
Date: 2017-09-14

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ID: oai:publications.aston.ac.uk:91
Date: 2017-08-29

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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>In this paper we present a new approach to ontology learning. Its basis lies in a dynamic and iterative view of knowledge acquisition for ontologies. The Abraxas approach is founded on three resources, a set of texts, a set of learning patterns and a set of ontological triples, each of which must remain in equilibrium. As events occur which disturb this equilibrium various actions are triggered to re-establish a balance between the resources. Such events include acquisition of a further text from external resources such as the Web or the addition of ontological triples to the ontology. We develop the concept of a knowledge gap between the coverage of an ontology and the corpus of texts as a measure triggering actions. We present an overview of the algorithm and its functionalities.</dc:description><dc:format>application/pdf</dc:format><dc:identifier>http://publications.aston.ac.uk/91/1/Iria_lrec_abraxas.pdf</dc:identifier><dc:language>en</dc:language><dc:source>[Proceedings of the 5th edition of the international conference on language resources and evaluation]</dc:source><dc:title>An incremental tri-partite approach to ontology learning</dc:title><rioxxterms:author>Iria, José</rioxxterms:author><rioxxterms:author>Brewster, Christopher</rioxxterms:author><rioxxterms:author>Ciravegna, Fabio</rioxxterms:author><rioxxterms:author>Wilks, Yorick</rioxxterms:author><rioxxterms:publication_date>2006-05</rioxxterms:publication_date><rioxxterms:type>Book chapter</rioxxterms:type><rioxxterms:version>SMUR</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:89
Date: 2017-10-02

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ID: oai:publications.aston.ac.uk:88
Date: 2017-08-22

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ID: oai:publications.aston.ac.uk:87
Date: 2017-08-17

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ID: oai:publications.aston.ac.uk:85
Date: 2017-10-05

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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><ali:free_to_read/><dc:description>The fundamental failure of current approaches to ontology learning is to view it as single pipeline with one or more specific inputs and a single static output. In this paper, we present a novel approach to ontology learning which takes an iterative view of knowledge acquisition for ontologies. Our approach is founded on three open-ended resources: a set of texts, a set of learning patterns and a set of ontological triples, and the system seeks to maintain these in equilibrium. As events occur which disturb this equilibrium, actions are triggered to re-establish a balance between the resources. We present a gold standard based evaluation of the final output of the system, the intermediate output showing the iterative process and a comparison of performance using different seed input. The results are comparable to existing performance in the literature.</dc:description><dc:format>application/pdf</dc:format><dc:identifier>http://publications.aston.ac.uk/85/1/Iria_lrec_abraxas.pdf</dc:identifier><dc:language>en</dc:language><dc:source>6th International Conference on Recent Advances in Natural Language Processing</dc:source><dc:title>Dynamic iterative ontology learning</dc:title><rioxxterms:author>Brewster, Christopher</rioxxterms:author><rioxxterms:author>Iria, José</rioxxterms:author><rioxxterms:author>Zhang, Ziqi</rioxxterms:author><rioxxterms:author>Ciravegna, Fabio</rioxxterms:author><rioxxterms:author>Guthrie, Louise</rioxxterms:author><rioxxterms:author>Wilks, Yorick</rioxxterms:author><rioxxterms:type>Conference Paper/Proceeding/Abstract</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:83
Date: 2017-08-03

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      <identifier>oai:publications.aston.ac.uk:83</identifier>
      <datestamp>2017-08-03T08:12:06Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><ali:free_to_read/><dc:description>In the context of the needs of the Semantic Web and Knowledge Management, we consider what the requirements are of ontologies. The ontology as an artifact of knowledge representation is in danger of becoming a Chimera. We present a series of facts concerning the foundations on which automated ontology construction must build. We discuss a number of different functions that an ontology seeks to fulfill, and also a wish list of ideal functions. Our objective is to stimulate discussion as to the real requirements of ontology engineering and take the view that only a selective and restricted set of requirements will enable the beast to fly.</dc:description><dc:format>application/pdf</dc:format><dc:identifier>http://publications.aston.ac.uk/83/1/dagstuhl05.pdf</dc:identifier><dc:language>en</dc:language><dc:source>[Proceedings of the Dagstuhl Seminar on Machine Learning for the Semantic Web]</dc:source><dc:title>The ontology: Chimaera or Pegasus</dc:title><rioxxterms:author>Brewster, Christopher</rioxxterms:author><rioxxterms:author>Iria, José</rioxxterms:author><rioxxterms:author>Ciravegna, Fabio</rioxxterms:author><rioxxterms:author>Wilks, Yorick</rioxxterms:author><rioxxterms:contributor>Kushmerick, N.</rioxxterms:contributor><rioxxterms:contributor>Ciravegna, F.</rioxxterms:contributor><rioxxterms:contributor>Doan, A.</rioxxterms:contributor><rioxxterms:contributor>Knoblock, C.</rioxxterms:contributor><rioxxterms:contributor>Stabb, S.</rioxxterms:contributor><rioxxterms:type>Book chapter</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:82
Date: 2017-09-27

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      <identifier>oai:publications.aston.ac.uk:82</identifier>
      <datestamp>2017-09-27T07:19:12Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><ali:free_to_read/><dc:description>We present a vision and a proposal for using Semantic Web technologies in the organic food industry. This is a very knowledge intensive industry at every step from the producer, to the caterer or restauranteur, through to the consumer. There is a crucial need for a concept of environmental audit which would allow the various stake holders to know the full environmental impact of their economic choices. This is a di?erent and parallel form of knowledge to that of price. Semantic Web technologies can be used e?ectively for the calculation and transfer of this type of knowledge (together with other forms of multimedia data) which could contribute considerably to the commercial and educational impact of the organic food industry. We outline how this could be achieved as our essential ob jective is to show how advanced technologies could be used to both reduce ecological impact and increase public awareness.</dc:description><dc:format>application/pdf</dc:format><dc:identifier>http://publications.aston.ac.uk/82/1/Brewster_SWCASE.pdf</dc:identifier><dc:language>en</dc:language><dc:source>ISWC Worskshop Semantic Web Case Studies and Best Practice for eBusiness (SWCASE 05) , 4th International Semantic Web Conference</dc:source><dc:title>AKTive Food:semantic web based knowledge conduits for the organic food industry</dc:title><rioxxterms:author>Brewster, Christopher</rioxxterms:author><rioxxterms:author>Glaser, Hugh</rioxxterms:author><rioxxterms:author>Haughton, Barny</rioxxterms:author><rioxxterms:type>Book chapter</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:81
Date: 2017-07-26

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      <identifier>oai:publications.aston.ac.uk:81</identifier>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>With this paper, we propose a set of techniques to largely automate the process of KA, by using technologies based on Information Extraction (IE) , Information Retrieval and Natural Language Processing. We aim to reduce all the impeding factors mention above and thereby contribute to the wider utility of the knowledge management tools. In particular we intend to reduce the introspection of knowledge engineers or the extended elicitations of knowledge from experts by extensive textual analysis using a variety of methods and tools, as texts are largely available and in them - we believe - lies most of an organization's memory.</dc:description><dc:language>en</dc:language><dc:publisher>CEUR-WS.org</dc:publisher><dc:source>Proceeding of the IJCAI-2001 Workshop on Ontology Learning</dc:source><dc:title>Knowledge acquisition for knowledge management: position paper</dc:title><rioxxterms:author>Brewster, Christopher A.</rioxxterms:author><rioxxterms:author>Ciravegna, Fabio</rioxxterms:author><rioxxterms:author>Wilks, Yorick</rioxxterms:author><rioxxterms:type>Book chapter</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:80
Date: 2017-08-22

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      <identifier>oai:publications.aston.ac.uk:80</identifier>
      <datestamp>2017-08-22T11:55:52Z</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>Automatic ontology building is a vital issue in many fields where they are currently built manually. This paper presents a user-centred methodology for ontology construction based on the use of Machine Learning and Natural Language Processing. In our approach, the user selects a corpus of texts and sketches a preliminary ontology (or selects an existing one) for a domain with a preliminary vocabulary associated to the elements in the ontology (lexicalisations). Examples of sentences involving such lexicalisation (e.g. ISA relation) in the corpus are automatically retrieved by the system. Retrieved examples are validated by the user and used by an adaptive Information Extraction system to generate patterns that discover other lexicalisations of the same objects in the ontology, possibly identifying new concepts or relations. New instances are added to the existing ontology or used to tune it. This process is repeated until a satisfactory ontology is obtained. The methodology largely automates the ontology construction process and the output is an ontology with an associated trained leaner to be used for further ontology modifications.</dc:description><dc:language>en</dc:language><dc:publisher>Springer</dc:publisher><dc:source>978-3-540-36271-5</dc:source><dc:title>User-centred ontology learning for knowledge management</dc:title><rioxxterms:author>Brewster, Christopher</rioxxterms:author><rioxxterms:author>Ciravegna, Fabio</rioxxterms:author><rioxxterms:author>Wilks, Yorick</rioxxterms:author><rioxxterms:contributor>Andersson, Birger</rioxxterms:contributor><rioxxterms:contributor>Bergholtz, Maria</rioxxterms:contributor><rioxxterms:contributor>Johannesson, Paul</rioxxterms:contributor><rioxxterms:publication_date>2002-06</rioxxterms:publication_date><rioxxterms:type>Book chapter</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1007/3-540-36271-1_18</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:79
Date: 2017-08-25

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      <identifier>oai:publications.aston.ac.uk:79</identifier>
      <datestamp>2017-08-25T07:12:08Z</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>Ontologies have become a key component in the Semantic Web and Knowledge management. One accepted goal is to construct ontologies from a domain specific set of texts. An ontology reflects the background knowledge used in writing and reading a text. However, a text is an act of knowledge maintenance, in that it re-enforces the background assumptions, alters links and associations in the ontology, and adds new concepts. This means that background knowledge is rarely expressed in a machine interpretable manner. When it is, it is usually in the conceptual boundaries of the domain, e.g. in textbooks or when ideas are borrowed into other domains. We argue that a partial solution to this lies in searching external resources such as specialized glossaries and the internet. We show that a random selection of concept pairs from the Gene Ontology do not occur in a relevant corpus of texts from the journal Nature. In contrast, a significant proportion can be found on the internet. Thus, we conclude that sources external to the domain corpus are necessary for the automatic construction of ontologies.</dc:description><dc:language>en</dc:language><dc:source>Proceedings of the Semantic Web Workshop</dc:source><dc:title>Background and foreground knowledge in dynamic ontology construction</dc:title><rioxxterms:author>Brewster, Christopher</rioxxterms:author><rioxxterms:author>Ciravegna, Fabio</rioxxterms:author><rioxxterms:author>Wilks, Yorick</rioxxterms:author><rioxxterms:publication_date>2003</rioxxterms:publication_date><rioxxterms:type>Book chapter</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:77
Date: 2017-09-05

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      <identifier>oai:publications.aston.ac.uk:77</identifier>
      <datestamp>2017-09-05T07:18:02Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>The evaluation of ontologies is vital for the growth of the Semantic Web. We consider a number of problems in evaluating a knowledge artifact like an ontology. We propose in this paper that one approach to ontology evaluation should be corpus or data driven. A corpus is the most accessible form of knowledge and its use allows a measure to be derived of the ‘fit’ between an ontology and a domain of knowledge. We consider a number of methods for measuring this ‘fit’ and propose a measure to evaluate structural fit, and a probabilistic approach to identifying the best ontology.</dc:description><dc:language>en</dc:language><dc:source>[LREC 2004 Proceedings]</dc:source><dc:title>Data driven ontology evaluation</dc:title><rioxxterms:author>Brewster, Christopher</rioxxterms:author><rioxxterms:author>Alani, Harith</rioxxterms:author><rioxxterms:author>Dasmahapatra, Srinandan</rioxxterms:author><rioxxterms:author>Wilks, Yorick</rioxxterms:author><rioxxterms:publication_date>2004</rioxxterms:publication_date><rioxxterms:type>Book chapter</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:76
Date: 2017-07-20

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      <datestamp>2017-07-20T07:06:33Z</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>Ontologies have become widely accepted as the main method for representing knowledge in Knowledge Management (KM) applica-tions. Given the continuous and rapid change and dynamic nature of knowledge in all fields, automated methods for construct-ing ontologies are of great importance. All ontologies or taxonomies currently in use have been hand built and require consider-able manpower to keep up to date. Taxono-mies are less logically rigorous than ontolo-gies, and in this paper we consider the re-quirements for a system which automatically constructed taxonomies. There are a number of potentially useful methods for construct-ing hierarchically organised concepts from a collection of texts and there are a number of automatic methods which permit one to as-sociate one word with another. The impor-tant issue for the successful development of this research area is to identify techniques for labelling the relation between two candi-date terms, if one exists. We consider a number of possible approaches and argue that the majority are unsuitable for our re-quirements.</dc:description><dc:language>en</dc:language><dc:source>[Proceedings of the 5th Annual CLUK Research Colloquium]</dc:source><dc:title>Techniques for automated taxonomy building: towards ontologies for knowledge management</dc:title><rioxxterms:author>Brewster, Christopher A.</rioxxterms:author><rioxxterms:type>Book chapter</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:75
Date: 2017-08-22

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      <identifier>oai:publications.aston.ac.uk:75</identifier>
      <datestamp>2017-08-22T07:18:12Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Knowledge maintenance is a major challenge for both knowledge management and the Semantic Web. Operating over the Semantic Web, there will be a network of collaborating agents, each with their own ontologies or knowledge bases. Change in the knowledge state of one agent may need to be propagated across a number of agents and their associated ontologies. The challenge is to decide how to propagate a change of knowledge state. The effects of a change in knowledge state cannot be known in advance, and so an agent cannot know who should be informed unless it adopts a simple ‘tell everyone – everything’ strategy. This situation is highly reminiscent of the classic Frame Problem in AI. We argue that for agent-based technologies to succeed, far greater attention must be given to creating an appropriate model for knowledge update. In a closed system, simple strategies are possible (e.g. ‘sleeping dog’ or ‘cheap test’ or even complete checking). However, in an open system where cause and effect are unpredictable, a coherent cost-benefit based model of agent interaction is essential. Otherwise, the effectiveness of every act of knowledge update/maintenance is brought into question.</dc:description><dc:language>en</dc:language><dc:source>[Proceedings of the 6th Annual CLUK Research Colloquium]</dc:source><dc:title>Knowledge maintenance and the frame problem</dc:title><rioxxterms:author>Brewster, Christopher</rioxxterms:author><rioxxterms:publication_date>2003</rioxxterms:publication_date><rioxxterms:type>Book chapter</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:73
Date: 2017-09-04

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    <header>
      <identifier>oai:publications.aston.ac.uk:73</identifier>
      <datestamp>2017-09-04T07:20:49Z</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>AKT is a major research project applying a variety of technologies to knowledge management. Knowledge is a dynamic, ubiquitous resource, which is to be found equally in an expert's head, under terabytes of data, or explicitly stated in manuals. AKT will extend knowledge management technologies to exploit the potential of the semantic web, covering the use of knowledge over its entire lifecycle, from acquisition to maintenance and deletion. In this paper we discuss how HLT will be used in AKT and how the use of HLT will affect different areas of KM, such as knowledge acquisition, retrieval and publishing.</dc:description><dc:language>en</dc:language><dc:source>Proceedings of the ACL2001 Workshop on Human Language Technology and Knowledge Management</dc:source><dc:title>Using HLT for acquiring, retrieving and publishing knowledge in AKT:position paper</dc:title><rioxxterms:author>Bontcheva, Kalina</rioxxterms:author><rioxxterms:author>Brewster, Christopher</rioxxterms:author><rioxxterms:author>Cunningham, Hamish</rioxxterms:author><rioxxterms:author>Guthrie, Louise</rioxxterms:author><rioxxterms:author>Ciravegna, Fabio</rioxxterms:author><rioxxterms:author>Gaizauskas, Robert</rioxxterms:author><rioxxterms:author>Wilks, Yorick</rioxxterms:author><rioxxterms:publication_date>2001</rioxxterms:publication_date><rioxxterms:type>Book chapter</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:72
Date: 2017-09-08

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    <header>
      <identifier>oai:publications.aston.ac.uk:72</identifier>
      <datestamp>2017-09-08T07:13:19Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>In view of the need to provide tools to facilitate the re-use of existing knowledge structures such as ontologies, we present in this paper a system, AKTiveRank, for the ranking of ontologies. AKTiveRank uses as input the search terms provided by a knowledge engineer and, using the output of an ontology search engine, ranks the ontologies. We apply a number of metrics in an attempt to investigate their appropriateness for ranking ontologies, and compare the results with a questionnaire-based human study. Our results show that AKTiveRank will have great utility although there is potential for improvement.</dc:description><dc:language>en</dc:language><dc:publisher>ACM</dc:publisher><dc:source>978-1-59593-163-4</dc:source><dc:title>Ontology ranking based on the analysis of concept structures</dc:title><rioxxterms:author>Alani, Harith</rioxxterms:author><rioxxterms:author>Brewster, Christopher</rioxxterms:author><rioxxterms:publication_date>2005-10</rioxxterms:publication_date><rioxxterms:type>Book chapter</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1145/1088622.1088633</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:71
Date: 2017-07-24

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    <header>
      <identifier>oai:publications.aston.ac.uk:71</identifier>
      <datestamp>2017-07-24T07:22:56Z</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>Representing knowledge using domain ontologies has shown to be a useful mechanism and format for managing and exchanging information. Due to the difficulty and cost of building ontologies, a number of ontology libraries and search engines are coming to existence to facilitate reusing such knowledge structures. The need for ontology ranking techniques is becoming crucial as the number of ontologies available for reuse is continuing to grow. In this paper we present AKTiveRank, a prototype system for ranking ontologies based on the analysis of their structures. We describe the metrics used in the ranking system and present an experiment on ranking ontologies returned by a popular search engine for an example query.</dc:description><dc:language>en</dc:language><dc:source>[Proceedings of the Workshop on Evaluating Ontologies for the Web]</dc:source><dc:title>Metrics for ranking ontologies</dc:title><rioxxterms:author>Alani, Harith</rioxxterms:author><rioxxterms:author>Brewster, Christopher A.</rioxxterms:author><rioxxterms:type>Book chapter</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:70
Date: 2017-09-08

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    <header>
      <identifier>oai:publications.aston.ac.uk:70</identifier>
      <datestamp>2017-09-08T07:13:22Z</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>Ontology search and reuse is becoming increasingly important as the quest for methods to reduce the cost of constructing such knowledge structures continues. A number of ontology libraries and search engines are coming to existence to facilitate locating and retrieving potentially relevant ontologies. The number of ontologies available for reuse is steadily growing, and so is the need for methods to evaluate and rank existing ontologies in terms of their relevance to the needs of the knowledge engineer. This paper presents AKTiveRank, a prototype system for ranking ontologies based on a number of structural metrics.</dc:description><dc:language>en</dc:language><dc:publisher>Springer</dc:publisher><dc:source>The Semantic Web - ISWC 2006</dc:source><dc:title>Ranking ontologies with AKTiveRank</dc:title><rioxxterms:author>Alani, Harith</rioxxterms:author><rioxxterms:author>Brewster, Christopher</rioxxterms:author><rioxxterms:author>Shadbolt, Nigel</rioxxterms:author><rioxxterms:contributor>Cruz, Isabel</rioxxterms:contributor><rioxxterms:contributor>Decker, Stefan</rioxxterms:contributor><rioxxterms:contributor>Allemang, Dean</rioxxterms:contributor><rioxxterms:contributor>Preist, Chris</rioxxterms:contributor><rioxxterms:contributor>Schwabe, Daniel</rioxxterms:contributor><rioxxterms:contributor>Mika, Peter</rioxxterms:contributor><rioxxterms:contributor>Uschold, Mike</rioxxterms:contributor><rioxxterms:contributor>Aroyo, Lora M.</rioxxterms:contributor><rioxxterms:type>Book chapter</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1007/11926078_1</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:68
Date: 2017-08-22

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    <header>
      <identifier>oai:publications.aston.ac.uk:68</identifier>
      <datestamp>2017-08-22T11:55:52Z</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>Objective: To introduce a new technique for co-registration of Magnetoencephalography (MEG) with magnetic resonance imaging (MRI). We compare the accuracy of a new bite-bar with fixed fiducials to a previous technique whereby fiducial coils were attached proximal to landmarks on the skull. Methods: A bite-bar with fixed fiducial coils is used to determine the position of the head in the MEG co-ordinate system. Co-registration is performed by a surface-matching technique. The advantage of fixing the coils is that the co-ordinate system is not based upon arbitrary and operator dependent fiducial points that are attached to landmarks (e.g. nasion and the preauricular points), but rather on those that are permanently fixed in relation to the skull. Results: As a consequence of minimizing coil movement during digitization, errors in localization of the coils are significantly reduced, as shown by a randomization test. Displacement of the bite-bar caused by removal and repositioning between MEG recordings is minimal (∼0.5 mm), and dipole localization accuracy of a somatosensory mapping paradigm shows a repeatability of ∼5 mm. The overall accuracy of the new procedure is greatly improved compared to the previous technique. Conclusions: The test-retest reliability and accuracy of target localization with the new design is superior to techniques that incorporate anatomical-based fiducial points or coils placed on the circumference of the head. © 2003 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.</dc:description><dc:language>en</dc:language><dc:source>1872-8952</dc:source><dc:title>Co-registration of magnetoencephalography with magnetic resonance imaging using bite-bar-based fiducials and surface-matching</dc:title><rioxxterms:author>Adjamian, Peyman</rioxxterms:author><rioxxterms:author>Barnes, Gareth R.</rioxxterms:author><rioxxterms:author>Hillebrand, Arjan</rioxxterms:author><rioxxterms:author>Holliday, Ian E.</rioxxterms:author><rioxxterms:author>Singh, Krish D.</rioxxterms:author><rioxxterms:author>Furlong, Paul L.</rioxxterms:author><rioxxterms:author>Harrington, E.</rioxxterms:author><rioxxterms:author>Barclay, C.W.</rioxxterms:author><rioxxterms:author>Route, P.J.G.</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.clinph.2003.10.023</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:67
Date: 2017-09-05

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      <identifier>oai:publications.aston.ac.uk:67</identifier>
      <datestamp>2017-09-05T07:02:27Z</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>Using magnetoencephalography, we studied the spatiotemporal properties of cortical responses in terms of event-related synchronization and event-related desynchronization to a range of stripe patterns in subjects with no neurological disorders. These stripes are known for their tendency to induce a range of abnormal sensations, such as illusions, nausea, dizziness, headache and attacks of pattern-sensitive epilepsy. The optimal stimulus must have specific physical properties, and maximum abnormalities occur at specific spatial frequency and contrast. Despite individual differences in the severity of discomfort experienced, psychophysical studies have shown that most observers experience some degree of visual anomaly on viewing such patterns. In a separate experiment, subjects reported the incidence of illusions and discomfort to each pattern. We found maximal cortical power in the gamma range (30-60 Hz) confined to the region of the primary visual cortex in response to patterns of 2-4 cycles per degree, peaking at 3 cycles per degree. This coincides with the peak of mean illusions and discomfort, also maximal for patterns of 2-4 cycles per degree. We show that gamma band activity in V1 is a narrow band function of spatial frequency. We hypothesize that the intrinsic properties of gamma oscillations may underlie visual discomfort and play a role in the onset of seizures.</dc:description><dc:language>en</dc:language><dc:relation>http://www.scopus.com/inward/record.url?scp=3242815204&amp;partnerID=8YFLogxK</dc:relation><dc:source>1460-9568</dc:source><dc:title>Induced visual illusions and gamma oscillations in human primary visual cortex</dc:title><rioxxterms:author>Adjamian, Peyman</rioxxterms:author><rioxxterms:author>Holliday, Ian E.</rioxxterms:author><rioxxterms:author>Barnes, Gareth R.</rioxxterms:author><rioxxterms:author>Hillebrand, Arjan</rioxxterms:author><rioxxterms:author>Hadjipapas, Avgis</rioxxterms:author><rioxxterms:author>Singh, Krish D.</rioxxterms:author><rioxxterms:publication_date>2004-07</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1111/j.1460-9568.2004.03495.x</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:65
Date: 2017-08-22

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      <identifier>oai:publications.aston.ac.uk:65</identifier>
      <datestamp>2017-08-22T11:55:51Z</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:description>Gamma activity to stationary grating stimuli was studied non-invasively using MEG recordings in humans. Using a spatial filtering technique, we localized gamma activity to primary visual cortex. We tested the hypothesis that spatial frequency properties of visual stimuli may be related to the temporal frequency characteristics of the associated cortical responses. We devised a method to assess temporal frequency differences between stimulus-related responses that typically exhibit complex spectral shapes. We applied this methodology to either single-trial (induced) or time-averaged (evoked) responses in four frequency ranges (0-40, 20-60, 40-80 and 60-100 Hz) and two time windows (either the entire duration of stimulus presentation or the first second following stimulus onset). Our results suggest that stimuli of varying spatial frequency induce responses that exhibit significantly different temporal frequency characteristics. These effects were particularly accentuated for induced responses in the classical gamma frequency band (20-60 Hz) analyzed over the entire duration of stimulus presentation. Strikingly, examining the first second of the responses following stimulus onset resulted in significant loss in stimulus specificity, suggesting that late signal components contain functionally relevant information. These findings advocate a functional role of gamma activity in sensory representation. We suggest that stimulus specific frequency characteristics of MEG signals can be mapped to processes of neuronal synchronization within the framework of coupled dynamical systems.</dc:description><dc:language>en</dc:language><dc:source>1095-9572</dc:source><dc:title>Stimuli of varying spatial scale induce gamma activity with distinct temporal characteristics in human visual cortex</dc:title><rioxxterms:author>Hadjipapas, Avgis</rioxxterms:author><rioxxterms:author>Adjamian, Peyman</rioxxterms:author><rioxxterms:author>Swettenham, Jennifer B.</rioxxterms:author><rioxxterms:author>Holliday, Ian E.</rioxxterms:author><rioxxterms:author>Barnes, Gareth 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.neuroimage.2007.01.002</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:63
Date: 2017-08-28

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      <identifier>oai:publications.aston.ac.uk:63</identifier>
      <datestamp>2017-08-28T07:01:14Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>The muscarinic receptor from the cerebral cortex, heart, and lacrimal gland can be solubilized in the zwitterionic detergent 3-(3-cholamidopropyl)dimethylammonio-2-hydroxy-1-propane sulfonate (CHAPSO) with retention of high affinity [3H]N-methyls-copolamine binding. However, in this detergent there are significant differences in the binding properties of the receptors, compared with those observed in membranes and digitonin solution. Some agents retain a degree of selectivity. In the heart and cortex, agonists can bind with high affinity to a receptor-GTP-binding protein complex. A second, lower affinity, agonist binding state is also present, which resembles a class of sites seen in membranes but not in digitonin solution. The high affinity agonist binding state has been resolved from the lower affinity state on sucrose density gradient centrifugation. Hydrodynamic analysis suggests that the high affinity state is approximately 110,000 Da larger than the lower affinity state. The binding properties of the receptor in CHAPSO can be altered to those seen in digitonin by exchanging detergents after CHAPSO solubilization.</dc:description><dc:language>en</dc:language><dc:source>1521-0111</dc:source><dc:title>Binding and hydrodynamic properties of muscarinic receptor subtypes solubilized in 3-(3-cholamidopropyl)dimethylammonio-2-hydroxy-1-propanesulfonate</dc:title><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Birdsall, N.J.</rioxxterms:author><rioxxterms:author>Curtis, C.</rioxxterms:author><rioxxterms:author>Eveleigh, P.</rioxxterms:author><rioxxterms:author>Hulme, E.C.</rioxxterms:author><rioxxterms:author>Pedder, E.K.</rioxxterms:author><rioxxterms:author>Wheatley, Mark</rioxxterms:author><rioxxterms:publication_date>1989-10-26</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:62
Date: 2017-08-22

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      <identifier>oai:publications.aston.ac.uk:62</identifier>
      <datestamp>2017-08-22T11:55:51Z</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:description>[3H]Inositol hexakisphosphate (InsP6) binds with a heterogeneous distribution to frozen sections of unfixed rat brain and is displaced by unlabelled InsP6. The pattern of binding correlates with binding to neuronal cell bodies. [3H]InsP6 binding to cerebellar membranes has been further characterised, is reversible, and saturable, and exhibits high specificity for inositol polyphosphates. The IC50 for competition by unlabelled InsP6 is approximately 100nM, whereas inositol 1,3,4,5,6 pentakisphosphate (Ins(13456)P5), inositol 1,3,4,5 tetrakisphosphate (Ins(1345)P4), and inositol 1,4,5 trisphosphate (Ins(145)P3) bind with an affinity at least one order of magnitude lower. [3H]InsP6 binding is clearly distinct from previously characterised Ins(145)P3 (ref. 1, 2) and Ins(1345)P4 (ref. 3) binding, both in terms of pharmacology and brain distribution.</dc:description><dc:language>en</dc:language><dc:source>1090-2104</dc:source><dc:title>Identification of a novel inositol phosphate recognition site: specific [3H]inositol hexakisphosphate binding to brain regions and cerebellar membranes</dc:title><rioxxterms:author>Hawkins, Phillip T.</rioxxterms:author><rioxxterms:author>Reynolds, D.J.M.</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Hanley, Michael R.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/0006-291X(90)92099-L</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:61
Date: 2017-06-09

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      <identifier>oai:publications.aston.ac.uk:61</identifier>
      <datestamp>2017-06-09T10:43:53Z</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>A neuronal cell line (NG115-401L-C3) was stimulated by mitogenic (angiotensin) and non-mitogenic (bradykinin) peptides and examined for the time course of changes in the levels of radiolabelled inositol phosphates and phospholipids. Both peptides stimulated the time-dependent production of Ins(1,4,5)P3 and related metabolites. Bradykinin caused a much larger increase in Ins(1,4,5)P3 than did angiotensin. However, both peptides stimulated similar rises in the levels of Ins(1,3,4)P3 and InsP4. Bradykinin but not angiotensin, caused a rapid (within 2 s) fall in the levels of PtdIns(4,5)P2 and PtdIns(4)P. Serum pretreatment of the cells caused a 2-3-fold potentiation of both the responses to bradykinin and angiotensin. Although significant levels of PtdIns(3)P were detected in resting cells neither mitogenic (angiotensin, insulin-like growth factor I, transforming growth factor beta) nor non-mitogenic (bradykinin, nerve growth factor interleukin-1) receptor activation changed its levels, arguing against regulation of either PtdIns 3-kinase or PtdIns(3)P phosphatase. We conclude that, as judged by the levels of its product. PtdIns(3)P, the enzyme PtdIns 3-kinase is not activated. This questions the significance of this activity in the receptor-mediated initiation of DNA synthesis.</dc:description><dc:language>en</dc:language><dc:source>1470-8728</dc:source><dc:title>Changes in inositol lipids and phosphates after stimulation of the MAS-transfected NG115-401L-C3 cell line by mitogenic and non-mitogenic stimuli</dc:title><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Hawkins, Phillip T.</rioxxterms:author><rioxxterms:author>Benton, H.P.</rioxxterms:author><rioxxterms:author>Hanley, Michael R.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:60
Date: 2017-08-22

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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>1557-7988</dc:source><dc:title>Inositol phospholipids and phosphates for investigation of intact cell phospholipase C substrates and products</dc:title><rioxxterms:author>Hanley, Michael R.</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Hawkins, Phillip T.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/0076-6879(91)97141-K</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:59
Date: 2017-08-28

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      <identifier>oai:publications.aston.ac.uk:59</identifier>
      <datestamp>2017-08-28T07:01:15Z</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>1. Standard and high-performance anion-exchange-chromatographic techniques have been used to purify myo-[3H]inositol pentakisphosphates from various myo-[3H]inositol-prelabelled cells. Slime mould (Dictyostelium discoideum) contained 8 microM-myo-[3H]inositol 1,3,4,5,6-pentakisphosphate 16 microM-myo-[3H]inositol 1,2,3,4,6-pentakisphosphate and 36 microM-D-myo-[3H]inositol 1,2,4,5,6-pentakisphosphate [calculated intracellular concentrations; Stephens &amp; Irvine (1990) Nature (London) 346 580-583]; germinating mung-bean (Phaseolus aureus) seedlings contained both D- and L-myo-[3H]inositol 1,2,4,5,6-pentakisphosphate (which was characterized by 31P and two-dimensional proton n.m.r.) and D- and/or L-myo-[3H]inositol 1,2,3,4,5-pentakisphosphate; HL60 cells contained myo-[3H]inositol 1,3,4,5,6-pentakisphosphate (in a 500-fold excess over the other species), myo-[3H]inositol 1,2,3,4,6-pentakisphosphate and D- and/or L-myo-[3H]inositol 1,2,4,5,6-pentakisphosphate; and NG-115-401L-C3 cells contained myo-[3H]inositol 1,3,4,5,6-pentakisphosphate (in a 100-fold excess over the other species), D- and/or L-myo-[3H]inositol 1,2,4,5,6-pentakisphosphate, myo-[3H]inositol 1,2,3,4,6-pentakisphosphate and D- and/or L-myo-[3H]inositol 1,2,3,4,5-pentakisphosphate. 2. Multiple soluble ATP-dependent myo-inositol pentakisphosphate kinase activities have been detected in slime mould, rat brain and germinating mung-bean seedling homogenates. In slime-mould cytosolic fractions, the three myo-inositol pentakisphosphates that were present in intact slime moulds could be phosphorylated to myo-[3H]inositol hexakisphosphate: the relative first-order rate constants for these reactions were, in the order listed above, 1:8:31 respectively (with first-order rate constants in the intact cell of 0.1, 0.8 and 3.1 s-1, assuming a cytosolic protein concentration of 50 mg/ml), and the Km values of the activities for their respective inositol phosphate substrates (in the presence of 5 mM-ATP) were 1.6 microM, 3.8 microM and 1.4 microM. At least two forms of myo-inositol pentakisphosphate kinase activity could be resolved from a slime-mould cytosolic fraction by both pharmacological and chromatographic criteria. Rat brain cytosol and a soluble fraction derived from germinating mung-bean seedlings could phosphorylate myo-inositol D/L-1,2,4,5,6-, D/L-1,2,3,4,5-, 1,2,3,4,6- and 1,3,4,5,6-pentakisphosphates to myo-inositol hexakisphosphate: the relative first-order rate constants were 57:27:77:1 respectively for brain cytosol (with first-order rate constants in the intact cell of 0.0041, 0.0019, 0.0056 and 0.000073 s-1 respectively, assuming a cytosolic protein concentration of 50 mg/ml) and 1:11:12:33 respectively for mung-bean cytosol (with first-order rate constants in a supernatant fraction with a protein concentration of 10 mg/ml of 0.0002, 0.0022, 0.0024 and 0.0066 s-1 respectively).</dc:description><dc:language>en</dc:language><dc:source>1470-8728</dc:source><dc:title>myo-inositol pentakisphosphates. Structure, biological occurrence and phosphorylation to myo-inositol hexakisphosphate</dc:title><rioxxterms:author>Stephens, L.R.</rioxxterms:author><rioxxterms:author>Hawkins, Phillip T.</rioxxterms:author><rioxxterms:author>Stanley, Alison F.</rioxxterms:author><rioxxterms:author>Moore, T.</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Morris, P.J.</rioxxterms:author><rioxxterms:author>Hanley, Michael R.</rioxxterms:author><rioxxterms:author>Kay, R.R.</rioxxterms:author><rioxxterms:author>Irvine, R.F.</rioxxterms:author><rioxxterms:publication_date>1991-06-06</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:58
Date: 2017-08-22

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      <identifier>oai:publications.aston.ac.uk:58</identifier>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>Calcitonin gene-related peptide (CGRP) shows diversity both in its effects and its receptors. It is likely to have roles as a neurotransmitter, neuromodulator, local hormone and trophic factor. Its effects include rapid changes in neuronal activity, relaxation of many type of smooth muscle, actions on metabolism and changes in gene expression. Receptor heterogenecity has been revealed from experiments comparing agonist potency ratios and antagonists affinities. the evidence from these approaches is reviewed in this article and a speculative receptor classification scheme is proposed. Some of the likely future directions for CGRP research are discussed. © 1993.</dc:description><dc:language>en</dc:language><dc:source>1879-016X</dc:source><dc:title>Calcitonin gene-related peptide:multiple actions, multiple receptors</dc:title><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:publication_date>1992</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/0163-7258(92)90036-Y</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:57
Date: 2017-07-26

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      <identifier>oai:publications.aston.ac.uk:57</identifier>
      <datestamp>2017-07-26T13:34:26Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>1 The L6 myocyte cell line expresses high affinity receptors for calcitonin gene-related peptide (CGRP) which are coupled to activation of adenylyl cyclase. The biochemical pharmacology of these receptors has been examined by radioligand binding or adenosine 3':5'-cyclic monophosphate (cyclic AMP) accumulation. 2 In intact cells at 37 degrees C, human and rat alpha- and beta-CGRP all activated adenylyl cyclase with EC50s of about 1.5 nM. A number of CGRP analogues containing up to five amino acid substitutions showed similar potencies. In membrane binding studies at 22 degrees C in 1 mM Mg2+, the above all bound to a single site with IC50s of 0.1-0.4 nM. 3 The fragment CGRP(8-37) acted as a competitive antagonist of CGRP stimulation of adenylyl cyclase with a calculated Kd of 5 nM. The Kd determined in membrane binding assays was lower (0.5 nM). 4 The N-terminal extended human alpha-CGRP analogue Tyro-CGRP activated adenylyl cyclase and inhibited [125I]-iodohistidyl-CGRP binding less potently than human alpha-CGRP (EC50 for cyclase = 12 nM, IC50 for binding = 4 nM). 5 The pharmacological profile of the L6 CGRP receptor suggests that it most closely resembles sites on skeletal muscle, cardiac myocytes and hepatocytes. The L6 cell line should be a stable homogeneous model system in which to study CGRP mechanisms and pharmacology."</dc:description><dc:language>en</dc:language><dc:source>1476-5381</dc:source><dc:title>Pharmacological characterization of a receptor for calcitonin gene-related peptide on rat, L6 myocytes</dc:title><rioxxterms:author>Poyner, D.R.</rioxxterms:author><rioxxterms:author>Andrew, D.P.</rioxxterms:author><rioxxterms:author>Brown, D.</rioxxterms:author><rioxxterms:author>Bose, C.</rioxxterms:author><rioxxterms:author>Hanley, M.R.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:56
Date: 2017-08-22

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ID: oai:publications.aston.ac.uk:55
Date: 2017-08-22

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ID: oai:publications.aston.ac.uk:54
Date: 2017-06-09

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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 CHO-K1 cell line responds to the peptide amylin by a rapid elevation of cAMP. The related peptide calcitonin gene-related peptide (CGRP) is 100 times less potent at stimulating adenylate cyclase than is amylin. The actions of amylin at this receptor are concentration dependent and not antagonized by the CGRP antagonist CGRP-(8-37). Although these cells have receptors for calcitonin, amylin is unable to take part in any high affinity interaction with these receptors, as assessed by radioligand binding. The CHO-K1 cell line has receptors for amylin that are distinct from those for calcitonin and CGRP.</dc:description><dc:language>en</dc:language><dc:source>0026-895X</dc:source><dc:title>Stimulation of adenylate cyclase by amylin in CHO-K1 cells</dc:title><rioxxterms:author>D'Santos, C.S.</rioxxterms:author><rioxxterms:author>Gatti, A.</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Hanley, Michael R.</rioxxterms:author><rioxxterms:publication_date>1992-05-01</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:53
Date: 2017-07-26

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      <identifier>oai:publications.aston.ac.uk:53</identifier>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>The binding of [3H]inositol hexakisphosphate ([3H] InsP6) to rat cerebellar membranes has been characterized with the objective of establishing the role, if any, of a membrane protein receptor. In the presence of EDTA, we have previously identified an InsP6-binding site with a capacity of approximately 20 pmol/mg protein (Hawkins, P. T., Reynolds, D. J. M., Poyner, D. R., and Hanley, M. R. (1990) Biochem. Biophys. Res. Commun. 167, 819-827). However, in the presence of 1 mM Mg2+, the capacity of [3H]InsP6 binding to membranes was increased approximately 9-fold. This enhancing effect of Mg2+ was reversed by addition of 10 microM of several cation chelators, suggesting that the increased binding required trace quantities of other metal cations. This is supported by experiments where it was possible to saturate binding by addition of excess membranes, despite not significantly depleting radioligand, pointing to removal of some other factor. Removal of endogenous cations from the binding assay by pretreatment with chelex resin also prevents the Mg(2+)-induced potentiation. Consideration of the specificity of the chelators able to abolish this potentiation suggested involvement of Fe3+ or Al3+. Both these ions (but not several others) were able to increase [3H]InsP6 binding to chelex-pretreated membranes at concentrations of 1 microM. It is possible to demonstrate synergy between Fe3+ and Mg2+ under these conditions. We propose that [3H]InsP6 may interact with membranes through non-protein recognition possibly via phospholipids, in a manner dependent upon trace metals. The implications of this for InsP6 biology are considered.</dc:description><dc:language>en</dc:language><dc:source>1083-351X</dc:source><dc:title>Characterization of metal ion-induced [3H]inositol hexakisphosphate binding to rat cerebellar membranes</dc:title><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Cooke, F.</rioxxterms:author><rioxxterms:author>Hanley, Michael R.</rioxxterms:author><rioxxterms:author>Reynolds, D.J.</rioxxterms:author><rioxxterms:author>Hawkins, Phillip T.</rioxxterms:author><rioxxterms:publication_date>1993-01-15</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://www.scopus.com/inward/record.url?scp=0027518290&amp;partnerID=8YFLogxK</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:52
Date: 2017-07-20

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      <identifier>oai:publications.aston.ac.uk:52</identifier>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>The activation of phosphoinositide 3-hydroxykinase (P13K) is currently believed to represent the critical regulatory event which leads to the production of a novel intracellular signal. We have examined the control of this pathway by a number of cell-surface receptors in NG115-401L-C3 neuronal cells. Insulin-like growth factor-I stimulated the accumulation of 3-phosphorylated inositol lipids in intact cells and the appearance of P13K in antiphosphotyrosine-antibody-directed immunoprecipitates prepared from lysed cells, suggesting that P13K had been activated by a mechanism involving a protein tyrosine kinase. In contrast, P13K in these cells was not regulated by a variety of G-protein-coupled receptors, nerve growth factor acting via a low affinity receptor, or receptors for transforming growth factor-beta and interleukin-1. The receptor-specificity of P13K activation in these cells places significant constraints on the possible physiological function(s) of this pathway.</dc:description><dc:language>en</dc:language><dc:source>1470-8728</dc:source><dc:title>Receptor regulation of phosphoinositide 3-hydroxykinase in the NG115-401L-C3 neuronal cell line: stimulation by insulin-like growth factor-I</dc:title><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Hanley, Michael R.</rioxxterms:author><rioxxterms:author>Jackson, T.R.</rioxxterms:author><rioxxterms:author>Hawkins, Phillip T.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:51
Date: 2017-07-24

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    <header>
      <identifier>oai:publications.aston.ac.uk:51</identifier>
      <datestamp>2017-07-24T09:46:26Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>1. The ability of myo-inositol polyphosphates to inhibit iron-catalysed hydroxyl radical formation was studied in a hypoxanthine/xanthine oxidase system [Graf, Empson and Eaton (1987) J. Biol. Chem. 262, 11647-11650]. Fe3+ present in the assay reagents supported some radical formation, and a standard assay, with 5 microM Fe3+ added, was used to investigate the specificity of compounds which could inhibit radical generation. 2. InsP6 (phytic acid) was able to inhibit radical formation in this assay completely. In this respect it was similar to the effects of the high affinity Fe3+ chelator Desferral, and dissimilar to the effects of EDTA which, even at high concentrations, still allowed detectable radical formation to take place. 3. The six isomers of InsP5 were purified from an alkaline hydrolysate of InsP6 (four of them as two enantiomeric mixtures) and they were compared with InsP6 in this assay. Ins(1,2,3,4,6)P5 and D/L-Ins(1,2,3,4,5)P5 were similar to InsP6 in that they caused a complete inhibition of iron-catalysed radical formation at &gt; 30 microM. Ins(1,3,4,5,6)P5 and D/L-Ins(1,2,4,5,6)P5, however, were markedly less potent than InsP6, and did not inhibit radical formation completely; even when Ins(1,3,4,5,6)P5 was added up to 600 microM, significant radical formation was still detected. Thus InsP5s lacking 2 or 1/3 phosphates are in this respect qualitatively different from InsP6 and the other InsP5s. 4. scyllo-Inositol hexakisphosphate was also tested, and although it caused a greater inhibition than Ins(1,3,4,5,6)P5, it too still allowed detectable free radical formation even at 600 microM. 5. We conclude that the 1,2,3 (equatorial-axial-equatorial) phosphate grouping in InsP6 has a conformation that uniquely provides a specific interaction with iron to inhibit totally its ability to catalyse hydroxyl radical formation; we suggest that a physiological function of InsP6 might be to act as a 'safe' binding site for iron during its transport through the cytosol or cellular organelles</dc:description><dc:language>en</dc:language><dc:source>1470-8728</dc:source><dc:title>Inhibition of iron-catalysed hydroxyl radical formation by inositol polyphosphates: a possible physiological function for myo-inositol hexakisphosphate</dc:title><rioxxterms:author>Hawkins, Phillip T.</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Jackson, T.R.</rioxxterms:author><rioxxterms:author>Letcher, A.J.</rioxxterms:author><rioxxterms:author>Lander, Dawn</rioxxterms:author><rioxxterms:author>Irvine, R.F.</rioxxterms:author><rioxxterms:publication_date>1993-10-19</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:50
Date: 2017-08-22

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      <identifier>oai:publications.aston.ac.uk:50</identifier>
      <datestamp>2017-08-22T07:01:58Z</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>1470-8752</dc:source><dc:title>Regulation of membrane potential by G-protein-coupled receptors in L6 skeletal myocytes: the role of second messengers</dc:title><rioxxterms:author>Gosling, Martin</rioxxterms:author><rioxxterms:author>Smith, John W.</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:publication_date>1994-04-18</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:49
Date: 2017-08-22

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ID: oai:publications.aston.ac.uk:48
Date: 2017-06-09

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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>Myo-Inositol hexakisphosphate (InsP6), which is found in soil and most, if not all, plant and animal cells, has been estimated to have an affinity for Fe3+ in the range of 10(25) to 10(30) M-1. In this report, we demonstrate that the Fe-InsP6 complex has siderophore activity and is able to reverse the iron-restricted growth inhibition of Pseudomonas aeruginosa by ethylene diamine di(o-hydroxyphenyl)acetic acid. With 55Fe-InsP6 in transport studies, iron uptake is strongly iron regulated, being repressed after growth in iron-replete conditions and inhibited by treatment with potassium cyanide and carbonyl cyanide m-chlorophenylhydrazone. The kinetics of iron transport revealed a Km of 100 nM. Self-displacement of binding of [3H]InsP6 to isolated membranes by InsP6 revealed a single class of binding sites (Kd = 143 +/- 6 nM; Hill coefficient, 1.1 +/- 0.1). The binding of [3H]InsP6 to membranes was not dependent on whether cells had been grown under conditions of high or low iron concentrations. We believe that this is the first report of inositol polyphosphate activity in prokaryotic cells.</dc:description><dc:language>en</dc:language><dc:source>0021-9193</dc:source><dc:title>Siderophore activity of myo-inositol hexakisphosphate in Pseudomonas aeruginosa</dc:title><rioxxterms:author>Smith, Anthony W.</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Hughes, H.K.</rioxxterms:author><rioxxterms:author>Lambert, Peter A.</rioxxterms:author><rioxxterms:publication_date>1994-06-14</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:47
Date: 2017-08-22

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ID: oai:publications.aston.ac.uk:46
Date: 2017-07-26

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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>1. During osmotic swelling, cultured osteoblastic cells (ROS 17/2.8) exhibited activation of large amplitude Cl- currents in the whole-cell configuration of the patch-clamp technique. Effects of hypotonic shock on cell volume and membrane conductance were rapidly reversed on return to isotonic conditions. 2. Voltage command pulses in the range -80 to +50 mV produce instantaneous activation of Cl- currents. At potentials more positive than +50 mV the current exhibited time-dependent inactivation. The instantaneous current-voltage relationship was outwardly rectifying. 3. The anion permeability sequence of the induced current was SCN- (2.2) &gt; I- (1.9) &gt; Br- (1.5) &gt; Cl- (1.0) &gt; F- (0.8) &gt; gluconate- (0.2). This corresponds to Eisenman's sequence I. 4. The volume-sensitive Cl- current was effectively inhibited by the Cl- channel blockers 4,4'-diisothiocyanatostilbene-2,2-disulphonic acid (DIDS) and 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB). Outward currents were more effectively suppressed by DIDS than inward currents. The concentrations for 50% inhibition (IC50) of outward and inward currents were 81 and 298 μM, respectively. NPPB was equally effective at inhibiting outward and inward currents (IC50 of 64 μM). The current was relatively insensitive to diphenylamine-2-carboxylate (DPC), 500 μM producing only 22.5 ± 4.0% inhibition. 5. Inhibitors of protein kinase A (H-89, 1 μM) and tyrosine kinase (tyrphostin A25, 200 μM) were without effect upon activation of Cl- currents in response to hypotonic shock. Under isotonic conditions, elevation of intracellular Ca2+ by ionomycin (1 μM) or activation of protein kinase C by 12-O-tetradecanoylphorbol 13-acetate (TPA, 0.1 μM) failed to evoke increases in basal Cl- conductance levels. 6. It is concluded that an outwardly rectifying Cl- conductance is activated upon osmotic swelling and may be involved in cell volume regulation of ROS 17/2.8 cells.</dc:description><dc:language>en</dc:language><dc:source>1469-7793</dc:source><dc:title>Characterization of a volume-sensitive chloride current in rat osteoblast-like (ROS 17/2.8) cells</dc:title><rioxxterms:author>Gosling, Martin</rioxxterms:author><rioxxterms:author>Smith, J.W.</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:contributor>Poyner, David</rioxxterms:contributor><rioxxterms:publication_date>1995-06-15</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://www.scopus.com/inward/record.url?scp=0029011650&amp;partnerID=8YFLogxK</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:45
Date: 2017-08-22

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      <identifier>oai:publications.aston.ac.uk:45</identifier>
      <datestamp>2017-08-22T11:55:50Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>The effects of extracellular application of arginine vasopressin (AVP) upon membrane currents in L6 skeletal myocytes was investigated using the whole-cell configuration of the patch-clamp technique. At O mV AVP produced large amplitude, transient outward currents that reversed when the clamping potential was changed to -100 mV (negative to EK) The effects of alterations in the extracellular K+ concentration upon the current reversal potential suggested that the current elicited by AVP was carried mainly by K+ ions. Intracellular dialysis with 10 μM inositol 1,4,5-trisphosphate (InsP3) elicited similar currents but only in 6/14 cells. Inclusion of 5 mg ml-1 heparin in the intracellular solutions was ineffective at inhibiting the current responses to AVP. The AVP-induced current was totally abolished when the intracellular EGTA concentration was increased from 0.05 mM to 10 mM or Ca2+ was removed from the extracellular perfusing solution. These results suggest that AVP produces activation of a Ca2+-sensitive K+ conductance in L6 skeletal myocytes by a process dependent upon extracellular Ca2+ and not intracellular Ca2+ release. © 1995 Academic Press. All rights reserved.</dc:description><dc:language>en</dc:language><dc:source>1090-2104</dc:source><dc:title>Activation of calcium-sensitive potassium channels in L6 skeletal myocytes by arginine vasopressin requires extracellular calcium</dc:title><rioxxterms:author>Gosling, Martin</rioxxterms:author><rioxxterms:author>Smith, J.W.</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1006/bbrc.1995.2891</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:44
Date: 2017-08-22

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    <header>
      <identifier>oai:publications.aston.ac.uk:44</identifier>
      <datestamp>2017-08-22T11:55:50Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>The first syntheses of the natural products myo-inositol 1,2,3-trisphosphate and (+/-)-myo-inositol 1,2-bisphosphate are described. The protected key intermediates 4,5,6-tri-O-benzoyl-myo-inositol and (+/-)-3,4,5,6-tetra-O-benzyl-myo-inositol were phosphorylated with dibenzyl N,N-di-isopropylphosphoramidite in the presence of 1H-tetrazole and subsequent oxidation of the phosphite. The crystal structures of the synthetic intermediates (+/-)-1-O-(tert-butyldiphenylsilyl)-2,3,O-cyclohexylidene-myo-inos itol and (+/-)-4,5,6-tri-O-benzoyl-1-O-(tert-butyldiphenylsilyl)-2,3-O-cycl ohexylidene- myo-inositol are reported. myo-Inositol 1,2,3-trisphosphate (+/-)-myo-inositol 1,2-bisphosphate, and all isomeric myo-inositol tetrakisphosphates were evaluated for their ability to alter HO. production in the iron-catalysed Haber-Weiss reaction. The results demonstrated that a 1,2,3-grouping of phosphates in myo-inositol was necessary for inhibition also that (+/-)-myo-inositol 1,2-bisphosphate potentiated HO. production. myo-Inositol 1,2,3-trisphosphate resembled myo-inositol hexakisphosphate (phytic acid) in its ability to act as a siderophore by promoting iron-uptake into Pseudomonas aeruginosa.</dc:description><dc:language>en</dc:language><dc:source>1873-426X</dc:source><dc:title>Synthesis and iron binding studies of myo-inositol 1,2,3-trisphosphate and (+/-)-myo-inositol 1,2-bisphosphate, and iron binding studies of all myo-inositol tetrakisphosphates</dc:title><rioxxterms:author>Spiers, Ian D.</rioxxterms:author><rioxxterms:author>Barker, Christopher J.</rioxxterms:author><rioxxterms:author>Chung, Sung-Kee</rioxxterms:author><rioxxterms:author>Chang, Young-Tae</rioxxterms:author><rioxxterms:author>Freeman, Sally</rioxxterms:author><rioxxterms:author>Gardiner, John M.</rioxxterms:author><rioxxterms:author>Hirst, Peter H.</rioxxterms:author><rioxxterms:author>Lambert, Peter A.</rioxxterms:author><rioxxterms:author>Michell, Robert H.</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Schwalbe, Carl H.</rioxxterms:author><rioxxterms:author>Smith, Anthony W.</rioxxterms:author><rioxxterms:author>Solomons, Kevin R. H.</rioxxterms:author><rioxxterms:publication_date>1996-10-11</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/0008-6215(95)00361-4</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:43
Date: 2017-07-26

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    <header>
      <identifier>oai:publications.aston.ac.uk:43</identifier>
      <datestamp>2017-07-26T13:34:22Z</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>1. The responses of the electrically stimulated guinea-pig ileum and vas deferens to human and rat calcitonin gene-related peptide (CGRP) and amylin were investigated. 2. The inhibition of contraction of the ileum produced by human alpha CGRP was antagonized by human alpha CGRP8-37 (apparent pA2 estimated at 7.15 +/- 0.23) &gt; human alpha CGRP19-37 (apparent pA2 estimated as 6.67 +/- 0.33) &gt; [Tyr0]-human alpha CGRP28-37. The amylin antagonist, AC187, was three fold less potent than CGRP8-37 in antagonizing human alpha CGRP. 3. Both human beta- and rat alpha CGRP inhibited contractions of the ileum, but this was less sensitive to inhibition by CGRP8-37 than the effect of human alpha CGRP. However, CGRP19-37 was twenty times more effective in inhibiting the response to rat alpha CGRP (apparent pA2 estimated as 8.0 +/- 0.1) compared to human alpha CGRP. 4. Rat amylin inhibited contractions in about 10% of ileal preparations; this effect was not antagonized by any CGRP fragment. Human amylin had no action on this preparation. 5. Both human and rat alpha CGRP inhibited electrically stimulated contractions of the vas deferens, which were not antagonized by 3 microM CGRP8-37 or 10 microM AC187. 6. Rat amylin inhibited the stimulated contractions of the vas deferens (EC50 = 77 +/- 9 nM); human amylin was less potent (EC50 = 213 +/- 22 nM). The response to rat amylin was antagonized by 10 microM CGRP8-37 (EC50 = 242 +/- 25 nM) and 10 microM AC187 (EC50 = 610 +/- 22 nM). 7. It is concluded that human alpha CGRP relaxes the guinea-pig ileum via CGRP1-like receptors, but that human beta CGRP and rat alpha CGRP may use additional receptors. These are distinct CGRP2-like and amylin receptors on guinea-pig vas deferens.</dc:description><dc:language>en</dc:language><dc:source>0007-1188</dc:source><dc:title>Multiple receptors for calcitonin gene-related peptide and amylin on guinea-pig ileum and vas deferens</dc:title><rioxxterms:author>Tomlinson, A. Elaine</rioxxterms:author><rioxxterms:author>Poyner, David</rioxxterms:author><rioxxterms:publication_date>1996-03</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://www.scopus.com/inward/record.url?scp=0029926264&amp;partnerID=8YFLogxK</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:42
Date: 2017-06-09

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    <header>
      <identifier>oai:publications.aston.ac.uk:42</identifier>
      <datestamp>2017-06-09T10:43:48Z</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>1. The effects of arachidonic acid upon the volume-sensitive Cl- current present in cultured osteoblastic cells (ROS 17/2.8) was studied using the whole-cell patch-clamp technique. 2. Arachidonate produced two distinct phases of inhibition, a rapid phase occurring within 10-15 s of application preceding a slower phase that occurred 2 min after onset of arachidonate superfusion. Accompanying the slower inhibitory phase was an acceleration of the time-dependent inactivation exhibited by the current at strongly depolarized potentials (&gt; + 50 mV). The half-maximal inhibitory concentrations (IC50) were 177 +/- 31 and 10 +/- 4 microM for the two phases respectively. 3. Arachidonate was still effective in the presence of inhibitors of cyclo-oxygenase (indomethacin, 10 microM), lipoxygenase (nordihydroguaretic acid, 10-100 microM) and cytochrome P450 (SKF525A, 100 microM; ethoxyresorufin, 10 microM; metyrapone, 500 microM; piperonyl butoxide, 500 microM; cimetidine, 1 mM). The effects of arachidonate could not be produced by another cis unsaturated fatty acid, oleic acid. 4. Measurements of cell volume showed that arachidonate effectively inhibited the regulatory volume decrease elicited by ROS 17/2.8 cells in response to a reduction in extracellular osmolarity. 5. It is concluded that the volume-sensitive Cl- conductance in ROS 17/2.8 cells is directly modulated by arachidonate and may represent a physiological mechanism by which volume regulation can be controlled in these cells.</dc:description><dc:language>en</dc:language><dc:source>0022-3751</dc:source><dc:title>Effects of arachidonic acid upon the volume-sensitive chloride current in rat osteoblast-like (ROS 17/2.8) cells.</dc:title><rioxxterms:author>Gosling, M.</rioxxterms:author><rioxxterms:author>Poyner, David</rioxxterms:author><rioxxterms:author>Smith, J.W.</rioxxterms:author><rioxxterms:publication_date>1996-06-15</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:41
Date: 2017-07-26

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    <header>
      <identifier>oai:publications.aston.ac.uk:41</identifier>
      <datestamp>2017-07-26T13:34:22Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>The overexpression of epidermal growth factor receptor (EGFr) has been implicated as a causative factor and a poor prognostic marker in a number of carcinomas. Therefore, strategies that down-regulate EGFr expression may be therapeutically useful. We designed antisense ODNs complementary to the initiation codon region of the EGFr mRNA and evaluated their efficacy in several tumor-derived cells, including the A431 cell line that express amplified levels of EGFr. A 15-mer phosphorothioate (PS) antisense ODN (erbB1AS15) induced a concentration-dependent reduction in proliferation that was accompanied by a change in the morphology of A431 cells into more tightly clustered and discrete colonies. A 15-mer sense (PS) control oligodeoxynucleotide (ODN) and a phosphodiester (PO) version of erbB1AS15 had little or no effect on cell number of morphology, and erbB1AS15 (PS) did not induce these effects in control cell lines expressing lower levels of EGFr. The effects of erbB1AS15 (PS) on A431 cells were not mediated by a true antisense mechanism in that there was no reduction in the level of EGFr mRNA or protein over a 24-hr period, as determined by Northern and Western blotting, respectively. However, autophosphorylation of the receptor was significantly reduced by erbB1AS15 (PS) and not by control ODNs. The results of further studies suggested that this effect was mediated by a direct, dose-dependent inhibition of the EGFr tyrosine kinase enzyme and was not due to impairment of either ligand-binding or receptor dimerization. These data suggest that erbB1AS15 (PS) can inhibit proliferation and alter the morphology of A431 cells by a sequence-selective, but nonantisense mechanism affecting receptor tyrosine kinase activity.</dc:description><dc:language>en</dc:language><dc:source>0026-895X</dc:source><dc:title>A nonantisense sequence-selective effect of a phosphorothioate oligodeoxynucleotide directed against the epidermal growth factor receptor in A431 cells</dc:title><rioxxterms:author>Coulson, Judy M.</rioxxterms:author><rioxxterms:author>Poyner, David</rioxxterms:author><rioxxterms:author>Chantry, Andrew</rioxxterms:author><rioxxterms:author>Irwin, William J.</rioxxterms:author><rioxxterms:author>Akhtar, Saghir</rioxxterms:author><rioxxterms:publication_date>1996-08</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://www.scopus.com/inward/record.url?scp=0029812567&amp;partnerID=8YFLogxK</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:40
Date: 2017-08-22

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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:publications.aston.ac.uk:40</identifier>
      <datestamp>2017-08-22T11:55:50Z</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 effects of a 15-mer antisense c-myc phosphorothioate modified oligodeoxynucleotide (OdN) upon the volume-sensitive Cl- current in ROS 17/2.8 cells were investigated using the whole-cell configuration of the patch clamp technique. At 5 microM, the OdN reversibly inhibited the current in a voltage- and time-dependent fashion. This was evident from the reduction in the peak current as assessed at the termination of each voltage pulse and an acceleration of the time-dependent inactivation present at strongly depolarised potentials. The kinetic modifications induced by the OdN suggest it may act by blocking the pore of open channels when the cell membrane potential is depolarised.</dc:description><dc:language>en</dc:language><dc:source>1090-2104</dc:source><dc:title>Direct inhibitory effects of an antisense oligodeoxynucleotide upon the volume-sensitive chloride current in rat osteoblast-like (ROS 17/2.8) cells</dc:title><rioxxterms:author>Gosling, Martin</rioxxterms:author><rioxxterms:author>Akhtar, Saghir</rioxxterms:author><rioxxterms:author>Smith, J.W.</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1006/bbrc.1996.1460</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:39
Date: 2017-08-22

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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>1. Potency orders were determined for a series of agonists and antagonists on the calcitonin gene-related peptide (CGRP) receptor of rat L6 myocytes. The agents tested were all shown to have been active against CGRP, amylin or adrenomedullin receptors. 2. AC187 had a PIC50 Of 6.8 ± 0.10, making it 14 fold less potent as an antagonist than CGRP8-37 (PIC50, 7.95 ± 0.14). Amyline8-37 was equipotent to AC187 (PIC50, 6.6 ± 0.16) and CGRP19-37 was a fold less potent than either (pIC50 6.1 ± 0.24). 3. [Ala11]-CGRP8-37 was 6 fold less potent than CGRP8-37, (pIC50 7.13 ± 0.14), whereas [Ala18] CGRP8-37 was approximately equipotent to CGRP8-37 (pIC50, 7.52 ± 0.15). However, [Ala11,Ala18]- CGRP8-37 was over 300 fold less potent than CGRP8-37 (pIC50, 5.30 ± 0.04). 4. [Tyr0]-CGRP28-37, amylin19-37 and adrenomedullin22-52 were inactive as antagonists at concentrations of up to 1 μM. 5. Biotinyl-human α-CGRP was 150 fold less potent than human α-CGRP itself (EC50 values of 48 ± 17 nM and 0.31 ± 0.13 nM, respectively). At 1 μM, [Cys(acetomethoxy)(2'7)]-CGRP was inactive as an agonist. 6. These results confirm a role for Arg11 in maintaining the high affinity binding of CGRP8-37. Arg18 is of less direct significance for high affinity binding, but it may be important in maintaining the amphipathic nature of CGRP and its analogues.</dc:description><dc:language>en</dc:language><dc:source>1476-5381</dc:source><dc:title>The selectivity and structural determinants of peptide antagonists at the CGRP receptor of rat, L6 myocytes</dc:title><rioxxterms:author>Howitt, Stephen G.</rioxxterms:author><rioxxterms:author>Poyner, David</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1038/sj.bjp.0701212</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:38
Date: 2017-08-22

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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>1470-8752</dc:source><dc:title>Molecular pharmacology of receptors for calcitonin-gene-related peptide, amylin and adrenomedullin</dc:title><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1042/bst0251032</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:37
Date: 2017-08-22

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      <identifier>oai:publications.aston.ac.uk:37</identifier>
      <datestamp>2017-08-22T11:55:49Z</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>1. Structure-activity relationships for the binding of human α-calcitonin gene-related peptide 8-37 (hαCGRP8-37) have been investigated at the CGRP receptors expressed by human SK-N-MC (neuroblastoma) and Col 29 (colonic epithelia) cells by radioligand binding assays and functional assays (hαCGRP stimulation of adenylate cyclase). 2. On SK-N-MC cells the potency order was hαCGRP8-37 &gt; hαCGRP19-37 = AC187 &gt; rat amylin8-37 &gt; hα[Tyr0]-CGRP28-37 (apparent pKBS of 7.49 ± 0.25, 5.89 ± 0.20, 6.18 ± 0.19, 5.85 ± 0.19 and 5.25 ± 0.07). The SK-N-MC receptor appeared CGRP1-like. 3. On Col 29 cells, only hαCGRP8-37 of the above compounds was able to antagonize the actions of hαCGRP (apparent pKB = 6.48 ± 0.28). Its receptor appeared CGRP2-like. 4. hα[Ala11,18]-CGRP8-37, where the amphipathic nature of the N-terminal α-helix has been reduced, bound to SK-N-MC cells a 100 fold less strongly than hαCGRP8-37. 5. On SK-N-MC cells, hαCGRP(8-18, 28-37) (M433) and mastoparan-hαCGRP28-37 (M432) had apparent pKBS of 6.64 ± 0.16 and 6.42 ± 0.26, suggesting that residues 19-27 play a minor role in binding. The physico-chemical properties of residues 8-18 may be more important than any specific side-chain interactions. 6. M433 was almost as potent as hαCGRP8-37 on Col 29 cells (apparent pKB = 6.17 ± 0.20). Other antagonists were inactive.</dc:description><dc:language>en</dc:language><dc:source>1476-5381</dc:source><dc:title>Structural determinants for binding to CGRP receptors expressed by human SK-N-MC and Col 29 cells:Studies with chimeric and other peptides</dc:title><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Soomets, Ursel</rioxxterms:author><rioxxterms:author>Howitt, Stephen G.</rioxxterms:author><rioxxterms:author>Langel, Ulo</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1038/sj.bjp.0702032</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:36
Date: 2017-08-22

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      <identifier>oai:publications.aston.ac.uk:36</identifier>
      <datestamp>2017-08-22T11:55:49Z</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>It has previously been shown that myo-inositol hexakisphosphate (myo- InsP6) mediates iron transport into Pseudomonas aeruginosa and overcomes iron-dependent growth inhibition. In this study, the iron transport properties of myo-inositol trisphosphate and tetrakisphosphate regio-isomers were studied. Pseudomonas aeruginosa accumulated iron (III) at similar rates whether complexed with myo-Ins(1,2,3)P3 or myo-InsP6. Iron accumulation from other compounds, notably D/L myo-Ins(1,2,4,5)P4 and another inositol trisphosphate regio-isomer, D-myo-Ins(1,4,5)P3, was dramatically increased. Iron transport profiles from myo-InsP6 into mutants lacking the outer membrane porins oprF, oprD and oprP were similar to the wild-type, indicating that these porins are not involved in the transport process. The rates of reduction of iron (III) to iron (II) complexed to any of the compounds by a Ps. aeruginosa cell lysate were similar, suggesting that a reductive mechanism is not the rate-determining step.</dc:description><dc:language>en</dc:language><dc:source>1365-2672</dc:source><dc:title>Inositol polyphosphate-mediated iron transport in Pseudomonas aeruginosa</dc:title><rioxxterms:author>Hirst, Peter H.</rioxxterms:author><rioxxterms:author>Riley, A.M.</rioxxterms:author><rioxxterms:author>Mills, S.J.</rioxxterms:author><rioxxterms:author>Spiers, Ian D.</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Freeman, Sally</rioxxterms:author><rioxxterms:author>Potter, B.V.</rioxxterms:author><rioxxterms:author>Smith, Anthony W.</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.1365-2672.1999.00697.x</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:35
Date: 2017-08-22

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    <header>
      <identifier>oai:publications.aston.ac.uk:35</identifier>
      <datestamp>2017-08-22T11:55:49Z</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>1. The receptors which mediate the effects of calcitonin gene-related peptide (CGRP), amylin and adrenomedullin on the guinea-pig vas deferens have been investigated. 2. All three peptides cause concentration dependant inhibitions of the electrically stimulated twitch response (pD 2s for CGRP, amylin and adrenomedullin of 7.90 ± 0.11, 7.70 ± 0.19 and 7.25 ± 0.10 respectively). 3. CGRP 8-37 (1 μM) and AC187 (10 μM) showed little antagonist activity against adrenomedullin. 4. Adrenomedullin 22-52 by itself inhibited the electrically stimulated contractions of the vas deferens and also antagonized the responses to CGRP, amylin and adrenomedullin. 5. [ 125I]-adrenomedullin labelled a single population of binding sites in vas deferens membranes with a pIC 50 of 8.91 and a capacity of 643 fmol mg -1. Its selectivity profile was adrenomedullin &gt; AC187 &gt; CGRP = amylin. It was clearly distinct from a site labelled by [ 125I]-CGRP (pIC 50 = 8.73, capacity = 114 fmol mg -1, selectivity CGRP &gt; amylin = AC187 &gt; adrenomedullin). [ 125I]-amylin bound to two sites with a total capacity of 882 fmol mg -1. 6. Although CGRP has been shown to act at a CGRP 2 receptor on the vas deferens with low sensitivity to CGRP 8-37, this antagonist displaced [ 125I]-CGRP with high affinity from vas deferens membranes. This affinity was unaltered by increasing the temperature from 4°C to 25°C, suggesting the anomalous behaviour of CGRP 8-37 is not due to temperature differences between binding and functional assays.</dc:description><dc:language>en</dc:language><dc:source>1476-5381</dc:source><dc:title>Characterization of receptors for calcitonin gene-related peptide and adrenomedullin on the guinea-pig vas deferens</dc:title><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Taylor, Gillian M.</rioxxterms:author><rioxxterms:author>Tomlinson, A. Elaine</rioxxterms:author><rioxxterms:author>Richardson, Alan G.</rioxxterms:author><rioxxterms:author>Smith, David M.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1038/sj.bjp.0702437</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:34
Date: 2017-08-22

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    <header>
      <identifier>oai:publications.aston.ac.uk:34</identifier>
      <datestamp>2017-08-22T11:55:49Z</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>A previous study has suggested that a G to A base change at position 169 of the GHRH-receptor gene in human somatotrophinomas is a mutation and confers hypersensitivity to GHRH. The alternative base converts codon 57 from GCG to AGC, resulting in replacement of alanine (Ala) with threonine (Thr). In the present study, two of five human GH-secreting somatotrophinomas were found to possess the codon 57 AGC sequence. The GCG allele was also detected, indicating heterozygosity. However, the patients' normal blood-derived DNA also yielded the same sequence pattern, indicating that the Ala=&gt; Thr amino acid change is a normal polymorphism, and not a somatic mutation. Nevertheless, in vitro, the tumors possessing the Ala=&gt; Thr amino acid change responded very strongly to GHRH in terms of cAMP formation, being increased 40- and 200-fold, in comparison to the 2-fold increases by tumors without the alternative GHRH-receptor sequence. Likewise, the in vitro response of GH secretion to GHRH was elevated. One of the two tumors with the alternative Thr residue, and the highest responder to GHRH, possessed a gsp muration, despite the fact that these defects are thought to reduce responsiveness to GHRH. These results fail to confirm that the GCG =&gt; AGC at codon 57 of the GHRH-receptor gene is a mutation, but do support the concept that the alternative form with Thr confers increased sensitivity to GHRH. (C) 2000 Academic Press.</dc:description><dc:language>en</dc:language><dc:source>1090-2104</dc:source><dc:title>A polymorphism in the growth hormone (GH)-releasing hormone (GHRH) receptor gene is associated with elevated response to GHRH by human pituitary somatotrophinomas in vitro</dc:title><rioxxterms:author>Adams, Eric F.</rioxxterms:author><rioxxterms:author>Symowski, Hedwig</rioxxterms:author><rioxxterms:author>Buchfelder, Michael</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:publication_date>2000-08-18</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1006/bbrc.2000.3247</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:33
Date: 2017-08-22

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      <identifier>oai:publications.aston.ac.uk:33</identifier>
      <datestamp>2017-08-22T11:45:17Z</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>1873-3735</dc:source><dc:title>The perils of using the human genome sequence:Lessons from CALCRL</dc:title><rioxxterms:author>Conner, Alex C.</rioxxterms:author><rioxxterms:author>Poyner, David 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/S0165-6147(00)01721-1</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:32
Date: 2017-08-08

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      <identifier>oai:publications.aston.ac.uk:32</identifier>
      <datestamp>2017-08-08T07:00:49Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>The SAR of Asperlicin analogues is reported, leading to bioactive 1,4-benzodiazepine-2-ones, which were prepared in a 3 step reaction sequence. The Asperlicin substructure was built up using Tryptophan and readily available 2-amino-acetophenones. This template, containing a 1,4-benzodiazepin-2-one moiety with a 3-indolmethyl side chain, was transformed into mono- and di-substituted 3-indol-3 '-yl-methyl-1,4-benzodi-azepine-2-ones by selective alkylation and acylation reactions. The SAR optimization of the 1,4-benzodiazepine scaffold has included variations at the 5-, 7-, 8-position, at the N1, N-indole nitrogen and the configuration of the C3-position. The most active Asperlicin analogue, having an IC50 of 1.6 microM on the CCKA receptor subtype, was obtained from Tryptophan in only 3 steps in an overall yield of 48%.</dc:description><dc:language>en</dc:language><dc:source>1029-2322</dc:source><dc:title>Synthesis and evaluation of asperlicin analogues as non-peptidal cholecystokinin-antagonists</dc:title><rioxxterms:author>Lattmann, Eric</rioxxterms:author><rioxxterms:author>Billington, David C.</rioxxterms:author><rioxxterms:author>Poyner, David</rioxxterms:author><rioxxterms:author>Howitt, Stephen B.</rioxxterms:author><rioxxterms:author>Offel, Michael</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:31
Date: 2017-08-22

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      <identifier>oai:publications.aston.ac.uk:31</identifier>
      <datestamp>2017-08-22T11:45:17Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>The 4th International Symposium on CGRP was expertly organized, at a difficult time, by Inger Jansen-Olesen and Lars Edvinsson and held on 28-30 September 2001 at the Royal Danish School of Pharmacy, Copenhagen, Denmark.</dc:description><dc:language>en</dc:language><dc:source>1873-3735</dc:source><dc:title>CGRP receptors:A headache to study, but will antagonists prove therapeutic in migraine?</dc:title><rioxxterms:author>Brain, Susan. D.</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Hill, Raymond G.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/S0165-6147(02)01945-4</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:30
Date: 2017-10-02

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    <header>
      <identifier>oai:publications.aston.ac.uk:30</identifier>
      <datestamp>2017-10-02T07:01:47Z</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 calcitonin family of peptides comprises calcitonin, amylin two calcitonin gene-related peptides (CGRPs), and adrenomedullin. The first calcitonin receptor was cloned in 1991. Its pharmacology is complicated by the existence of several splice variants. The receptors for the other members the family are made up of subunits. The calcitonin-like receptor (CL receptor) requires a single transmembrane domain protein, termed receptor activity modifying protein, RAMP1, to function as a CGRP receptor. RAMP2 and -3 enable the same CL receptor to behave as an adrenomedullin receptor. Although the calcitonin receptor does not require RAMP to bind and respond to calcitonin, it can associate with the RAMPs, resulting in a series of receptors that typically have high affinity for amylin and varied affinity for CGRP. This review aims to reconcile what is observed when the receptors are reconstituted in vitro with the properties they show in native cells and tissues. Experimental conditions must be rigorously controlled because different degrees of protein expression may markedly modify pharmacology in such a complex situation. Recommendations, which follow International Union of Pharmacology guidelines, are made for the nomenclature of these multimeric receptors.</dc:description><dc:language>en</dc:language><dc:relation>http://www.scopus.com/inward/record.url?scp=0036266044&amp;partnerID=8YFLogxK</dc:relation><dc:source>1521-0081</dc:source><dc:title>International Union of Pharmacology. XXXII. The mammalian calcitonin gene-related peptides, adrenomedullin, amylin, and calcitonin receptors</dc:title><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Sexton, Patrick M.</rioxxterms:author><rioxxterms:author>Marshall, Ian</rioxxterms:author><rioxxterms:author>Smith, David M.</rioxxterms:author><rioxxterms:author>Quirion, Remi</rioxxterms:author><rioxxterms:author>Born, Walter</rioxxterms:author><rioxxterms:author>Muff, Roman</rioxxterms:author><rioxxterms:author>Fischer, Jan A.</rioxxterms:author><rioxxterms:author>Foord, Steven M.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1124/pr.54.2.233</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:29
Date: 2017-08-22

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      <identifier>oai:publications.aston.ac.uk:29</identifier>
      <datestamp>2017-08-22T11:45:17Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>A novel synthetic approach towards N1-alkylated 3-propyl-1,4-benzodiazepines was developed in five synthetic steps from 2-amino-4-chlorobenzophenone, in which the N-oxide 4 served as a key intermediate. The structure-activity relationship optimization of this 3-prophyl-1,4-benzodiazepine template was carried out on the N1-position by selective alkylation reactions and resulted in a ligand with an improved affinity on the cholecystokinin (CCK2) receptor. The N-allyl-3-propyl-benzodiazepine 6d displayed an affinity towards the CCK2 (CCK-B) receptor of 170 nM in a radiolabelled receptor-binding assay. The anxiolytic activity of this allyl-3-propyl-1,4-benzodiazepine 6d was subsequently determined in in-vivo psychotropic assays. This novel ligand had ED50 values of 4.7 and 5.2 mg kg-1 in the black and white box test and the x-maze, respectively, and no significant sedation/muscle relaxation was observed.</dc:description><dc:language>en</dc:language><dc:source>2042-7158</dc:source><dc:title>Synthesis and evaluation of N1-substituted-3-propyl-1,4-benzodiazepine-2-ones as cholecystokinin (CCK2) receptor ligands</dc:title><rioxxterms:author>Lattmann, Eric</rioxxterms:author><rioxxterms:author>Sattayasai, Jintana</rioxxterms:author><rioxxterms:author>Billington, David C.</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Puapairoj, Prapawadee</rioxxterms:author><rioxxterms:author>Tiamkao, Siriporn</rioxxterms:author><rioxxterms:author>Airarat, Wanchai</rioxxterms:author><rioxxterms:author>Singh, Harjit</rioxxterms:author><rioxxterms:author>Offel, Michael</rioxxterms:author><rioxxterms:author>Poyner, David</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1211/0022357021779005</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:28
Date: 2017-08-22

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    <header>
      <identifier>oai:publications.aston.ac.uk:28</identifier>
      <datestamp>2017-08-22T11:45:17Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>1. The calcitonin receptor-like receptor (CRLR) and specific receptor activity modifying proteins (RAMPs) together form receptors for calcitonin gene-related peptide (CGRP) and/or adrenomedullin in transfected cells. 2. There is less evidence that innate CGRP and adrenomedullin receptors are formed by CRLR/RAMP combinations. We therefore examined whether CGRP and/or adrenomedullin binding correlated with CRLR and RAMP mRNA expression in human and rat cell lines known to express these receptors. Specific human or rat CRLR antibodies were used to examine the presence of CRLR in these cells. 3. We confirmed CGRP subtype 1 receptor (CGRP(1)) pharmacology in SK-N-MC neuroblastoma cells. L6 myoblast cells expressed both CGRP(1) and adrenomedullin receptors whereas Rat-2 fibroblasts expressed only adrenomedullin receptors. In contrast we could not confirm CGRP(2) receptor pharmacology for Col-29 colonic epithelial cells, which, instead were CGRP(1)-like in this study. 4. L6, SK-N-MC and Col-29 cells expressed mRNA for RAMP1 and RAMP2 but Rat-2 fibroblasts had only RAMP2. No cell line had detectable RAMP3 mRNA. 5. SK-N-MC, Col-29 and Rat-2 fibroblast cells expressed CRLR mRNA. By contrast, CRLR mRNA was undetectable by Northern analysis in one source of L6 cells. Conversely, a different source of L6 cells had mRNA for CRLR. All of the cell lines expressed CRLR protein. Thus circumstances where CRLR mRNA is apparently absent by Northern analysis do not exclude the presence of this receptor. 6. These data strongly support CRLR, together with appropriate RAMPs as binding sites for CGRP and adrenomedullin in cultured cells.</dc:description><dc:language>en</dc:language><dc:source>1476-5381</dc:source><dc:title>Comparison of the expression of calcitonin receptor-like receptor (CRLR) and receptor activity modifying proteins (RAMPs) with CGRP and adrenomedullin binding in cell lines</dc:title><rioxxterms:author>Choksi, Tejal</rioxxterms:author><rioxxterms:author>Hay, Debbie L.</rioxxterms:author><rioxxterms:author>Legon, Stephen</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Hagner, Stefanie</rioxxterms:author><rioxxterms:author>Bloom, Stephen R.</rioxxterms:author><rioxxterms:author>Smith, David M.</rioxxterms:author><rioxxterms:contributor>Poyner, David</rioxxterms:contributor><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1038/sj.bjp.0704761</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:27
Date: 2017-08-22

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    <header>
      <identifier>oai:publications.aston.ac.uk:27</identifier>
      <datestamp>2017-08-22T11:45:16Z</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>1. The ability of the CGRP antagonist BIBN4096BS to antagonize CGRP and adrenomedullin has been investigated on cell lines endogenously expressing receptors of known composition. 2. On human SK-N-MC cells (expressing human calcitonin receptor-like receptor (CRLR) and receptor activity modifying protein 1 (RAMP1)), BIBN4096BS had a pA 2 of 9.95 although the slope of the Schild plot (1.37±0.16) was significantly greater than 1. 3. On rat L6 cells (expressing rat CRLR and RAMP1), BIBN4096BS had a pA 2 of 9.25 and a Schild slope of 0.89±0.05, significantly less than 1. 4. On human Colony (Col) 29 cells, CGRP 8-37 had a significantly lower pA 2 than on SK-N-MC cells (7.34±0.19 (n=7) compared to 8.35±0.18, (n=6)). BIBN4096BS had a pA 2 of 9.98 and a Schild plot slope of 0.86±0.19 that was not significantly different from 1. At concentrations in excess of 3 nM, it was less potent on Col 29 cells than on SK-N-MC cells. 5. On Rat 2 cells, expressing rat CRLR and RAMP2, BIBN4096BS was unable to antagonize adrenomedullin at concentrations up to 10 μM. CGRP 8-37 had a pA 2 of 6.72 against adrenomedullin. 6. BIBN4096BS shows selectivity for the human CRLR/RAMP1 combination compared to the rat counterpart. It can discriminate between the CRLR/RAMP1 receptor expressed on SK-N-MC cells and the CGRP-responsive receptor expressed by the Col 29 cells used in this study. Its slow kinetics may explain its apparent 'non-competive' behaviour. At concentrations of up to 10 μM, it has no antagonist actions at the adrenomedullin, CRLR/RAMP2 receptor, unlike CGRP 8-37.</dc:description><dc:language>en</dc:language><dc:source>1476-5381</dc:source><dc:title>A comparison of the actions of BIBN4096BS and CGRP 8-37 on CGRP and adrenomedullin receptors expressed on SK-N-MC, L6, Col 29 and Rat 2 cells</dc:title><rioxxterms:author>Hay, Debbie L.</rioxxterms:author><rioxxterms:author>Howitt, Stephen G.</rioxxterms:author><rioxxterms:author>Conner, Alex C.</rioxxterms:author><rioxxterms:author>Doods, Henri</rioxxterms:author><rioxxterms:author>Schindler, Marcus</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1038/sj.bjp.0704844</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:26
Date: 2017-06-09

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      <identifier>oai:publications.aston.ac.uk:26</identifier>
      <datestamp>2017-06-09T10:43:43Z</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>Adrenomedullin is a vascular tissue peptide and a member of the calcitonin family of peptides, which includes calcitonin calcitonin-gene-related peptide (CGRP) and amylin. Its many biological actions are mediated via CGRP type 1 (CGRP(1)) receptors and by specific adrenomedullin receptors. Although the pharmacology of these receptors is distinct, they are both represented in molecular terms by the type II family G-protein-coupled receptor, calcitonin-receptor-like receptor (CRLR). The specificity here is defined by co-expression of receptor-activity-modifying proteins (RAMPs). CGRP(1) receptors are represented by CRLR and RAMP1, and specific adrenomedullin receptors by CRLR and RAMP2 or 3. Here we discuss how CRLR/RAMP2 relates to adrenomedullin binding, pharmacology and pathophysiology, and how chemical cross-linking of receptor-ligand complexes in tissue relates to that in CRLR/RAMP2-expressing cells. CRLR, like other type II family G-protein-coupled receptors, signals via G(s) and adenylate cyclase activation. We demonstrated that adrenomedullin signalling in cell lines expressing specific adrenomedullin receptors followed this expected pattern.</dc:description><dc:language>en</dc:language><dc:source>0300-5127</dc:source><dc:title>Adrenomedullin: receptor and signal transduction</dc:title><rioxxterms:author>Smith, David M.</rioxxterms:author><rioxxterms:author>Coppock, H.A.</rioxxterms:author><rioxxterms:author>Withers, D.J.</rioxxterms:author><rioxxterms:author>Owji, A.A.</rioxxterms:author><rioxxterms:author>Hay, D.L.</rioxxterms:author><rioxxterms:author>Choksi, T.P.</rioxxterms:author><rioxxterms:author>Chakravarty, P.</rioxxterms:author><rioxxterms:author>Legon, S.</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:publication_date>2002-08-28</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:25
Date: 2017-09-26

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<record>
    <header>
      <identifier>oai:publications.aston.ac.uk:25</identifier>
      <datestamp>2017-09-26T07:01:32Z</datestamp>
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      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>The receptor for calcitonin-gene-related peptide (CGRP) is a heterodimer formed by calcitonin-receptor-like receptor (CRLR), a type II (family B) G-protein-coupled receptor, and receptor-activity-modifying protein 1 (RAMP1), a single-membrane-pass protein. It is likely that the first seven or so amino acids of CGRP (which form a disulphide-bonded loop) interact with the transmembrane domain of CRLR to cause receptor activation. The rest of the CGRP molecule falls into three domains. Residues 28-37 and 8-18 are normally required for high-affinity binding, while residues 19-27 form a hinge region. The 28-37 region is almost certainly in direct contact with the receptor; 8-18 may make additional receptor contacts or may stabilize an appropriate conformation of 28-37. It is likely that these regions of CGRP interact both with CRLR and with the extracellular domain of RAMP1.</dc:description><dc:language>en</dc:language><dc:relation>http://www.scopus.com/inward/record.url?scp=0036671940&amp;partnerID=8YFLogxK</dc:relation><dc:source>1470-8752</dc:source><dc:title>Interaction of calcitonin-gene-related peptide with its receptors</dc:title><rioxxterms:author>Conner, Alex C.</rioxxterms:author><rioxxterms:author>Hay, Debbie L.</rioxxterms:author><rioxxterms:author>Howitt, S.G.</rioxxterms:author><rioxxterms:author>Kilk, K.</rioxxterms:author><rioxxterms:author>Langel, U.</rioxxterms:author><rioxxterms:author>Wheatley, Mark</rioxxterms:author><rioxxterms:author>Smith, David M.</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1042/BST0300451</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:23
Date: 2017-08-22

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      <datestamp>2017-08-22T11:45:16Z</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>One hundred sixty-eight multiply substituted 1,4-benzodiazepines have been prepared by a five-step solid-phase combinatorial approach using syn-phase crowns as a solid support and a hydroxymethyl-phenoxy-acetamido linkage (Wang linker). The substituents of the 1,4-benzodiazepine scaffold have been varied in the -3, -5, -7, and 8-positions and the combinatorial library was evaluated in a cholecystokinin (CCK) radioligand binding assay. 3-Alkylated 1,4-benzodiazepines with selectivity towards the CCK-B (CCK2) receptor have been optimized on the lipophilic side chain, the ketone moiety, and the stereochemistry at the 3-position. Various novel 3-alkylated compounds were synthesized and [S]3-propyl-5-phenyl-1,4-benzodiazepin-2-one, [S]NV-A, has shown a CCK-B selective binding at about 180 nM. Fifty-eight compounds of this combinatorial library were purified by preparative TLC and 25 compounds were isolated and fully characterized by TLC, IR, APCI-MS, and 1H/13C-NMR spectroscopy.</dc:description><dc:language>en</dc:language><dc:source>1029-2322</dc:source><dc:title>Combinatorial solid phase synthesis of multiply substituted 1,4-benzodiazepines and affinity studies on the CCK2 receptor (Part 1)</dc:title><rioxxterms:author>Lattmann, Eric</rioxxterms:author><rioxxterms:author>Billington, David C.</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Arayarat, Pornthip</rioxxterms:author><rioxxterms:author>Howitt, Stephen B.</rioxxterms:author><rioxxterms:author>Lawrence, Spencer</rioxxterms:author><rioxxterms:author>Offel, Michael</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1080/10559610213504</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:22
Date: 2017-08-14

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<record>
    <header>
      <identifier>oai:publications.aston.ac.uk:22</identifier>
      <datestamp>2017-08-14T07:02:33Z</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>1. The role of individual residues in the 8-18 helix of CGRP 8-37 in promoting high-affinity binding to CGRP 1 receptors expressed on rat L6 and human SK-N-MC cells has been examined. The relative potencies of various derivatives were estimated from their ability to inhibit the human αCGRP-mediated increase in cyclic AMP production and the binding of [ 125I]-human αCGRP. 3. Arg 11 and Arg 18 were replaced by serines to give [Ser 11.18]CGRP 8-37. These bound with pKi values &lt;6 to SK-N-MC cells and had apparent pA 2 values of 5.81 ± 0.04 and 5.31 ± 0.11 on SK-N-MC and L6 cells. CGRP 8-37 had a pKi of 8.22 on SK-N-MC cells and pK b values on the above cell lines of 8.95±0.04 and 8.76±0.04. 3. The arginines were replaced with glutamic acid residues. [Glu 11]CGRP 8-37 had a pK b of 7.14±0.14 on SK-N-MC cells (pKi=7.05±0.05) and 6.99±0.08 on L6 cells. [Glu 18]CGRP 8-37 had a pK b of 7.10±0.0.08 on SK-N-MC cells (pKi=6.91±0.23) and 7.12±0.09 on L6 cells. 4. Leu 12, Leu 15 and Leu 16 were replaced by benzoyl-phenylalanine (bpa) residues. On SK-N-MC cells, the apparent pA 2 values of [bpa 12]-, [bpa 15]- and [bpa 16]CGRP 8-37 were respectively 7.43±0.23, 8.34±0.11 and 5.66±0.16 (pKi values of 7.14±0.17, 7.66±0.21 and &lt;6): on L6 cells they were 7.96±0.36, 8.28±0.21 and 6.09±0.04 (all n=3). 5. It is concluded that the Arg 11 and Arg 18 are involved in specific electrostatic interactions with other residues, either on the CGRP 1 receptors or elsewhere on CGRP 8-37. Leu 16 is in a conformationally restricted site when CGRP 8-37 binds to CGRP 1 receptors, unlike Leu 12 and Leu 15.</dc:description><dc:language>en</dc:language><dc:relation>http://www.scopus.com/inward/record.url?scp=0037275217&amp;partnerID=8YFLogxK</dc:relation><dc:source>1476-5381</dc:source><dc:title>The role of the 8-18 helix of CGRP 8-37 in mediating high affinity binding to CGRP receptors; coulombic and steric interactions</dc:title><rioxxterms:author>Howitt, Stephen G.</rioxxterms:author><rioxxterms:author>Kilk, Kalle</rioxxterms:author><rioxxterms:author>Wang, Yang</rioxxterms:author><rioxxterms:author>Smith, David M.</rioxxterms:author><rioxxterms:author>Langel, Ulo</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:publication_date>2003-01-23</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1038/sj.bjp.0705040</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:21
Date: 2017-08-21

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<record>
    <header>
      <identifier>oai:publications.aston.ac.uk:21</identifier>
      <datestamp>2017-08-21T07:02:50Z</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>Adrenomedullin (AM), a potent vasoactive peptide, is elevated in certain disease states such as sepsis. Its role as a physiologically relevant peptide has been confirmed with the advent of the homozygous lethal AM peptide knockout mouse. So far, there have been few and conflicting studies which examine the regulatory role of AM at the receptor level. In this article, we discuss the few studies that have been presented on the desensitisation of AM receptors and also present novel data on the desensitisation of endogenous AM receptors in Rat-2 fibroblasts. © 2003 Elsevier Science B.V. All rights reserved.</dc:description><dc:language>en</dc:language><dc:relation>http://www.scopus.com/inward/record.url?scp=12244290339&amp;partnerID=8YFLogxK</dc:relation><dc:source>1873-1686</dc:source><dc:title>Desensitisation of adrenomedullin and CGRP receptors</dc:title><rioxxterms:author>Hay, Debbie L.</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Smith, David M.</rioxxterms:author><rioxxterms:publication_date>2003-04-15</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1016/S0167-0115(03)00032-6</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:20
Date: 2017-08-28

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<record>
    <header>
      <identifier>oai:publications.aston.ac.uk:20</identifier>
      <datestamp>2017-08-28T07:02:20Z</datestamp>
      <setSpec>7374617475733D707562</setSpec>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>1. Adrenomedullin (AM) has two known receptors formed by the calcitonin receptor-like receptor (CL) and receptor activity-modifying protein (RAMP) 2 or 3: We report the effects of the antagonist fragments of human AM and CGRP (AM 22-52 and CGRP 8-37) in inhibiting AM at human (h), rat (r) and mixed species CL/RAMP2 and CL/RAMP3 receptors transiently expressed in Cos 7 cells or endogenously expressed as rCL/rRAMP2 complexes by Rat 2 and L6 cells. 2. AM 22-52 (10 μM) antagonised AM at all CL/RAMP2 complexes (apparent pA 2 values: 7.34±0.14 (hCL/hRAMP2), 7.28±0.06 (Rat2), 7.00±0.05 (L6), 6.25±0.17(rCL/hRAMP2)). CGRP 8-37 (10 μM) resembled AM 22-52 except on the rCL/hRAMP2 complex, where it did not antagonise AM (apparent PA 2 values: 7.04±0.13 (hCL/hRAMP2), 6.72±0.06 (Rat2), 7.03±0. 12 (L6)). 3. On CL/RAMP3 receptors, 10 μM CGRP 8-37 was an effective antagonist at all combinations (apparent pA 2 values: 6.96±0.08 (hCL/hRAMP3), 6.18±0.18 (rCL/rRAMP3), 6.48±0.20 (rCL/ hRAMP3)). However, 10 μm AM 22-52 only antagonised AM at the hCL/hRAMP3 receptor (apparent PA 2 6.73±0.14). 4. BIBN4096BS (10 μM) did not antagonise AM at any of the receptors. 5. Where investigated (all-rat and rat/human combinations), the agonist potency order on the CL/ RAMP3 receptor was AM∼βCGRP&gt;αCGRP. 6. rRAMP3 showed three apparent polymorphisms, none of which altered its coding sequence. 7. This study shows that on CL/RAMP complexes, AM 22-52 has significant selectivity for the CL/ RAMP2 combination over the CL/RAMP3 combination. On the mixed species receptor, CGRP 8-37 showed the opposite selectivity. Thus, depending on the species, it is possible to discriminate pharmacologically between CL/RAMP2 and CL/RAMP3 AM receptors.</dc:description><dc:language>en</dc:language><dc:relation>http://www.scopus.com/inward/record.url?scp=0142153874&amp;partnerID=8YFLogxK</dc:relation><dc:source>1476-5381</dc:source><dc:title>CL/RAMP2 and CL/RAMP3 produce pharmacologically distinct adrenomedullin receptors:a comparison of effects of adrenomedullin 22-52, CGRP 8-37 and BIBN4096BS</dc:title><rioxxterms:author>Hay, Debbie L.</rioxxterms:author><rioxxterms:author>Howitt, Stephen G.</rioxxterms:author><rioxxterms:author>Conner, Alex C.</rioxxterms:author><rioxxterms:author>Schindler, Marcus</rioxxterms:author><rioxxterms:author>Smith, David M.</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:publication_date>2003-10-02</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1038/sj.bjp.0705472</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:19
Date: 2017-08-22

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<record>
    <header>
      <identifier>oai:publications.aston.ac.uk:19</identifier>
      <datestamp>2017-08-22T11:45:15Z</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>Adrenomedullin (AM) has two specific receptors formed by the calcitonin-receptor-like receptor (CL) and receptor activity-modifying protein (RAMP) 2 or 3. These are known as AM1 and AM2 receptors, respectively. In addition, AM has appreciable affinity for the CGRP1 receptor, composed of CL and RAMP1. The AM1 receptor has a high degree of selectivity for AM over CGRP and other peptides, and AM 22-52 is an effective antagonist at this receptor. By contrast, the AM2 receptor shows less specificity for AM, having appreciable affinity for βCGRP. Here, CGRP8-37 is either equipotent or more effective as an antagonist than AM22-52, depending on the species from which the receptor components are derived. Thus, under the appropriate circumstances it seems that βCGRP might be able to activate both CGRP 1 and AM2 receptors and AM could activate both AM 1 and AM2 receptors as well as CGRP1 receptors. Current peptide antagonists are not sufficiently selective to discriminate between these three receptors. The CGRP-selectivity of RAMP1 and RAMP3 may be conferred by a putative disulfide bond from the N-terminus to the middle of the extracellular domain of these molecules. This is not present in RAMP2. Copyright © 2004 Humana Press Inc. All rights of any nature whatsoever reserved.</dc:description><dc:language>en</dc:language><dc:source>1559-1166</dc:source><dc:title>The pharmacology of adrenomedullin receptors and their relationship to CGRP receptors</dc:title><rioxxterms:author>Hay, Debbie L.</rioxxterms:author><rioxxterms:author>Conner, Alex C.</rioxxterms:author><rioxxterms:author>Howitt, Stephen G.</rioxxterms:author><rioxxterms:author>Smith, David M.</rioxxterms:author><rioxxterms:author>Poyner, David</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1385/JMN:22:1-2:105</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:18
Date: 2017-08-22

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<record>
    <header>
      <identifier>oai:publications.aston.ac.uk:18</identifier>
      <datestamp>2017-08-22T11:45:15Z</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>RAMPs (receptor activity-modifying proteins) are single-pass transmembrane proteins that associate with certain family-B GPCRs (G-protein-coupled receptors). Specifically for the CT (calcitonin) receptor-like receptor and the CT receptor, this results in profound changes in ligand binding and receptor pharmacology, allowing the generation of six distinct receptors with preferences for CGRP (CT gene-related peptide) adrenomedullin, amylin and CT. There are three RAMPs: RAMP1-RAMP3. The N-terminus appears to be the main determinant of receptor pharmacology whereas the transmembrane domain contributes to association of the RAMP with the GPCR. The N-terminus of all members of the RAMP family probably contains two disulphide bonds; a potential third disulphide is found in RAMP1 and RAMP3. The N-terminus appears to be in close proximity to the ligand and plays a key role in its binding, either directly or indirectly. BIBN4096BS, a CGRP antagonist, targets RAMP1 and this gives the compound very high selectivity for the human CGRP(1) receptor.</dc:description><dc:language>en</dc:language><dc:source>1470-8752</dc:source><dc:title>Heterodimers and family-B GPCRs:RAMPs, CGRP and adrenomedullin</dc:title><rioxxterms:author>Conner, A.C.</rioxxterms:author><rioxxterms:author>Simms, J.</rioxxterms:author><rioxxterms:author>Hay, D.L.</rioxxterms:author><rioxxterms:author>Mahmoud, K.</rioxxterms:author><rioxxterms:author>Howitt, S.G.</rioxxterms:author><rioxxterms:author>Wheatley, M.</rioxxterms:author><rioxxterms:author>Poyner, D.R.</rioxxterms:author><rioxxterms:publication_date>2004</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1042/BST0320843</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:17
Date: 2017-08-22

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<record>
    <header>
      <identifier>oai:publications.aston.ac.uk:17</identifier>
      <datestamp>2017-08-22T11:45:15Z</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>Historically, CGRP receptors have been classified as CGRP(1) or CGRP(2) subtypes, chiefly depending on their affinity for the antagonist CGRP(8-37). It has been shown that the complex between calcitonin receptor-like receptor (CRLR or CL) and receptor activity modifying protein (RAMP) 1 provides a molecular correlate for the CGRP(1) receptor; however this does not explain the range of affinities seen for CGRP(8-37) in isolated tissues. It is suggested that these may largely be explained by a combination of methodological factors and CGRP-responsive receptors generated by CL and RAMP2 or RAMP3 and complexes of RAMPs with the calcitonin receptor.</dc:description><dc:language>en</dc:language><dc:source>1873-5169</dc:source><dc:title>The pharmacology of CGRP-responsive receptors in cultured and transfected cells</dc:title><rioxxterms:author>Hay, D.L.</rioxxterms:author><rioxxterms:author>Conner, A.C.</rioxxterms:author><rioxxterms:author>Howitt, S.G.</rioxxterms:author><rioxxterms:author>Takhshid, M.A.</rioxxterms:author><rioxxterms:author>Simms, J.</rioxxterms:author><rioxxterms:author>Mahmoud, K.</rioxxterms:author><rioxxterms:author>Poyner, David</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.peptides.2004.06.007</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:16
Date: 2017-09-28

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      <identifier>oai:publications.aston.ac.uk:16</identifier>
      <datestamp>2017-09-28T07:02:02Z</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>Calcitonin receptor like-receptor is a family B G-protein coupled receptor (GPCR). It requires receptor activity modifying protein (RAMP) 1 to give a calcitonin gene-related peptide (CGRP) receptor. Little is known of how members of this receptor family function. Proline residues often form important kinks in alpha-helices. Therefore, all proline residues within the transmembrane helices of the receptor (Pro241, Pro244 in helix 4, Pro275 in helix 5, Pro321 and Pro331 in helix 6) were mutated to alanine. Pro241 Pro275, and Pro321 are highly conserved throughout all family B GPCRs. The binding of CGRP and its ability to stimulate cAMP production were investigated in mutant and wild-type receptors after transient transfection into COS-7 cells with RAMP1. The P321A mutation significantly decreased the pEC(50) for CGRP and reduced its affinity but did not change cell-surface expression. Antagonist binding [CGRP(8-37) and 1-piperidinecarboxamide N-[2-[[5amino-1-[[4-(4-pyridinyl)-1-piperazinyl]carbonyl]pentyl]amino]-1-[(3 5-dibromo-4-hydroxyphenyl)methyl]-2-oxoethyl]-4-(1,4-dihydro-2-oxo-3(2H)-quina zolinyl) (BIBN4096BS)] was little altered by the mutation. Adrenomedullin-mediated signaling was disrupted when P321A was coexpressed with RAMP1, RAMP2, or RAMP3. The P331A mutant produced a moderate reduction in CGRP binding and receptor activation. Mutation of the other residues had no effect on receptor function. Thus, Pro321 and Pro331 are required for agonist binding and receptor activation. Modeling suggested that Pro321 induces a bend in helix 6, bringing its C terminus near that of helix 3, as seen in many family A GPCRs. This is abolished in P321A. P321A-I325P predicted to restore this conformation, showed wild-type activation. Modeling can also rationalize the effects of transmembrane proline mutants previously reported for another family B GPCR, the VPAC(1) receptor.</dc:description><dc:language>en</dc:language><dc:relation>http://www.scopus.com/inward/record.url?scp=11244331476&amp;partnerID=8YFLogxK</dc:relation><dc:source>1521-0111</dc:source><dc:title>A key role for transmembrane prolines in calcitonin receptor-like receptor agonist binding and signalling:implications for family B G-protein-coupled receptors</dc:title><rioxxterms:author>Conner, Alex C.</rioxxterms:author><rioxxterms:author>Hay, Debbie L.</rioxxterms:author><rioxxterms:author>Simms, John</rioxxterms:author><rioxxterms:author>Howitt, Stephen G.</rioxxterms:author><rioxxterms:author>Schindler, Marcus</rioxxterms:author><rioxxterms:author>Smith, David M.</rioxxterms:author><rioxxterms:author>Wheatley, Mark</rioxxterms:author><rioxxterms:author>Poyner, David R.</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.67.1.20</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:15
Date: 2017-08-22

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    <header>
      <identifier>oai:publications.aston.ac.uk:15</identifier>
      <datestamp>2017-08-22T11:45:15Z</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>Calcitonin (CT) receptors dimerize with receptor activity-modifying proteins (RAMPs) to create high-affinity amylin (AMY) receptors, but there is no reliable means of pharmacologically distinguishing these receptors. We used agonists and antagonists to define their pharmacology, expressing the CT (a) receptor alone or with RAMPs in COS-7 cells and measuring cAMP accumulation. Intermedin short, otherwise known as adrenomedullin 2, mirrored the action of αCGRP, being a weak agonist at CT(a), AMY 2(a), and AMY3(a) receptors but considerably more potent at AMY1(a) receptors. Likewise, the linear calcitonin gene-related peptide (CGRP) analogs (Cys(ACM)2,7)hαCGRP and (Cys(Et) 2,7)haCGRP were only effective at AMY1(a) receptors, but they were partial agonists. As previously observed in COS-7 cells, there was little induction of the AMY2(a) receptor phenotype; thus, AMY 2(a) was not examined further in this study. The antagonist peptide salmon calcitonin8-32 (sCT8-32) did not discriminate strongly between CT and AMY receptors; however, AC187 was a more effective antagonist of AMY responses at AMY receptors, and AC413 additionally showed modest selectivity for AMY1(a) over AMY3(a) receptors. CGRP8-37 also demonstrated receptor-dependent effects. CGRP 8-37 more effectively antagonized AMY at AMY1(a) than AMY3(a) receptors, although it was only a weak antagonist of both, but it did not inhibit responses at the CT(a) receptor. Low CGRP 8-37 affinity and agonism by linear CGRP analogs at AMY 1(a) are the classic signature of a CGRP2 receptor. Our data indicate that careful use of combinations of agonists and antagonists may allow pharmacological discrimination of CT(a), AMY1(a), and AMY3(a) receptors, providing a means to delineate the physiological significance of these receptors. Copyright © 2005 The American Society for Pharmacology and Experimental Therapeutics.</dc:description><dc:language>en</dc:language><dc:source>1521-0111</dc:source><dc:title>Pharmacological discrimination of calcitonin receptor:receptor activity-modifying protein complexes</dc:title><rioxxterms:author>Hay, Debbie L.</rioxxterms:author><rioxxterms:author>Christopoulos, George</rioxxterms:author><rioxxterms:author>Christopoulos, Arthur</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Sexton, Patrick M.</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.104.008615</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:14
Date: 2017-09-01

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<record>
    <header>
      <identifier>oai:publications.aston.ac.uk:14</identifier>
      <datestamp>2017-09-01T07:03:22Z</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:description>Our conceptual understanding of the molecular architecture of G-protein coupled receptors (GPCRs) has transformed over the last decade. Once considered as largely independent functional units (aside from their interaction with the G-protein itself), it is now clear that a single GPCR is but part of a multifaceted signaling complex, each component providing an additional layer of sophistication. Receptor activity-modifying proteins (RAMPs) provide a notable example of proteins that interact with GPCRs to modify their function. They act as pharmacological switches, modifying GPCR pharmacology for a particular subset of receptors. However, there is accumulating evidence that these ubiquitous proteins have a broader role, regulating signaling and receptor trafficking. This article aims to provide the reader with a comprehensive appraisal of RAMP literature and perhaps some insight into the impact that their discovery has had on those who study GPCRs. © 2005 Elsevier Inc. All rights reserved.</dc:description><dc:language>en</dc:language><dc:relation>http://www.scopus.com/inward/record.url?scp=28444464430&amp;partnerID=8YFLogxK</dc:relation><dc:source>1879-016X</dc:source><dc:title>GPCR modulation by RAMPs</dc:title><rioxxterms:author>Hay, Debbie L.</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Sexton, Patrick M.</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.pharmthera.2005.06.015</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:13
Date: 2017-09-28

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<record>
    <header>
      <identifier>oai:publications.aston.ac.uk:13</identifier>
      <datestamp>2017-09-28T07:02:19Z</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 calcitonin gene-related peptide (CGRP) receptor is a heterodimer of a family B G-protein-coupled receptor, calcitonin receptor-like receptor (CLR), and the accessory protein receptor activity modifying protein 1. It couples to Gs, but it is not known which intracellular loops mediate this. We have identified the boundaries of this loop based on the relative position and length of the juxtamembrane transmembrane regions 3 and 4. The loop has been analyzed by systematic mutagenesis of all residues to alanine, measuring cAMP accumulation, CGRP affinity, and receptor expression. Unlike rhodopsin, ICL2 of the CGRP receptor plays a part in the conformational switch after agonist interaction. His-216 and Lys-227 were essential for a functional CGRP-induced cAMP response. The effect of (H216A)CLR is due to a disruption to the cell surface transport or surface stability of the mutant receptor. In contrast, (K227A)CLR had wild-type expression and agonist affinity, suggesting a direct disruption to the downstream signal transduction mechanism of the CGRP receptor. Modeling suggests that the loop undergoes a significant shift in position during receptor activation, exposing a potential G-protein binding pocket. Lys-227 changes position to point into the pocket, potentially allowing it to interact with bound G-proteins. His-216 occupies a position similar to that of Tyr-136 in bovine rhodopsin, part of the DRY motif of the latter receptor. This is the first comprehensive analysis of an entire intracellular loop within the calcitonin family of G-protein-coupled receptor. These data help to define the structural and functional characteristics of the CGRP-receptor and of family B G-protein-coupled receptors in general. © 2006 by The American Society for Biochemistry and Molecular Biology, Inc.</dc:description><dc:language>en</dc:language><dc:relation>http://www.scopus.com/inward/record.url?scp=33644985933&amp;partnerID=8YFLogxK</dc:relation><dc:source>1083-351X</dc:source><dc:title>The second intracellular loop of the calcitonin gene-related peptide receptor provides molecular determinants for signal transduction and cell surface expression</dc:title><rioxxterms:author>Conner, Alex C.</rioxxterms:author><rioxxterms:author>Simms, John</rioxxterms:author><rioxxterms:author>Howitt, Stephen G.</rioxxterms:author><rioxxterms:author>Wheatley, Mark</rioxxterms:author><rioxxterms:author>Poyner, David R.</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.M510064200</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:12
Date: 2017-08-22

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<record>
    <header>
      <identifier>oai:publications.aston.ac.uk:12</identifier>
      <datestamp>2017-08-22T11:45:14Z</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>Receptor activity modifying proteins (RAMPs) are a family of single-pass transmembrane proteins that dimerize with G-protein-coupled receptors. They may alter the ligand recognition properties of the receptors (particularly for the calcitonin receptor-like receptor, CLR). Very little structural information is available about RAMPs. Here, an ab initio model has been generated for the extracellular domain of RAMP1. The disulfide bond arrangement (Cys 27-Cys82, Cys40-Cys72, and Cys 57-Cys104) was determined by site-directed mutagenesis. The secondary structure (a-helices from residues 29-51, 60-80, and 87-100) was established from a consensus of predictive routines. Using these constraints, an assemblage of 25,000 structures was constructed and these were ranked using an all-atom statistical potential. The best 1000 conformations were energy minimized. The lowest scoring model was refined by molecular dynamics simulation. To validate our strategy, the same methods were applied to three proteins of known structure; PDB:1HP8, PDB:1V54 chain H (residues 21-85), and PDB:1T0P. When compared to the crystal structures, the models had root mean-square deviations of 3.8 Å, 4.1 Å, and 4.0 Å, respectively. The model of RAMP1 suggested that Phe93, Tyr 100, and Phe101 form a binding interface for CLR, whereas Trp74 and Phe92 may interact with ligands that bind to the CLR/RAMP1 heterodimer. © 2006 by the Biophysical Society.</dc:description><dc:language>en</dc:language><dc:source>1542-0086</dc:source><dc:title>Characterization of the structure of RAMP1 by mutagenesis and molecular modeling</dc:title><rioxxterms:author>Simms, John</rioxxterms:author><rioxxterms:author>Hay, Debbie L.</rioxxterms:author><rioxxterms:author>Wheatley, Mark</rioxxterms:author><rioxxterms:author>Poyner, David R.</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.106.084582</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:11
Date: 2017-08-22

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<record>
    <header>
      <identifier>oai:publications.aston.ac.uk:11</identifier>
      <datestamp>2017-08-22T11:45:14Z</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>1 Adrenomedullin (AM) and calcitonin gene-related peptide (CGRP) have structural similarities, interact with each others receptors (calcitonin receptor-like receptor (CLR)/receptor-activity-modifying proteins (RAMPs)) and show overlapping biological activities. AM and CGRP receptors are chiefly coupled to cAMP production. In this study, a method of primary dissociated cell culture was used to investigate the presence of AM and CGRP receptors and their effects on cAMP production in embryonic spinal cord cells. 2 Both neuronal and non-neuronal CLR immunopositive cells were present in our model. 3 High affinity, specific [ 125I]-AM binding sites (K(d) 79±9 pM and B(max) 571±34 fmol mg -1 protein) were more abundant than specific [ 125I]-CGRP binding sites (K(d) 12±0.7 pM and B(max) 32±2 fmol mg -1 protein) in embryonic spinal cord cells. 4 Specific [ 125I]-AM binding was competed by related molecules with a ligand selectivity profile of rAM&gt;hAM(22-52)&gt;rCGRPα&gt;CGRP(8-37) ≫[r-(r*,s*)]-N-[2-[[5-amino-1-[[4-(4-pyridinyl)-1-piperazinyl] carbonyl]pentyl]amino]-1-[(3,5-dibromo-4-hydroxyphenyl)methyl]-2-oxoethyl]-4-(1, 4-dihydro-2-oxo-3(2H)-quinazolinyl)-,1-piperidinecarboxamide (BIBN4096BS). 5 Specific [ 125I]-CGRP binding was competed by rCGRPα&gt;rAM≥ CGRP(8-37)≥BIBN4096BS&gt;hAM(22-52). 6 Cellular levels of cAMP were increased by AM (pEC"5"0 10.2±0.2) and less potently by rCGRPα (pEC"5"0 8.9±0.4). rCGRPα-induced cAMP accumulation was effectively inhibited by CGRP(8-37) (pA"2 7.63±0.44) and hAM(22-52) (pA"2 6.18±0.21) while AM-stimulation of cAMP levels was inhibited by CGRP(8-37) (pA"2 7.41±0.15) and AM(22-52) (pA"2 7.26±0.18). BIBN4096BS only antagonized the effects of CGRP (pA"2 8.40±0.30) on cAMP accumulation. 7 These pharmacological profiles suggest that effects of CGRP are mediated by the CGRP"1 (CLR/RAMP1) receptor in our model while those of AM are related to the activation of the AM"1 (CLR/RAMP2) receptor subtype. © 2006 Nature Publishing Group All rights reserved.</dc:description><dc:language>en</dc:language><dc:source>1476-5381</dc:source><dc:title>Characterization and effects on cAMP accumulation of adrenomedullin and calcitonin gene-related peptide (CGRP) receptors in dissociated rat spinal cord cell culture</dc:title><rioxxterms:author>Takhshid, Mohammad A.</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Chabot, Jean-Guy</rioxxterms:author><rioxxterms:author>Fournier, Alain</rioxxterms:author><rioxxterms:author>Ma, Weiya</rioxxterms:author><rioxxterms:author>Zheng, Wen-Hua</rioxxterms:author><rioxxterms:author>Owji, Ali A.</rioxxterms:author><rioxxterms:author>Quirion, Remi</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1038/sj.bjp.0706750</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:9
Date: 2017-07-26

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    <header>
      <identifier>oai:publications.aston.ac.uk:9</identifier>
      <datestamp>2017-07-26T13:34:11Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><dc:description>In April 2007, the Biochemical Society held a meeting to compare and contrast ligand binding and activation of Family A and B GPCRs (G-protein-coupled receptors). Being the largest class, Family A GPCRs usually receive the most attention, although a previous Biochemical Society meeting has focused on Family B GPCRs. The aim of the present meeting was to bring researchers of both families together in order to identify commonalities between the two. The present article introduces the proceedings of the meeting, briefly commenting on the focus of each of the following articles. ©The Authors.</dc:description><dc:language>en</dc:language><dc:source>0300-5127</dc:source><dc:title>Family resemblances? Ligand binding and activation of family A and B G-protein-coupled receptors</dc:title><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Wheatley, M.</rioxxterms:author><rioxxterms:publication_date>2007-08-01</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://www.scopus.com/inward/record.url?scp=34548165300&amp;partnerID=8YFLogxK</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:7
Date: 2017-08-22

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    <header>
      <identifier>oai:publications.aston.ac.uk:7</identifier>
      <datestamp>2017-08-22T11:45:14Z</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>Historically, calcitonin gene-related peptide (CGRP) receptors have been divided into two classes, CGRP(1) and CGRP(2).After the cloning of calcitonin receptor-like receptor (CLR) and receptor activity-modifying proteins (RAMPs), it became clear that the CGRP(1) receptor was a complex between CLR and RAMP1. It is now apparent that the CGRP(2) receptor phenotype is the result of CGRP acting at receptors for amylin and adrenomedullin. Accordingly, the term "CGRP(2)" receptor should no longer be used, and the "CGRP(1)" receptor should be known as the "CGRP" receptor.</dc:description><dc:language>en</dc:language><dc:source>1521-0081</dc:source><dc:title>International Union of Pharmacology. LXIX. Status of the calcitonin gene-related peptide subtype 2 receptor</dc:title><rioxxterms:author>Hay, Debbie L.</rioxxterms:author><rioxxterms:author>Poyner, David R.</rioxxterms:author><rioxxterms:author>Quirion, Remi</rioxxterms:author><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>NA</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1124/pr.108.00372</rioxxterms:version_of_record></rioxx></metadata></record>
ID: oai:publications.aston.ac.uk:3
Date: 2017-09-19

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<record>
    <header>
      <identifier>oai:publications.aston.ac.uk:3</identifier>
      <datestamp>2017-09-19T07:03:34Z</datestamp>
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    <metadata>
      <rioxx xmlns="http://www.rioxx.net/schema/v2.0/rioxx/" xmlns:ali="http://ali.niso.org/2014/ali/1.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:rioxxterms="http://docs.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.rioxx.net/schema/v2.0/rioxx/ http://www.rioxx.net/schema/v2.0/rioxx/rioxx.xsd"><ali:free_to_read/><ali:license_ref start_date="2008-02-27">http://creativecommons.org/licenses/by/4.0</ali:license_ref><dc:description>Darwin originally pointed out that there is something about infants which prompts adults to respond to and care for them, in order to increase individual fitness, i.e. reproductive success, via increased survivorship of one's own offspring. Lorenz proposed that it is the specific structure of the infant face that serves to elicit these parental responses, but the biological basis for this remains elusive. Here, we investigated whether adults show specific brain responses to unfamiliar infant faces compared to adult faces, where the infant and adult faces had been carefully matched across the two groups for emotional valence and arousal, as well as size and luminosity. The faces also matched closely in terms of attractiveness. Using magnetoencephalography (MEG) in adults, we found that highly specific brain activity occurred within a seventh of a second in response to unfamiliar infant faces but not to adult faces. This activity occurred in the medial orbitofrontal cortex (mOFC), an area implicated in reward behaviour, suggesting for the first time a neural basis for this vital evolutionary process. We found a peak in activity first in mOFC and then in the right fusiform face area (FFA). In mOFC the first significant peak (p&lt;0.001) in differences in power between infant and adult faces was found at around 130 ms in the 10-15 Hz band. These early differences were not found in the FFA. In contrast, differences in power were found later, at around 165 ms, in a different band (20-25 Hz) in the right FFA, suggesting a feedback effect from mOFC. These findings provide evidence in humans of a potential brain basis for the "innate releasing mechanisms" described by Lorenz for affection and nurturing of young infants. This has potentially important clinical applications in relation to postnatal depression, and could provide opportunities for early identification of families at risk.</dc:description><dc:format>application/pdf</dc:format><dc:identifier>http://publications.aston.ac.uk/3/1/Specific_and_rapid_neural_signature_for_parental_instinct.pdf</dc:identifier><dc:language>en</dc:language><dc:relation>http://www.scopus.com/inward/record.url?scp=45749091796&amp;partnerID=8YFLogxK</dc:relation><dc:source>1932-6203</dc:source><dc:title>A specific and rapid neural signature for parental instinct</dc:title><rioxxterms:author>Kringelbach, Morten L.</rioxxterms:author><rioxxterms:author>Lehtonen, Annukka</rioxxterms:author><rioxxterms:author>Squire, Sarah</rioxxterms:author><rioxxterms:author>Harvey, Allison G.</rioxxterms:author><rioxxterms:author>Craske, Michelle G.</rioxxterms:author><rioxxterms:author>Holliday, Ian E.</rioxxterms:author><rioxxterms:author>Green, Alexander L.</rioxxterms:author><rioxxterms:author>Aziz, Tipu Z.</rioxxterms:author><rioxxterms:author>Hansen, Peter C.</rioxxterms:author><rioxxterms:author>Cornelissen, Piers L.</rioxxterms:author><rioxxterms:author>Stein, Alan</rioxxterms:author><rioxxterms:publication_date>2008-02-27</rioxxterms:publication_date><rioxxterms:type>Journal Article/Review</rioxxterms:type><rioxxterms:version>SMUR</rioxxterms:version><rioxxterms:version_of_record>http://dx.doi.org/10.1371/journal.pone.0001664</rioxxterms:version_of_record></rioxx></metadata></record>

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