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Study of Cysteine-Rich Protein 61 Genetic Polymorphism in Predisposition to Fracture Nonunion: A Case Control
Background. Many factors are responsible for this impaired healing, especially in long bones, but a possible genetic predisposition for the development of this complication remains unknown till now. In the present study, we aim to examine the CYR61 gene polymorphism in fracture nonunion patients and...
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Published in: | Genetics Research International 2015-01, Vol.2015, p.68-72 |
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description | Background. Many factors are responsible for this impaired healing, especially in long bones, but a possible genetic predisposition for the development of this complication remains unknown till now. In the present study, we aim to examine the CYR61 gene polymorphism in fracture nonunion patients and the correlation with clinical findings. Materials and Methods. We performed SNP analysis of the CYR61 gene in 250 fracture nonunion patients and 250 healthy subjects were genotyped in this hospital-based case control study, and 56 cases were further evaluated for mRNA expression of CYR61 by real-time quantitative reverse-transcription PCR. Results. CYR61 gene TT, TG, and GG genotype frequencies of total fracture nonunion cases were 41.6%, 49.2%, and 9.20% and 54.4%, 39.2%, and 6.40% in healthy controls. Heterozygous TG genotype was found statistically significant in fracture nonunion cases compared with that in controls, whereas homozygous mutant GG genotype was not found significant. Moreover, we found that TG + GG genotypes were significantly different in serum expression of CYR61 mRNA when compared with cases (TT genotypes). Conclusions. Our result signifies that genotype of CYR61 affects the mRNA expression and acts as a risk factor that could synergistically increase the susceptibility of a patient to develop fracture nonunion. |
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Many factors are responsible for this impaired healing, especially in long bones, but a possible genetic predisposition for the development of this complication remains unknown till now. In the present study, we aim to examine the CYR61 gene polymorphism in fracture nonunion patients and the correlation with clinical findings. Materials and Methods. We performed SNP analysis of the CYR61 gene in 250 fracture nonunion patients and 250 healthy subjects were genotyped in this hospital-based case control study, and 56 cases were further evaluated for mRNA expression of CYR61 by real-time quantitative reverse-transcription PCR. Results. CYR61 gene TT, TG, and GG genotype frequencies of total fracture nonunion cases were 41.6%, 49.2%, and 9.20% and 54.4%, 39.2%, and 6.40% in healthy controls. Heterozygous TG genotype was found statistically significant in fracture nonunion cases compared with that in controls, whereas homozygous mutant GG genotype was not found significant. Moreover, we found that TG + GG genotypes were significantly different in serum expression of CYR61 mRNA when compared with cases (TT genotypes). Conclusions. Our result signifies that genotype of CYR61 affects the mRNA expression and acts as a risk factor that could synergistically increase the susceptibility of a patient to develop fracture nonunion.</description><identifier>ISSN: 2090-3154</identifier><identifier>ISSN: 2090-3162</identifier><identifier>EISSN: 2090-3162</identifier><identifier>DOI: 10.1155/2015/754872</identifier><identifier>PMID: 26783467</identifier><language>eng</language><publisher>Egypt: Hindawi Limiteds</publisher><subject>Angiogenesis ; Automation ; Bones ; Care and treatment ; CYR61 gene ; CYR61 protein ; Deoxyribonucleic acid ; DNA ; Enzymes ; Fractures ; Gene polymorphism ; Genetic aspects ; Genetic polymorphisms ; Genotype & phenotype ; Nonunion ; Patient outcomes ; Patients ; Physiological aspects ; Polymorphism ; Risk factors ; Single-nucleotide polymorphism ; Statistical analysis</subject><ispartof>Genetics Research International, 2015-01, Vol.2015, p.68-72</ispartof><rights>Copyright © 2015 Sabir Ali et al.</rights><rights>COPYRIGHT 2015 John Wiley & Sons, Inc.</rights><rights>Copyright © 2015 Sabir Ali et al. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Copyright © 2015 Sabir Ali et al. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-a508t-67d394de9f493f8d0ccf5776150b9d4737e3061d1e1b34abf9f87a119d02fa473</citedby><cites>FETCH-LOGICAL-a508t-67d394de9f493f8d0ccf5776150b9d4737e3061d1e1b34abf9f87a119d02fa473</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2407664528/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2407664528?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,25731,27901,27902,36989,36990,44566,53766,53768,74869</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26783467$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Durocher, Francine</contributor><creatorcontrib>Ali, Sabir</creatorcontrib><creatorcontrib>Hussain, Syed Rizwan</creatorcontrib><creatorcontrib>Singh, Ajai</creatorcontrib><creatorcontrib>Kumar, Vineet</creatorcontrib><creatorcontrib>Walliullah, Shah</creatorcontrib><creatorcontrib>Rizvi, Nazia</creatorcontrib><creatorcontrib>Yadav, Manish</creatorcontrib><creatorcontrib>Ahmad, Mohammad Kaleem</creatorcontrib><creatorcontrib>Mahdi, Abbas Ali</creatorcontrib><title>Study of Cysteine-Rich Protein 61 Genetic Polymorphism in Predisposition to Fracture Nonunion: A Case Control</title><title>Genetics Research International</title><addtitle>Genet Res Int</addtitle><description>Background. Many factors are responsible for this impaired healing, especially in long bones, but a possible genetic predisposition for the development of this complication remains unknown till now. In the present study, we aim to examine the CYR61 gene polymorphism in fracture nonunion patients and the correlation with clinical findings. Materials and Methods. We performed SNP analysis of the CYR61 gene in 250 fracture nonunion patients and 250 healthy subjects were genotyped in this hospital-based case control study, and 56 cases were further evaluated for mRNA expression of CYR61 by real-time quantitative reverse-transcription PCR. Results. CYR61 gene TT, TG, and GG genotype frequencies of total fracture nonunion cases were 41.6%, 49.2%, and 9.20% and 54.4%, 39.2%, and 6.40% in healthy controls. Heterozygous TG genotype was found statistically significant in fracture nonunion cases compared with that in controls, whereas homozygous mutant GG genotype was not found significant. Moreover, we found that TG + GG genotypes were significantly different in serum expression of CYR61 mRNA when compared with cases (TT genotypes). Conclusions. Our result signifies that genotype of CYR61 affects the mRNA expression and acts as a risk factor that could synergistically increase the susceptibility of a patient to develop fracture nonunion.</description><subject>Angiogenesis</subject><subject>Automation</subject><subject>Bones</subject><subject>Care and treatment</subject><subject>CYR61 gene</subject><subject>CYR61 protein</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Enzymes</subject><subject>Fractures</subject><subject>Gene polymorphism</subject><subject>Genetic aspects</subject><subject>Genetic polymorphisms</subject><subject>Genotype & phenotype</subject><subject>Nonunion</subject><subject>Patient outcomes</subject><subject>Patients</subject><subject>Physiological aspects</subject><subject>Polymorphism</subject><subject>Risk factors</subject><subject>Single-nucleotide polymorphism</subject><subject>Statistical analysis</subject><issn>2090-3154</issn><issn>2090-3162</issn><issn>2090-3162</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNqFkttrFDEUxgdRbKl98l0CvogybZLJZeKDsAy2KkUXL88hm0s3ZSZZkxll_3uznbp2RTDnIck5v_OFE76qeorgGUKUnmOI6DmnpOX4QXWMoYB1gxh-uD9TclSd5nwDy2KQMioeV0eY8bYhjB9Xw5dxMlsQHei2ebQ-2Pqz12uwTHF3AwyBSxvs6DVYxn47xLRZ-zyAUloma3zexOxHHwMYI7hISo9TsuBjDFMoyddgATqVLehiGFPsn1SPnOqzPb3bT6pvF2-_du_qq0-X77vFVa0obMeacdMIYqxwRDSuNVBrRzlniMKVMIQ33DaQIYMsWjVErZxwLVcICQOxU6V-Ur2ZdTfTarBG2_K66uUm-UGlrYzKy8NK8Gt5HX9IwlohoCgCL-4EUvw-2TzKwWdt-14FG6csEWewFQyKtqDP_0Jv4pRCGU9iAjljhOJ71LXqrfTBxfKu3onKBWEY8xKoUGf_oEoYO3gdg3W-5A8aXs0NOsWck3X7GRGUO4PInUHkbJBCP7v_LXv2tx0K8HIG1j4Y9dP_R-3DDCufigX-jL3cUQihBkJ824FuNw4FwiXFDi-slUXsF9u_1Ig</recordid><startdate>20150101</startdate><enddate>20150101</enddate><creator>Ali, Sabir</creator><creator>Hussain, Syed Rizwan</creator><creator>Singh, Ajai</creator><creator>Kumar, Vineet</creator><creator>Walliullah, Shah</creator><creator>Rizvi, Nazia</creator><creator>Yadav, Manish</creator><creator>Ahmad, Mohammad Kaleem</creator><creator>Mahdi, Abbas Ali</creator><general>Hindawi Limiteds</general><general>Hindawi Publishing Corporation</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>188</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20150101</creationdate><title>Study of Cysteine-Rich Protein 61 Genetic Polymorphism in Predisposition to Fracture Nonunion: A Case Control</title><author>Ali, Sabir ; Hussain, Syed Rizwan ; Singh, Ajai ; Kumar, Vineet ; Walliullah, Shah ; Rizvi, Nazia ; Yadav, Manish ; Ahmad, Mohammad Kaleem ; Mahdi, Abbas Ali</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-a508t-67d394de9f493f8d0ccf5776150b9d4737e3061d1e1b34abf9f87a119d02fa473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Angiogenesis</topic><topic>Automation</topic><topic>Bones</topic><topic>Care and treatment</topic><topic>CYR61 gene</topic><topic>CYR61 protein</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Enzymes</topic><topic>Fractures</topic><topic>Gene polymorphism</topic><topic>Genetic aspects</topic><topic>Genetic polymorphisms</topic><topic>Genotype & phenotype</topic><topic>Nonunion</topic><topic>Patient outcomes</topic><topic>Patients</topic><topic>Physiological aspects</topic><topic>Polymorphism</topic><topic>Risk factors</topic><topic>Single-nucleotide polymorphism</topic><topic>Statistical analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ali, Sabir</creatorcontrib><creatorcontrib>Hussain, Syed Rizwan</creatorcontrib><creatorcontrib>Singh, Ajai</creatorcontrib><creatorcontrib>Kumar, Vineet</creatorcontrib><creatorcontrib>Walliullah, Shah</creatorcontrib><creatorcontrib>Rizvi, Nazia</creatorcontrib><creatorcontrib>Yadav, Manish</creatorcontrib><creatorcontrib>Ahmad, Mohammad Kaleem</creatorcontrib><creatorcontrib>Mahdi, Abbas Ali</creatorcontrib><collection>Airiti Library</collection><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access Journals</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Biological Science Database</collection><collection>ProQuest - Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Genetics Research International</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ali, Sabir</au><au>Hussain, Syed Rizwan</au><au>Singh, Ajai</au><au>Kumar, Vineet</au><au>Walliullah, Shah</au><au>Rizvi, Nazia</au><au>Yadav, Manish</au><au>Ahmad, Mohammad Kaleem</au><au>Mahdi, Abbas Ali</au><au>Durocher, Francine</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Study of Cysteine-Rich Protein 61 Genetic Polymorphism in Predisposition to Fracture Nonunion: A Case Control</atitle><jtitle>Genetics Research International</jtitle><addtitle>Genet Res Int</addtitle><date>2015-01-01</date><risdate>2015</risdate><volume>2015</volume><spage>68</spage><epage>72</epage><pages>68-72</pages><issn>2090-3154</issn><issn>2090-3162</issn><eissn>2090-3162</eissn><abstract>Background. Many factors are responsible for this impaired healing, especially in long bones, but a possible genetic predisposition for the development of this complication remains unknown till now. In the present study, we aim to examine the CYR61 gene polymorphism in fracture nonunion patients and the correlation with clinical findings. Materials and Methods. We performed SNP analysis of the CYR61 gene in 250 fracture nonunion patients and 250 healthy subjects were genotyped in this hospital-based case control study, and 56 cases were further evaluated for mRNA expression of CYR61 by real-time quantitative reverse-transcription PCR. Results. CYR61 gene TT, TG, and GG genotype frequencies of total fracture nonunion cases were 41.6%, 49.2%, and 9.20% and 54.4%, 39.2%, and 6.40% in healthy controls. Heterozygous TG genotype was found statistically significant in fracture nonunion cases compared with that in controls, whereas homozygous mutant GG genotype was not found significant. Moreover, we found that TG + GG genotypes were significantly different in serum expression of CYR61 mRNA when compared with cases (TT genotypes). Conclusions. Our result signifies that genotype of CYR61 affects the mRNA expression and acts as a risk factor that could synergistically increase the susceptibility of a patient to develop fracture nonunion.</abstract><cop>Egypt</cop><pub>Hindawi Limiteds</pub><pmid>26783467</pmid><doi>10.1155/2015/754872</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Angiogenesis Automation Bones Care and treatment CYR61 gene CYR61 protein Deoxyribonucleic acid DNA Enzymes Fractures Gene polymorphism Genetic aspects Genetic polymorphisms Genotype & phenotype Nonunion Patient outcomes Patients Physiological aspects Polymorphism Risk factors Single-nucleotide polymorphism Statistical analysis |
title | Study of Cysteine-Rich Protein 61 Genetic Polymorphism in Predisposition to Fracture Nonunion: A Case Control |
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