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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en"><italic>MBL2</italic> Variations and Malaria Susceptibility in Indian Populations</title><author><name sortKey="Jha, Aditya Nath" sort="Jha, Aditya Nath" uniqKey="Jha A" first="Aditya Nath" last="Jha">Aditya Nath Jha</name><affiliation><nlm:aff id="aff1">CSIR–Centre for Cellular and Molecular Biology, Hyderabad, India</nlm:aff></affiliation></author><author><name sortKey="Sundaravadivel, Pandarisamy" sort="Sundaravadivel, Pandarisamy" uniqKey="Sundaravadivel P" first="Pandarisamy" last="Sundaravadivel">Pandarisamy Sundaravadivel</name><affiliation><nlm:aff id="aff1">CSIR–Centre for Cellular and Molecular Biology, Hyderabad, India</nlm:aff></affiliation></author><author><name sortKey="Singh, Vipin Kumar" sort="Singh, Vipin Kumar" uniqKey="Singh V" first="Vipin Kumar" last="Singh">Vipin Kumar Singh</name><affiliation><nlm:aff id="aff1">CSIR–Centre for Cellular and Molecular Biology, Hyderabad, India</nlm:aff></affiliation></author><author><name sortKey="Pati, Sudhanshu S" sort="Pati, Sudhanshu S" uniqKey="Pati S" first="Sudhanshu S." last="Pati">Sudhanshu S. Pati</name><affiliation><nlm:aff id="aff2">Ispat General Hospital, Rourkela, Orrisa, India</nlm:aff></affiliation></author><author><name sortKey="Patra, Pradeep K" sort="Patra, Pradeep K" uniqKey="Patra P" first="Pradeep K." last="Patra">Pradeep K. Patra</name><affiliation><nlm:aff id="aff3">Pt. Jawaharlal Nehru Memorial Medical College, Raipur, Chhattisgarh, India</nlm:aff></affiliation></author><author><name sortKey="Kremsner, Peter G" sort="Kremsner, Peter G" uniqKey="Kremsner P" first="Peter G." last="Kremsner">Peter G. Kremsner</name><affiliation><nlm:aff id="aff4">Institute of Tropical Medicine, University ofTübingen, Tübingen, Germany</nlm:aff></affiliation></author><author><name sortKey="Velavan, Thirumalaisamy P" sort="Velavan, Thirumalaisamy P" uniqKey="Velavan T" first="Thirumalaisamy P." last="Velavan">Thirumalaisamy P. Velavan</name><affiliation><nlm:aff id="aff4">Institute of Tropical Medicine, University ofTübingen, Tübingen, Germany</nlm:aff></affiliation></author><author><name sortKey="Singh, Lalji" sort="Singh, Lalji" uniqKey="Singh L" first="Lalji" last="Singh">Lalji Singh</name><affiliation><nlm:aff id="aff1">CSIR–Centre for Cellular and Molecular Biology, Hyderabad, India</nlm:aff></affiliation><affiliation><nlm:aff id="aff5">Banaras Hindu University, Varanasi, India</nlm:aff></affiliation><affiliation><nlm:aff id="aff6">Genome Foundation, Hyderabad, India</nlm:aff></affiliation></author><author><name sortKey="Thangaraj, Kumarasamy" sort="Thangaraj, Kumarasamy" uniqKey="Thangaraj K" first="Kumarasamy" last="Thangaraj">Kumarasamy Thangaraj</name><affiliation><nlm:aff id="aff1">CSIR–Centre for Cellular and Molecular Biology, Hyderabad, India</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">24126531</idno><idno type="pmc">3911836</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3911836</idno><idno type="RBID">PMC:3911836</idno><idno type="doi">10.1128/IAI.01041-13</idno><date when="2014">2014</date><idno type="wicri:Area/Pmc/Corpus">000160</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000160</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main"><italic>MBL2</italic> Variations and Malaria Susceptibility in Indian Populations</title><author><name sortKey="Jha, Aditya Nath" sort="Jha, Aditya Nath" uniqKey="Jha A" first="Aditya Nath" last="Jha">Aditya Nath Jha</name><affiliation><nlm:aff id="aff1">CSIR–Centre for Cellular and Molecular Biology, Hyderabad, India</nlm:aff></affiliation></author><author><name sortKey="Sundaravadivel, Pandarisamy" sort="Sundaravadivel, Pandarisamy" uniqKey="Sundaravadivel P" first="Pandarisamy" last="Sundaravadivel">Pandarisamy Sundaravadivel</name><affiliation><nlm:aff id="aff1">CSIR–Centre for Cellular and Molecular Biology, Hyderabad, India</nlm:aff></affiliation></author><author><name sortKey="Singh, Vipin Kumar" sort="Singh, Vipin Kumar" uniqKey="Singh V" first="Vipin Kumar" last="Singh">Vipin Kumar Singh</name><affiliation><nlm:aff id="aff1">CSIR–Centre for Cellular and Molecular Biology, Hyderabad, India</nlm:aff></affiliation></author><author><name sortKey="Pati, Sudhanshu S" sort="Pati, Sudhanshu S" uniqKey="Pati S" first="Sudhanshu S." last="Pati">Sudhanshu S. Pati</name><affiliation><nlm:aff id="aff2">Ispat General Hospital, Rourkela, Orrisa, India</nlm:aff></affiliation></author><author><name sortKey="Patra, Pradeep K" sort="Patra, Pradeep K" uniqKey="Patra P" first="Pradeep K." last="Patra">Pradeep K. Patra</name><affiliation><nlm:aff id="aff3">Pt. Jawaharlal Nehru Memorial Medical College, Raipur, Chhattisgarh, India</nlm:aff></affiliation></author><author><name sortKey="Kremsner, Peter G" sort="Kremsner, Peter G" uniqKey="Kremsner P" first="Peter G." last="Kremsner">Peter G. Kremsner</name><affiliation><nlm:aff id="aff4">Institute of Tropical Medicine, University ofTübingen, Tübingen, Germany</nlm:aff></affiliation></author><author><name sortKey="Velavan, Thirumalaisamy P" sort="Velavan, Thirumalaisamy P" uniqKey="Velavan T" first="Thirumalaisamy P." last="Velavan">Thirumalaisamy P. Velavan</name><affiliation><nlm:aff id="aff4">Institute of Tropical Medicine, University ofTübingen, Tübingen, Germany</nlm:aff></affiliation></author><author><name sortKey="Singh, Lalji" sort="Singh, Lalji" uniqKey="Singh L" first="Lalji" last="Singh">Lalji Singh</name><affiliation><nlm:aff id="aff1">CSIR–Centre for Cellular and Molecular Biology, Hyderabad, India</nlm:aff></affiliation><affiliation><nlm:aff id="aff5">Banaras Hindu University, Varanasi, India</nlm:aff></affiliation><affiliation><nlm:aff id="aff6">Genome Foundation, Hyderabad, India</nlm:aff></affiliation></author><author><name sortKey="Thangaraj, Kumarasamy" sort="Thangaraj, Kumarasamy" uniqKey="Thangaraj K" first="Kumarasamy" last="Thangaraj">Kumarasamy Thangaraj</name><affiliation><nlm:aff id="aff1">CSIR–Centre for Cellular and Molecular Biology, Hyderabad, India</nlm:aff></affiliation></author></analytic><series><title level="j">Infection and Immunity</title><idno type="ISSN">0019-9567</idno><idno type="eISSN">1098-5522</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Human mannose-binding lectin (MBL) encoded by the <italic>MBL2</italic> gene is a pattern recognition protein and has been associated with many infectious diseases, including malaria. We sought to investigate the contribution of functional <italic>MBL2</italic> gene variations to <named-content content-type="genus-species">Plasmodium falciparum</named-content> malaria in well-defined cases and in matched controls. We resequenced the 8.7 kb of the entire <italic>MBL2</italic> gene in 434 individuals clinically classified with malaria from regions of India where malaria is endemic. The study cohort included 176 patients with severe malaria, 101 patients with mild malaria, and 157 ethnically matched asymptomatic individuals. In addition, 830 individuals from 32 socially, linguistically, and geographically diverse endogamous populations of India were investigated for the distribution of functional <italic>MBL2</italic> variants. The <italic>MBL2 −221C</italic> (<italic>X</italic>) allelic variant is associated with increased risk of malaria (mild malaria odds ratio [OR] = 1.9, corrected <italic>P</italic> value [<italic>P</italic><sup>Corr</sup>] = 0.0036; severe malaria OR = 1.6, <italic>P</italic><sup><italic>Corr</italic></sup> = 0.02). The exon1 variants <italic>MBL2*B</italic> (severe malaria OR = 2.1, <italic>P</italic><sup><italic>Corr</italic></sup> = 0.036; mild versus severe malaria OR = 2.5, <italic>P</italic><sup><italic>Corr</italic></sup> = 0.039) and <italic>MBL2*C</italic> (mild versus severe malaria OR = 5.4, <italic>P</italic><sup><italic>Corr</italic></sup> = 0.045) increased the odds of having malaria. The exon1 <italic>MBL2*D/*B/*C</italic> variant increased the risk for severe malaria (OR = 3.4, <italic>P</italic><sup><italic>Corr</italic></sup> = 0.000045). The frequencies of low MBL haplotypes were significantly higher in severe malaria (14.2%) compared to mild malaria (7.9%) and asymptomatic (3.8%). The <italic>MBL2*LYPA</italic> haplotypes confer protection, whereas <italic>MBL2*LXPA</italic> increases the malaria risk. Our findings in Indian populations demonstrate that <italic>MBL2</italic> functional variants are strongly associated with malaria and infection severity.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Infect Immun</journal-id><journal-id journal-id-type="iso-abbrev">Infect. Immun</journal-id><journal-id journal-id-type="hwp">iai</journal-id><journal-id journal-id-type="pmc">iai</journal-id><journal-id journal-id-type="publisher-id">IAI</journal-id><journal-title-group><journal-title>Infection and Immunity</journal-title></journal-title-group><issn pub-type="ppub">0019-9567</issn><issn pub-type="epub">1098-5522</issn><publisher><publisher-name>American Society for Microbiology</publisher-name><publisher-loc>1752 N St., N.W., Washington, DC</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">24126531</article-id><article-id pub-id-type="pmc">3911836</article-id><article-id pub-id-type="publisher-id">01041-13</article-id><article-id pub-id-type="doi">10.1128/IAI.01041-13</article-id><article-categories><subj-group subj-group-type="heading"><subject>Host Response and Inflammation</subject></subj-group></article-categories><title-group><article-title><italic>MBL2</italic> Variations and Malaria Susceptibility in Indian Populations</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Jha</surname><given-names>Aditya Nath</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Sundaravadivel</surname><given-names>Pandarisamy</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Singh</surname><given-names>Vipin Kumar</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Pati</surname><given-names>Sudhanshu S.</given-names></name><xref ref-type="aff" rid="aff2"><sup>b</sup></xref></contrib><contrib contrib-type="author"><name><surname>Patra</surname><given-names>Pradeep K.</given-names></name><xref ref-type="aff" rid="aff3"><sup>c</sup></xref></contrib><contrib contrib-type="author"><name><surname>Kremsner</surname><given-names>Peter G.</given-names></name><xref ref-type="aff" rid="aff4"><sup>d</sup></xref></contrib><contrib contrib-type="author"><name><surname>Velavan</surname><given-names>Thirumalaisamy P.</given-names></name><xref ref-type="aff" rid="aff4"><sup>d</sup></xref></contrib><contrib contrib-type="author"><name><surname>Singh</surname><given-names>Lalji</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref><xref ref-type="aff" rid="aff5"><sup>e</sup></xref><xref ref-type="aff" rid="aff6"><sup>f</sup></xref></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Thangaraj</surname><given-names>Kumarasamy</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><aff id="aff1"><label>a</label>CSIR–Centre for Cellular and Molecular Biology, Hyderabad, India</aff><aff id="aff2"><label>b</label>Ispat General Hospital, Rourkela, Orrisa, India</aff><aff id="aff3"><label>c</label>Pt. Jawaharlal Nehru Memorial Medical College, Raipur, Chhattisgarh, India</aff><aff id="aff4"><label>d</label>Institute of Tropical Medicine, University ofTübingen, Tübingen, Germany</aff><aff id="aff5"><label>e</label>Banaras Hindu University, Varanasi, India</aff><aff id="aff6"><label>f</label>Genome Foundation, Hyderabad, India</aff></contrib-group><contrib-group><contrib contrib-type="editor"><name><surname>Adams</surname><given-names>J. H.</given-names></name><role>Editor</role></contrib></contrib-group><author-notes><corresp id="cor1">Address correspondence to Kumarasamy Thangaraj, <email>thangs@ccmb.res.in</email>.</corresp></author-notes><pub-date pub-type="ppub"><month>1</month><year>2014</year></pub-date><volume>82</volume><issue>1</issue><fpage>52</fpage><lpage>61</lpage><history><date date-type="received"><day>21</day><month>8</month><year>2013</year></date><date date-type="rev-request"><day>24</day><month>9</month><year>2013</year></date><date date-type="accepted"><day>30</day><month>9</month><year>2013</year></date></history><permissions><copyright-statement>Copyright © 2014, American Society for Microbiology. All Rights Reserved.</copyright-statement><copyright-year>2014</copyright-year><copyright-holder>American Society for Microbiology</copyright-holder></permissions><self-uri xlink:title="pdf" xlink:type="simple" xlink:href="zii00114000052.pdf"></self-uri><abstract><p>Human mannose-binding lectin (MBL) encoded by the <italic>MBL2</italic> gene is a pattern recognition protein and has been associated with many infectious diseases, including malaria. We sought to investigate the contribution of functional <italic>MBL2</italic> gene variations to <named-content content-type="genus-species">Plasmodium falciparum</named-content> malaria in well-defined cases and in matched controls. We resequenced the 8.7 kb of the entire <italic>MBL2</italic> gene in 434 individuals clinically classified with malaria from regions of India where malaria is endemic. The study cohort included 176 patients with severe malaria, 101 patients with mild malaria, and 157 ethnically matched asymptomatic individuals. In addition, 830 individuals from 32 socially, linguistically, and geographically diverse endogamous populations of India were investigated for the distribution of functional <italic>MBL2</italic> variants. The <italic>MBL2 −221C</italic> (<italic>X</italic>) allelic variant is associated with increased risk of malaria (mild malaria odds ratio [OR] = 1.9, corrected <italic>P</italic> value [<italic>P</italic><sup>Corr</sup>] = 0.0036; severe malaria OR = 1.6, <italic>P</italic><sup><italic>Corr</italic></sup> = 0.02). The exon1 variants <italic>MBL2*B</italic> (severe malaria OR = 2.1, <italic>P</italic><sup><italic>Corr</italic></sup> = 0.036; mild versus severe malaria OR = 2.5, <italic>P</italic><sup><italic>Corr</italic></sup> = 0.039) and <italic>MBL2*C</italic> (mild versus severe malaria OR = 5.4, <italic>P</italic><sup><italic>Corr</italic></sup> = 0.045) increased the odds of having malaria. The exon1 <italic>MBL2*D/*B/*C</italic> variant increased the risk for severe malaria (OR = 3.4, <italic>P</italic><sup><italic>Corr</italic></sup> = 0.000045). The frequencies of low MBL haplotypes were significantly higher in severe malaria (14.2%) compared to mild malaria (7.9%) and asymptomatic (3.8%). The <italic>MBL2*LYPA</italic> haplotypes confer protection, whereas <italic>MBL2*LXPA</italic> increases the malaria risk. Our findings in Indian populations demonstrate that <italic>MBL2</italic> functional variants are strongly associated with malaria and infection severity.</p></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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