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<journal>
<language>en</language>
<journal_id_issn>1726-7536</journal_id_issn>
<journal_id_issn_online>1735-8507</journal_id_issn_online>
<journal_id_pii></journal_id_pii>
<journal_id_doi></journal_id_doi>
<journal_id_isnet></journal_id_isnet>
<journal_id_iranmedex>69</journal_id_iranmedex>
<journal_id_magiran>2139</journal_id_magiran>
<journal_id_sid>288</journal_id_sid>
<pubdate PubStatus="epublish">
	<type>gregorian</type>
	<year>2013</year>
	<month>3</month>
	<day>19</day>
</pubdate>
<volume>14</volume>
<number>2</number>
<publish_type>online</publish_type>
<publish_edition>1</publish_edition>
<article_type>fulltext</article_type>
<articleset>

<article>
	<language>en</language>
	<article_id_issn></article_id_issn>
	<article_id_issn_online></article_id_issn_online>
	<article_id_pubmed>23926566</article_id_pubmed>
	<article_id_pii></article_id_pii>
	<article_id_doi></article_id_doi>
	<article_id_iranmedex></article_id_iranmedex>
	<article_id_magiran></article_id_magiran>
	<article_id_sid></article_id_sid>
	<title_fa></title_fa>
	<title>Evaluation of Interleukin-10 (G-1082A) Promoter Polymorphism in Preeclampsia</title>
	<subject_fa></subject_fa>
	<subject></subject>
	<content_type_fa></content_type_fa>
	<content_type></content_type>
	<abstract_fa></abstract_fa>
	<abstract>Background: Preeclampsia is a pregnancy-specific syndrome that may be life-threatening, especially to the fetus. Several causes have been reported that may have a possible role in the development of the disorder. Interleukin-10 affect maternal intravascular inflammation, as well as endothelial dysfunction. The aim of this study was to investigate the association between IL-10 G-1082A polymorphism and pre-eclampsia. 
Methods: A total of eighty-eight pregnant women with preeclampsia and 100 women with normal pregnancy attending the Gynecological unit of Government Maternity Hospital, Petlaburz, Hyderabad, India, were considered for the study. A standard amplification refractory mutation system (ARMS) PCR was carried out for genotyping IL-10 G-1082A promoter polymorphism in all the participants. Genotypic distribution of the control and patient groups were compared with values predicted by Hardy-Weinberg equilibrium using χ2 test. Odd ratios (OR) and their respective 95% confidence intervals were used to measure the strength of association between IL-10 gene polymorphism and preeclampsia.
Results: The frequencies of IL-10 G-1082A genotypes, GG, GA and AA, were 17.8%, 41.09% and 41.09% in women with preeclampsia and 25%, 28% and 47% in the controls respectively. There was no significant difference in the distribution of genotypes and alleles of IL-10 G-1082A between the two groups (Test power=0.66). 
Conclusion: The present study suggests that the IL-10 G-1082A gene promoter polymorphism is not a major genetic regulator in the etiology of preeclampsia.
</abstract>
	<keyword_fa></keyword_fa>
	<keyword>ARMS PCR, Cytokines, Interleukin-10, Polymorphism, Preeclampsia</keyword>
	<start_page>62</start_page>
	<end_page>67</end_page>
	<web_url>https://www.jri.ir/article/525</web_url>
	<pdf_url>https://www.jri.ir/documents/fullpaper/en/525.pdf</pdf_url>
	<author_list><author><first_name>Sowmya</first_name><middle_name></middle_name><last_name>Sabnavis</last_name><suffix></suffix><affiliation>Institute of Genetics and Hospital for Genetic Diseases, Begumpet, Hyderabad, India</affiliation><first_name_fa>Sowmya</first_name_fa><middle_name_fa></middle_name_fa><last_name_fa>Sabnavis</last_name_fa><suffix_fa></suffix_fa><email></email><code>1138</code><coreauthor></coreauthor><affiliation_fa></affiliation_fa></author><author><first_name>Aruna</first_name><middle_name></middle_name><last_name>Ramaiah</last_name><suffix></suffix><affiliation>Government Maternity Hospital, Petlaburz, Hyderabad, India</affiliation><first_name_fa>Aruna</first_name_fa><middle_name_fa></middle_name_fa><last_name_fa>Ramaiah</last_name_fa><suffix_fa></suffix_fa><email></email><code>1139</code><coreauthor></coreauthor><affiliation_fa></affiliation_fa></author><author><first_name>Tella</first_name><middle_name></middle_name><last_name>Sunitha</last_name><suffix></suffix><affiliation>Institute of Genetics and Hospital for Genetic Diseases, Begumpet, Hyderabad, India</affiliation><first_name_fa>تلا</first_name_fa><middle_name_fa></middle_name_fa><last_name_fa>سونيتا</last_name_fa><suffix_fa></suffix_fa><email></email><code>840</code><coreauthor></coreauthor><affiliation_fa></affiliation_fa></author><author><first_name>Pratibha</first_name><middle_name></middle_name><last_name>Nallari</last_name><suffix></suffix><affiliation>Department of Genetics, Osmania University, Hyderabad, India</affiliation><first_name_fa>Pratibha</first_name_fa><middle_name_fa></middle_name_fa><last_name_fa>Nallari</last_name_fa><suffix_fa></suffix_fa><email></email><code>943</code><coreauthor></coreauthor><affiliation_fa></affiliation_fa></author><author><first_name>Akka</first_name><middle_name></middle_name><last_name>Jyothy</last_name><suffix></suffix><affiliation>Institute of Genetics and Hospital for Genetic Diseases, Begumpet, Hyderabad, India</affiliation><first_name_fa></first_name_fa><middle_name_fa></middle_name_fa><last_name_fa></last_name_fa><suffix_fa></suffix_fa><email></email><code>842</code><coreauthor></coreauthor><affiliation_fa></affiliation_fa></author><author><first_name>Ananthapur</first_name><middle_name></middle_name><last_name>Venkateshwari</last_name><suffix></suffix><affiliation>Institute of Genetics and Hospital for Genetic Diseases, Begumpet, Hyderabad, India</affiliation><first_name_fa></first_name_fa><middle_name_fa></middle_name_fa><last_name_fa></last_name_fa><suffix_fa></suffix_fa><email>venkateshwari@yahoo.com</email><code>1140</code><coreauthor></coreauthor><affiliation_fa></affiliation_fa></author></author_list>
</article>

</articleset>
</journal>

