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	<title>Polymorphisms in Turkish population &#187; Department</title>
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		<title>Association between mannose-binding lectin levels and gene polymorphisms in chronic periodontitis and response to treatment.</title>
		<link>http://polymorphisms.info/polymorphisms/chronic-periodontitis/association-between-mannose-binding-lectin-levels-and-gene-polymorphisms-in-chronic-periodontitis-and-response-to-treatment.html</link>
		<comments>http://polymorphisms.info/polymorphisms/chronic-periodontitis/association-between-mannose-binding-lectin-levels-and-gene-polymorphisms-in-chronic-periodontitis-and-response-to-treatment.html#comments</comments>
		<pubDate>Thu, 25 Feb 2010 20:02:02 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Chronic periodontitis]]></category>
		<category><![CDATA[allele]]></category>
		<category><![CDATA[Arch]]></category>
		<category><![CDATA[association]]></category>
		<category><![CDATA[Berdeli]]></category>
		<category><![CDATA[chronic periodontitis ELISA]]></category>
		<category><![CDATA[codon]]></category>
		<category><![CDATA[Dentistry]]></category>
		<category><![CDATA[Department]]></category>
		<category><![CDATA[Distribution]]></category>
		<category><![CDATA[DNA]]></category>
		<category><![CDATA[exon]]></category>
		<category><![CDATA[fragment]]></category>
		<category><![CDATA[Genomic]]></category>
		<category><![CDATA[immunosorbent]]></category>
		<category><![CDATA[Izmir]]></category>
		<category><![CDATA[Köse]]></category>
		<category><![CDATA[method]]></category>
		<category><![CDATA[Nalbantsoy]]></category>
		<category><![CDATA[Oral Biol]]></category>
		<category><![CDATA[outcome]]></category>
		<category><![CDATA[Ozçaka]]></category>
		<category><![CDATA[PCR-RFLP]]></category>
		<category><![CDATA[Periodontology]]></category>
		<category><![CDATA[plasma]]></category>
		<category><![CDATA[polymerase]]></category>
		<category><![CDATA[polymorphism]]></category>
		<category><![CDATA[population]]></category>
		<category><![CDATA[response]]></category>
		<category><![CDATA[therapy]]></category>
		<category><![CDATA[Turkey]]></category>
		<category><![CDATA[University]]></category>

		<guid isPermaLink="false">http://polymorphisms.info/?p=304</guid>
		<description><![CDATA[Arch Oral Biol. 2010 Feb 2.
Ozçaka O, Bıçakcı N, Nalbantsoy A, Köse T, Berdeli A.
Department of Periodontology, School of Dentistry, University of Ege, Izmir, Turkey.

BACKGROUND: The aims of the present study were: (1) to investigate mannose-binding lectin (MBL) gene exon-1 polymorphisms in Turkish subjects with chronic periodontitis (CP), (2) to assess the association between these [...]]]></description>
			<content:encoded><![CDATA[<p>Arch Oral Biol. 2010 Feb 2.</p>
<p>Ozçaka O, Bıçakcı N, Nalbantsoy A, Köse T, Berdeli A.</p>
<p>Department of Periodontology, School of Dentistry, University of Ege, Izmir, Turkey.</p>
<div>
<p>BACKGROUND: The aims of the present study were: (1) to investigate mannose-binding lectin (MBL) gene exon-1 polymorphisms in Turkish subjects with chronic periodontitis (CP), (2) to assess the association between these polymorphisms and plasma MBL levels, (3) to determine the effects of MBL genotypes on the outcomes of non-surgical periodontal therapy. METHODS: A total of 172 subjects were included in the present study. Genomic DNA was obtained from the peripheral blood of 83 CP patients and 89 periodontally healthy subjects. The MBL levels were measured by enzyme-linked immunosorbent assay (ELISA). The MBL gene exon-1 polymorphisms were genotyped by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. RESULTS: Subjects homozygous for the frequent allele A had higher MBL plasma levels compared with rare allele B carriers. This difference in MBL plasma levels was statistically significant both in CP patients and healthy subjects. The distribution of MBL gene codon 54 genotypes and allele frequencies did not differ significantly between study groups. All study subjects were the MBL gene codon 52 and 57 frequent allele A carriers. Codon 54 B allele carriers had similar clinical periodontal parameters compared with AA genotypes after non-surgical periodontal therapy. CONCLUSIONS: The present study failed to find any significant association between the MBL gene codon 54 polymorphisms and severe CP in a Turkish population. MBL gene rare allele carriers had lower MBL plasma levels in both study groups. It seems that MBL gene codon 54 B allele carriage may not influence the outcome of periodontal therapy. Copyright © 2010. Published by Elsevier Ltd.</p>
</div>
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		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Angiotensin-Converting Enzyme Gene Polymorphism in Overweight and Obese Turkish Patients with Insulin Resistance.</title>
		<link>http://polymorphisms.info/polymorphisms/angiotensin-converting-enzyme-gene-polymorphism-in-overweight-and-obese-turkish-patients-with-insulin-resistance.html</link>
		<comments>http://polymorphisms.info/polymorphisms/angiotensin-converting-enzyme-gene-polymorphism-in-overweight-and-obese-turkish-patients-with-insulin-resistance.html#comments</comments>
		<pubDate>Fri, 05 Feb 2010 20:37:16 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[polymorphisms]]></category>
		<category><![CDATA[ACE]]></category>
		<category><![CDATA[amplification]]></category>
		<category><![CDATA[Angiotensin]]></category>
		<category><![CDATA[Bastemir]]></category>
		<category><![CDATA[Biol]]></category>
		<category><![CDATA[Cell]]></category>
		<category><![CDATA[control]]></category>
		<category><![CDATA[Converting]]></category>
		<category><![CDATA[deletion]]></category>
		<category><![CDATA[Denizli]]></category>
		<category><![CDATA[Department]]></category>
		<category><![CDATA[Endocrinology]]></category>
		<category><![CDATA[enzyme]]></category>
		<category><![CDATA[frequency]]></category>
		<category><![CDATA[gene]]></category>
		<category><![CDATA[gene polymorphism]]></category>
		<category><![CDATA[genotype]]></category>
		<category><![CDATA[Guclu]]></category>
		<category><![CDATA[Karasu]]></category>
		<category><![CDATA[Kursunluoglu]]></category>
		<category><![CDATA[Medicine]]></category>
		<category><![CDATA[metabolism]]></category>
		<category><![CDATA[Overweight]]></category>
		<category><![CDATA[Pamukkale]]></category>
		<category><![CDATA[polymerase]]></category>
		<category><![CDATA[polymorphism]]></category>
		<category><![CDATA[population]]></category>
		<category><![CDATA[reaction]]></category>
		<category><![CDATA[resistance]]></category>
		<category><![CDATA[Turgut]]></category>
		<category><![CDATA[University]]></category>

		<guid isPermaLink="false">http://polymorphisms.info/?p=293</guid>
		<description><![CDATA[DNA Cell Biol. 2010 Jan 13.
Akin F, Turgut S, Bastemir M, Turgut G, Kursunluoglu R, Karasu U, Guclu A.
1 Department of Endocrinology and Metabolism, Faculty of Medicine, Pamukkale University , Denizli, Turkey .

The aim of this study was to analyze the distribution of the insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene in obese [...]]]></description>
			<content:encoded><![CDATA[<p>DNA Cell Biol. 2010 Jan 13.</p>
<p>Akin F, Turgut S, Bastemir M, Turgut G, Kursunluoglu R, Karasu U, Guclu A.</p>
<p>1 Department of Endocrinology and Metabolism, Faculty of Medicine, Pamukkale University , Denizli, Turkey .</p>
<div>
<p>The aim of this study was to analyze the distribution of the insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene in obese Turkish patients with insulin resistance (IR). Sixty-two obese Turkish patients with IR were enrolled in this study. One hundred healthy people without IR were recruited as the control group. ACE amplification was performed by polymerase chain reaction. The frequency of the DD genotype was significantly higher in obese patients with IR than in control subjects. Of sixty-two patients, 1 (1.6%) had an II genotype, 22 (35.5%) had an ID genotype, and 39 (62.9%) had a DD genotype. The frequency of the I allele in the patient group was significantly lower than in controls. We found that the frequency of the DD genotype was higher in obese Turkish patients with IR. ACE gene I/D polymorphism may be associated with obesity in the Turkish population.</p>
</div>
]]></content:encoded>
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		</item>
		<item>
		<title>The relationship between paraoxanase gene Leu-Met (55) and Gln-Arg (192) polymorphisms and coronary artery disease.]</title>
		<link>http://polymorphisms.info/paraoxanase-gene/the-relationship-between-paraoxanase-gene-leu-met-55-and-gln-arg-192-polymorphisms-and-coronary-artery-disease.html</link>
		<comments>http://polymorphisms.info/paraoxanase-gene/the-relationship-between-paraoxanase-gene-leu-met-55-and-gln-arg-192-polymorphisms-and-coronary-artery-disease.html#comments</comments>
		<pubDate>Wed, 03 Feb 2010 14:47:57 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Paraoxanase gene]]></category>
		<category><![CDATA[allele frequency]]></category>
		<category><![CDATA[amino acid change]]></category>
		<category><![CDATA[Arch]]></category>
		<category><![CDATA[Berdeli]]></category>
		<category><![CDATA[Biology]]></category>
		<category><![CDATA[control group]]></category>
		<category><![CDATA[control groups]]></category>
		<category><![CDATA[Department]]></category>
		<category><![CDATA[DESIGN]]></category>
		<category><![CDATA[Distribution]]></category>
		<category><![CDATA[enzymes]]></category>
		<category><![CDATA[genet]]></category>
		<category><![CDATA[genotype]]></category>
		<category><![CDATA[Genotypes]]></category>
		<category><![CDATA[Gln]]></category>
		<category><![CDATA[Glu]]></category>
		<category><![CDATA[Medical]]></category>
		<category><![CDATA[polymerase]]></category>
		<category><![CDATA[polymerase chain reaction]]></category>
		<category><![CDATA[polymorphisms]]></category>
		<category><![CDATA[PON]]></category>
		<category><![CDATA[population]]></category>
		<category><![CDATA[protein]]></category>
		<category><![CDATA[restriction]]></category>
		<category><![CDATA[restriction enzymes]]></category>
		<category><![CDATA[risk]]></category>
		<category><![CDATA[risk factor]]></category>
		<category><![CDATA[substitution]]></category>
		<category><![CDATA[susceptibility]]></category>

		<guid isPermaLink="false">http://polymorphisms.info/?p=291</guid>
		<description><![CDATA[Turk Kardiyol Dern Ars. 2009;37(7):473-478.
Taşkıran P, Cam SF, Sekuri C, Tüzün N, Alioğlu E, Altıntaş N, Berdeli A.
Department of Medical Biology and Genetics, Medicine Faculty of Celal Bayar University, Manisa, Turkey.
OBJECTIVES: Paraoxonase (PON1) is a high-density lipoprotein (HDL)-associated esterase that hydrolyses lipoperoxides. PON1 serves as a protective factor against oxidative modification of LDL, suggesting that [...]]]></description>
			<content:encoded><![CDATA[<p>Turk Kardiyol Dern Ars. 2009;37(7):473-478.</p>
<p>Taşkıran P, Cam SF, Sekuri C, Tüzün N, Alioğlu E, Altıntaş N, Berdeli A.</p>
<p>Department of Medical Biology and Genetics, Medicine Faculty of Celal Bayar University, Manisa, Turkey.</p>
<p>OBJECTIVES: Paraoxonase (PON1) is a high-density lipoprotein (HDL)-associated esterase that hydrolyses lipoperoxides. PON1 serves as a protective factor against oxidative modification of LDL, suggesting that it may play an important role in the prevention of atherosclerotic process. Research has focused on two polymorphisms: leucine (L allele) to methionine (M allele) substitution at codon 55, and glutamine (A allele) to arginine (B allele) substitution at codon 192. STUDY DESIGN: We examined amino acid changes at codon 55 and 192 in the PON1 gene by polymerase chain reaction and using restriction enzymes in 120 patients (92 men, 28 women; mean age 48.2+/-4.3 years) with premature coronary artery disease (CAD) and in 102 healthy subjects (80 men, 22 women; mean age 46.8+/-5.2 years) with no history of CAD and a normal electrocardiogram. RESULTS: Distribution of genotypes in the patient and control groups at codon 55 were 6.7% and 4.9% for MM, 46.7% and 29.4% for LM, 46.7% and 65.7% for LL, respectively. The frequency of genotypes at codon 192 were as follows: 4.2% and 2% for RR, 40% and 35.3% for QR, and 55.8% and 62.8% for QQ, respectively. While the frequency of PON1 55M allele was higher in the CAD group (0.3 vs. 0.2), PON1 192R allele frequency did not differ (p&gt;0.05). There was a significant relationship between the PON1 M/L55 polymorphism and CAD (p=0.017), whereas the R/Q192 polymorphism was not associated with CAD (p=0.445). CONCLUSION: These data suggest that the PON1 M/L55 polymorphism shows a significant relationship with CAD and the Q/R192 polymorphism is not a major risk factor causing susceptibility to CAD in our population.</p>
]]></content:encoded>
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		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Common MEFV mutations and polymorphisms in an elderly population: an association with E148Q polymorphism andrheumatoid factor levels.</title>
		<link>http://polymorphisms.info/cancer-kanser/common-mefv-mutations-and-polymorphisms-in-an-elderly-population-an-association-with-e148q-polymorphism-andrheumatoid-factor-levels-2.html</link>
		<comments>http://polymorphisms.info/cancer-kanser/common-mefv-mutations-and-polymorphisms-in-an-elderly-population-an-association-with-e148q-polymorphism-andrheumatoid-factor-levels-2.html#comments</comments>
		<pubDate>Mon, 24 Aug 2009 20:48:04 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Cancer (Kanser)]]></category>
		<category><![CDATA[analyse]]></category>
		<category><![CDATA[association]]></category>
		<category><![CDATA[Beger]]></category>
		<category><![CDATA[Biology]]></category>
		<category><![CDATA[Bolayirli]]></category>
		<category><![CDATA[Center]]></category>
		<category><![CDATA[Clin]]></category>
		<category><![CDATA[Curgunlu]]></category>
		<category><![CDATA[Dasdemir]]></category>
		<category><![CDATA[Department]]></category>
		<category><![CDATA[DNA]]></category>
		<category><![CDATA[Erdincler]]></category>
		<category><![CDATA[Genetics]]></category>
		<category><![CDATA[hsCRP]]></category>
		<category><![CDATA[Karaca]]></category>
		<category><![CDATA[Karaman]]></category>
		<category><![CDATA[Mediterranean]]></category>
		<category><![CDATA[Methods]]></category>
		<category><![CDATA[PCR-RFLP]]></category>
		<category><![CDATA[population]]></category>
		<category><![CDATA[rheumatoid]]></category>
		<category><![CDATA[Rheumatol]]></category>
		<category><![CDATA[Technical]]></category>
		<category><![CDATA[Turanli]]></category>
		<category><![CDATA[Turkey]]></category>
		<category><![CDATA[Yazici]]></category>

		<guid isPermaLink="false">http://polymorphisms.info/?p=252</guid>
		<description><![CDATA[Clin Exp Rheumatol. 2009 Mar-Apr;27(2):340-3. Links

Turanli ET, Beger T, Erdincler D, Curgunlu A, Karaman S, Karaca E, Dasdemir S, Bolayirli M, Yazici H.
Department of Molecular Biology and Genetics, and 2Molecular Biology and Biotechnology Research Center, Istanbul Technical University, Istanbul, Turkey. turanlie@itu.edu.tr
OBJECTIVES: To analyse the most common MEFV (Mediterranean fever gene) mutations and polymorphisms in an [...]]]></description>
			<content:encoded><![CDATA[<p><span title="Clinical and experimental rheumatology.">Clin Exp Rheumatol.</span> 2009 Mar-Apr;27(2):340-3.<span class="linkbar"><script></script> Links</span></p>
<dd class="abstract">
<div class="authors"><!--AuthorList--><strong>Turanli ET</strong>, <strong>Beger T</strong>, <strong>Erdincler D</strong>, <strong>Curgunlu A</strong>, <strong>Karaman S</strong>, <strong>Karaca E</strong>, <strong>Dasdemir S</strong>, <strong>Bolayirli M</strong>, <strong>Yazici H</strong>.</div>
<p class="affiliation">Department of Molecular Biology and Genetics, and 2Molecular Biology and Biotechnology Research Center, Istanbul Technical University, Istanbul, Turkey. turanlie@itu.edu.tr</p>
<p class="abstract">OBJECTIVES: To analyse the most common MEFV (Mediterranean fever gene) mutations and polymorphisms in an elderly population free of chronic inflammatory disease (n=164), and explore possible associations between hsCRP (high sensitive C-reactive protein) and RF (rheumatoid factor) levels with MEFV mutations and polymorphisms. METHODS: An elderly group free of chronic inflammatory disease was chosen among the outpatients of the division of geriatric medicine. Total genomic DNA was isolated from blood, and PCR-RFLP analysis was performed using established protocols. Sera were analyzed for hsCRP and RF levels. RESULTS: The frequencies for 694V (1.8%), 694I (1.8%), 680I (0.6%), 726A (2.1%) and 148Q (5%) alleles were found to be similar to Turkish historic controls, with a carrier frequency of 1/4. Further analyses with rheumatoid factor (RF) levels and mutations revealed a significant association between the presence of the E148Q polymorphism with increased RF levels (&gt;15 mg/dl) (xi2= 7.358, p=0.007, OR=5.41 95% CI 1.41-20.64). CONCLUSIONS: Common MEFV mutations and polymorphisms were similarly represented among the elderly population compared to historic controls. On the other hand, a significant association was found between the presence of E148Q polymorphism and increased RF levels. This suggests that the previously noted increased RF levels in elderly populations may somehow be related to the now described association of RF with MEFV E148Q polymorphism.</p>
</dd>
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		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Association of beta-1 and beta-2 adrenergic receptor gene polymorphisms with myocardial infarction.</title>
		<link>http://polymorphisms.info/gene-polymorphisms/association-of-beta-1-and-beta-2-adrenergic-receptor-gene-polymorphisms-with-myocardial-infarction.html</link>
		<comments>http://polymorphisms.info/gene-polymorphisms/association-of-beta-1-and-beta-2-adrenergic-receptor-gene-polymorphisms-with-myocardial-infarction.html#comments</comments>
		<pubDate>Mon, 24 Aug 2009 20:41:52 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Gene polymorphisms]]></category>
		<category><![CDATA[ADRB]]></category>
		<category><![CDATA[akinyilmaz]]></category>
		<category><![CDATA[Besevler]]></category>
		<category><![CDATA[Biology]]></category>
		<category><![CDATA[Department]]></category>
		<category><![CDATA[Faculty]]></category>
		<category><![CDATA[Gazi]]></category>
		<category><![CDATA[Glu]]></category>
		<category><![CDATA[Gly]]></category>
		<category><![CDATA[haplotype]]></category>
		<category><![CDATA[homozygote]]></category>
		<category><![CDATA[Kaya MG]]></category>
		<category><![CDATA[Medical]]></category>
		<category><![CDATA[Merdanoglu]]></category>
		<category><![CDATA[noncardiovascular]]></category>
		<category><![CDATA[PCR-RFLP]]></category>
		<category><![CDATA[polymorphism]]></category>
		<category><![CDATA[receptor]]></category>
		<category><![CDATA[University]]></category>

		<guid isPermaLink="false">http://polymorphisms.info/?p=246</guid>
		<description><![CDATA[Yilmaz A, Kaya MG, Merdanoglu U, Ergun MA, Cengel A, Menevse S.
Department of Medical Biology and Genetics, Faculty of Medicine, Gazi University, Besevler, Ankara, 06510, Turkey. akinyilmaz@gazi.edu.tr
Both beta(1)- and beta2-adrenergic receptors (beta(1)- and beta(2)-AR) have important roles in heart function mainly in response to catecholamines. Some specific polymorphisms in the beta(1)- and beta(2)-AR genes, named [...]]]></description>
			<content:encoded><![CDATA[<div class="authors"><!--AuthorList--><strong>Yilmaz A</strong>, <strong>Kaya MG</strong>, <strong>Merdanoglu U</strong>, <strong>Ergun MA</strong>, <strong>Cengel A</strong>, <strong>Menevse S</strong>.</div>
<p class="affiliation">Department of Medical Biology and Genetics, Faculty of Medicine, Gazi University, Besevler, Ankara, 06510, Turkey. akinyilmaz@gazi.edu.tr</p>
<p class="abstract">Both beta(1)- and beta2-adrenergic receptors (beta(1)- and beta(2)-AR) have important roles in heart function mainly in response to catecholamines. Some specific polymorphisms in the beta(1)- and beta(2)-AR genes, named ADRB1 and ADRB2, respectively, have been implicated in several cardiovascular and noncardiovascular phenotypes. In this study, we aimed to investigate the possible relationship between Ser49Gly and Arg389Gly polymorphisms of the ADRB1 and Arg16Gly and Gln27Glu polymorphisms of the ADRB2 gene with ST elevation myocardial infarction (MI) in a Turkish population. One hundred patients with ST elevation MI and 100 healthy control subjects were genotyped using the PCR-RFLP method. Although the Arg389 allele of the ADRB1 gene was associated with an elevated risk of MI, the Glu27 allele of the ADRB2 gene was associated with a decreased risk of MI. Carriers of the ADRB1 Arg389 allele (heterozygotes+homozygotes) had an approximately 3.5-fold increased risk for MI than Gly389 homozygotes (OR=3.59, 95% CI=0.96-13.47, P=0.045). For the ADRB2 Gln27Glu polymorphism, subjects having one or two copies of the Glu27 allele showed a decreased risk of MI compared with Gln27 homozygote subjects (OR=0.48, 95% CI=0.24-0.94, P=0.03). Haplotype analysis of these polymorphisms showed no significant differences between groups. These results suggest that the Arg389Gly and Gln27Glu polymorphisms may be associated with an altered risk of MI in this Turkish population.</p>
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		</item>
		<item>
		<title>Association of paraoxonase 55 and 192 gene polymorphisms on serum homocysteine concentrations in preeclampsia.</title>
		<link>http://polymorphisms.info/gene-polymorphisms/paraoxonase-gene-polymorphisms/association-of-paraoxonase-55-and-192-gene-polymorphisms-on-serum-homocysteine-concentrations-in-preeclampsia.html</link>
		<comments>http://polymorphisms.info/gene-polymorphisms/paraoxonase-gene-polymorphisms/association-of-paraoxonase-55-and-192-gene-polymorphisms-on-serum-homocysteine-concentrations-in-preeclampsia.html#comments</comments>
		<pubDate>Sun, 12 Jul 2009 06:17:12 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Paraoxonase]]></category>
		<category><![CDATA[Ankara]]></category>
		<category><![CDATA[Arzu]]></category>
		<category><![CDATA[Baskent]]></category>
		<category><![CDATA[Biochemistry]]></category>
		<category><![CDATA[chromatography]]></category>
		<category><![CDATA[Department]]></category>
		<category><![CDATA[Folia]]></category>
		<category><![CDATA[Gurdol]]></category>
		<category><![CDATA[homocysteine]]></category>
		<category><![CDATA[hyperhomocysteinaemia]]></category>
		<category><![CDATA[influence]]></category>
		<category><![CDATA[Isbilen]]></category>
		<category><![CDATA[Medicine]]></category>
		<category><![CDATA[paraoxonase]]></category>
		<category><![CDATA[PCR]]></category>
		<category><![CDATA[plasma]]></category>
		<category><![CDATA[population]]></category>
		<category><![CDATA[Preeclamptic]]></category>
		<category><![CDATA[RFLP]]></category>
		<category><![CDATA[thiolactonase]]></category>
		<category><![CDATA[Turkey]]></category>
		<category><![CDATA[University]]></category>
		<category><![CDATA[Yilmaz]]></category>

		<guid isPermaLink="false">http://polymorphisms.info/?p=240</guid>
		<description><![CDATA[Folia Biol (Praha). 2009;55(2):35-40
Isbilen E, Yilmaz H, Arzu Ergen H, Unlucerci Y, Isbir T, Gurdol F.
Department of Biochemistry, Faculty of Medicine, Baskent University, Ankara, Turkey.
Paraoxonase 1 (PON1) is thought to influence serum homocysteine concentrations, at least in part, due to its homocysteine thiolactonase activity and to play a role in preeclampsia and atherosclerosis. We investigated [...]]]></description>
			<content:encoded><![CDATA[<p><span title="Folia biologica.">Folia Biol (Praha).</span> 2009;55(2):35-40</p>
<p><strong>Isbilen E</strong>, <strong>Yilmaz H</strong>, <strong>Arzu Ergen H</strong>, <strong>Unlucerci Y</strong>, <strong>Isbir T</strong>, <strong>Gurdol F</strong>.</p>
<p>Department of Biochemistry, Faculty of Medicine, Baskent University, Ankara, Turkey.</p>
<p>Paraoxonase 1 (PON1) is thought to influence serum homocysteine concentrations, at least in part, due to its homocysteine thiolactonase activity and to play a role in preeclampsia and atherosclerosis. We investigated the effects of PON 55 and PON 192 polymorphisms on plasma total homocysteine (tHcy) concentrations in preeclamptic and healthy pregnants among Turkish population (N = 106). PON 55 and 192 genotypes were determined by PCR RFLP techniques. Plasma tHcy concentrations were measured by high-performance liquid chromatography. No differences were observed in the distribution of PON 1 55/192 genotypes and allele frequencies between the preeclamptic and healthy pregnants. tHcy level in the plasma of preeclamptic women was found to be increased in comparison with healthy pregnants (P &lt; 0.01). Preeclamptic women bearing the mutated PON 192 RR and wild-type PON1 55 LL genotypes had higher tHcy levels than those of the healthy pregnants with the corresponding genotypes, supporting the possibility that the hyperhomocysteinaemia seen in preeclamptic women is associated with the PON genotypes. However, no influence of the allelic distribution on plasma tHcy concentrations was detected in either group. Our results suggest that PON1 55 and 192 genotypes might have an important role in developing hyperhomocysteinaemia and may also have a role in the pathogenesis of preeclampsia in a Turkish population.</p>
]]></content:encoded>
			<wfw:commentRss>http://polymorphisms.info/gene-polymorphisms/paraoxonase-gene-polymorphisms/association-of-paraoxonase-55-and-192-gene-polymorphisms-on-serum-homocysteine-concentrations-in-preeclampsia.html/feed</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Novel GDAP1 Mutation in a Turkish Family with CMT2K (CMT2K with Novel GDAP1 Mutation).</title>
		<link>http://polymorphisms.info/cancer-kanser/kategorisiz/novel-gdap1-mutation-in-a-turkish-family-with-cmt2k-cmt2k-with-novel-gdap1-mutation.html</link>
		<comments>http://polymorphisms.info/cancer-kanser/kategorisiz/novel-gdap1-mutation-in-a-turkish-family-with-cmt2k-cmt2k-with-novel-gdap1-mutation.html#comments</comments>
		<pubDate>Wed, 29 Apr 2009 19:42:25 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Kategorilenmemiş]]></category>
		<category><![CDATA[autosomal]]></category>
		<category><![CDATA[axonal]]></category>
		<category><![CDATA[Biology]]></category>
		<category><![CDATA[Calapoglu]]></category>
		<category><![CDATA[chromosome]]></category>
		<category><![CDATA[CMT]]></category>
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		<category><![CDATA[missense]]></category>
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		<category><![CDATA[nilufersahin]]></category>
		<category><![CDATA[novel]]></category>
		<category><![CDATA[Ozcelik]]></category>
		<category><![CDATA[presence]]></category>
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		<guid isPermaLink="false">http://polymorphisms.info/?p=232</guid>
		<description><![CDATA[Neuromolecular Med. 2009 Apr 19.

Sahin-Calapoglu N, Tan M, Soyoz M, Calapoglu M, Ozcelik N.
Department of Medical Biology, Faculty of Medicine, Suleyman Demirel University, 32260 Cunur, Isparta, Turkey, nilufersahin@yahoo.com.
Mutations in the ganglioside-induced differentiation-associated protein 1 gene (GDAP1) cause Charcot-Marie-Tooth type 2 (CMT2), a severe autosomal recessive form of neuropathy associated with axonal phenotypes. It has been [...]]]></description>
			<content:encoded><![CDATA[<p><span title="Neuromolecular medicine."><a href="javascript:AL_get(this, 'jour', 'Neuromolecular Med.');">Neuromolecular Med.</a></span> 2009 Apr 19.</p>
<dd class="abstract">
<div class="authors"><!--AuthorList--><a href="http://polymorphisms.info/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Sahin-Calapoglu%20N%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Sahin-Calapoglu N</strong></a>, <a href="http://polymorphisms.info/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Tan%20M%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Tan M</strong></a>, <a href="http://polymorphisms.info/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Soyoz%20M%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Soyoz M</strong></a>, <a href="http://polymorphisms.info/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Calapoglu%20M%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Calapoglu M</strong></a>, <a href="http://polymorphisms.info/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Ozcelik%20N%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Ozcelik N</strong></a>.</div>
<p class="affiliation">Department of Medical Biology, Faculty of Medicine, Suleyman Demirel University, 32260 Cunur, Isparta, Turkey, nilufersahin@yahoo.com.</p>
<p class="abstract">Mutations in the ganglioside-induced differentiation-associated protein 1 gene (GDAP1) cause Charcot-Marie-Tooth type 2 (CMT2), a severe autosomal recessive form of neuropathy associated with axonal phenotypes. It has been screened in this study for the presence of mutations in the coding region of GDAP1, which maps to chromosome 8q21, in a family with CMT2. To date, 29 mutations in the GDAP1 have been reported in patients of different ethnic origins. Here, we report a novel missense mutation (c.836A&gt;G), and two polymorphisms: a silent variant (c.102G&gt;C), and a 5&#8242;-splice site mutation (IVS5+24C&gt;T) in GDPA1 gene identified in a five generation Turkish family with autosomal recessive CMT2.</p>
</dd>
]]></content:encoded>
			<wfw:commentRss>http://polymorphisms.info/cancer-kanser/kategorisiz/novel-gdap1-mutation-in-a-turkish-family-with-cmt2k-cmt2k-with-novel-gdap1-mutation.html/feed</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Genetic polymorphisms of FSHR, CYP17, CYP1A1, CAPN10, INSR, SERPINE1 genes in adolescent girls with polycystic ovary syndrome.</title>
		<link>http://polymorphisms.info/capn10/genetic-polymorphisms-of-fshr-cyp17-cyp1a1-capn10-insr-serpine1-genes-in-adolescent-girls-with-polycystic-ovary-syndrome.html</link>
		<comments>http://polymorphisms.info/capn10/genetic-polymorphisms-of-fshr-cyp17-cyp1a1-capn10-insr-serpine1-genes-in-adolescent-girls-with-polycystic-ovary-syndrome.html#comments</comments>
		<pubDate>Wed, 29 Apr 2009 19:39:16 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[CAPN10]]></category>
		<category><![CDATA[SERPINE1]]></category>
		<category><![CDATA[adolescence]]></category>
		<category><![CDATA[Ankara]]></category>
		<category><![CDATA[Besevler]]></category>
		<category><![CDATA[Bideci]]></category>
		<category><![CDATA[Biology]]></category>
		<category><![CDATA[CAPN]]></category>
		<category><![CDATA[Cinaz]]></category>
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		<category><![CDATA[Department]]></category>
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		<category><![CDATA[Gazi]]></category>
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		<category><![CDATA[INSR]]></category>
		<category><![CDATA[J Assist]]></category>
		<category><![CDATA[Medical]]></category>
		<category><![CDATA[Menevse]]></category>
		<category><![CDATA[nucleotide]]></category>
		<category><![CDATA[Onen]]></category>
		<category><![CDATA[PCOS]]></category>
		<category><![CDATA[PCR-RFLP]]></category>
		<category><![CDATA[polymorphism]]></category>
		<category><![CDATA[SERPINE]]></category>
		<category><![CDATA[SNPs]]></category>
		<category><![CDATA[study]]></category>
		<category><![CDATA[syndrome]]></category>
		<category><![CDATA[Turkey]]></category>
		<category><![CDATA[University]]></category>
		<category><![CDATA[Unsal]]></category>
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		<guid isPermaLink="false">http://polymorphisms.info/?p=230</guid>
		<description><![CDATA[J Assist Reprod Genet. 2009 Apr 22.

Unsal T, Konac E, Yesilkaya E, Yilmaz A, Bideci A, Ilke Onen H, Cinaz P, Menevse A.
Department of Medical Biology and Genetics, Faculty of Medicine, Gazi University, Besevler, 6500, Ankara, Turkey.
BACKGROUND: Polycystic ovary syndrome (PCOS), whose genetic basis is not completely well understood, is the most common endocrine disorder [...]]]></description>
			<content:encoded><![CDATA[<p><span title="Journal of assisted reproduction and genetics."><a href="javascript:AL_get(this, 'jour', 'J Assist Reprod Genet.');">J Assist Reprod Genet.</a></span> 2009 Apr 22.</p>
<dd class="abstract">
<div class="authors"><!--AuthorList--><a href="http://polymorphisms.info/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Unsal%20T%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Unsal T</strong></a>, <a href="http://polymorphisms.info/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Konac%20E%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Konac E</strong></a>, <a href="http://polymorphisms.info/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Yesilkaya%20E%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Yesilkaya E</strong></a>, <a href="http://polymorphisms.info/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Yilmaz%20A%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Yilmaz A</strong></a>, <a href="http://polymorphisms.info/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Bideci%20A%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Bideci A</strong></a>, <a href="http://polymorphisms.info/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Ilke%20Onen%20H%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Ilke Onen H</strong></a>, <a href="http://polymorphisms.info/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Cinaz%20P%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Cinaz P</strong></a>, <a href="http://polymorphisms.info/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Menevse%20A%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Menevse A</strong></a>.</div>
<p class="affiliation">Department of Medical Biology and Genetics, Faculty of Medicine, Gazi University, Besevler, 6500, Ankara, Turkey.</p>
<p class="abstract">BACKGROUND: Polycystic ovary syndrome (PCOS), whose genetic basis is not completely well understood, is the most common endocrine disorder in women and it typically develops during adolescence. The aim of this study is to investigate the possible association between single nucleotide polymorphisms (SNPs) of FSHR, CYP17, CYP1A1, CAPN10, INSR, SERPINE1 genes and PCOS in adolescent girls. METHODS: DNA samples from forty-four adolescent girls with PCOS and 50 healthy controls were analyzed by PCR-RFLP and direct DNA sequencing to determine the genotypic frequency of 17 different polymorphic loci on the FSHR (A307T, N680S), CYP17 (-34 T/C), CYP1A1 (T6235C), CAPN10 (44, 43, 19, 63), INSR (exon 17 C/T), SERPINE1 (4G/5G) genes. Genotyping of exon 12 (six polymorphisms) and intron 12 (one polymorphism) of INSR gene by direct DNA sequencing was performed for the first time in this study. RESULTS: No significant differences were observed in the genotype and allele distributions of above mentioned polymorphisms between cases and control groups. CONCLUSION: Our data does not support an association between SNPs of FSHR, CYP17, CYP1A1, CAPN10, INSR, SERPINE1 genes and susceptibility to PCOS or related traits in Turkish adolescent girls.</p>
</dd>
]]></content:encoded>
			<wfw:commentRss>http://polymorphisms.info/capn10/genetic-polymorphisms-of-fshr-cyp17-cyp1a1-capn10-insr-serpine1-genes-in-adolescent-girls-with-polycystic-ovary-syndrome.html/feed</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Melanocortin-4 receptor gene polymorphisms in obese patients.</title>
		<link>http://polymorphisms.info/gene-polymorphisms/melanocortin-4-receptor/melanocortin-4-receptor-gene-polymorphisms-in-obese-patients-2.html</link>
		<comments>http://polymorphisms.info/gene-polymorphisms/melanocortin-4-receptor/melanocortin-4-receptor-gene-polymorphisms-in-obese-patients-2.html#comments</comments>
		<pubDate>Wed, 29 Apr 2009 19:35:21 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Melanocortin-4 Receptor]]></category>
		<category><![CDATA[Ankara]]></category>
		<category><![CDATA[Besevler]]></category>
		<category><![CDATA[Biochem]]></category>
		<category><![CDATA[Biology]]></category>
		<category><![CDATA[cause]]></category>
		<category><![CDATA[com]]></category>
		<category><![CDATA[concordance]]></category>
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		<category><![CDATA[genet]]></category>
		<category><![CDATA[Keles]]></category>
		<category><![CDATA[Kolukisa]]></category>
		<category><![CDATA[Medical]]></category>
		<category><![CDATA[Melanocortin]]></category>
		<category><![CDATA[Menevse]]></category>
		<category><![CDATA[mutation]]></category>
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		<category><![CDATA[Ozkurt]]></category>
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		<guid isPermaLink="false">http://polymorphisms.info/?p=228</guid>
		<description><![CDATA[Biochem Genet. 2009 Apr;47(3-4):295-300.

Yurtcu E, Yilmaz A, Ozkurt Z, Kolukisa E, Yilmaz M, Keles H, Ergun MA, Yetkin I, Menevse A.
Department of Medical Biology and Genetics, Gazi University Faculty of Medicine, Besevler, Ankara, Turkey. erkan_yurtcu@yahoo.com
Obesity is a complex disease caused by both genetics and environmental factors. Melanocortin-4 receptor (MC4R) (MIM 155541) gene polymorphisms were reported [...]]]></description>
			<content:encoded><![CDATA[<p><span title="Biochemical genetics."><a href="javascript:AL_get(this, 'jour', 'Biochem Genet.');">Biochem Genet.</a></span> 2009 Apr;47(3-4):295-300.</p>
<dd class="abstract">
<div class="authors"><!--AuthorList--><a href="http://polymorphisms.info/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Yurtcu%20E%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Yurtcu E</strong></a>, <a href="http://polymorphisms.info/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Yilmaz%20A%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Yilmaz A</strong></a>, <a href="http://polymorphisms.info/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Ozkurt%20Z%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Ozkurt Z</strong></a>, <a href="http://polymorphisms.info/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Kolukisa%20E%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Kolukisa E</strong></a>, <a href="http://polymorphisms.info/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Yilmaz%20M%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Yilmaz M</strong></a>, <a href="http://polymorphisms.info/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Keles%20H%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Keles H</strong></a>, <a href="http://polymorphisms.info/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Ergun%20MA%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Ergun MA</strong></a>, <a href="http://polymorphisms.info/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Yetkin%20I%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Yetkin I</strong></a>, <a href="http://polymorphisms.info/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Menevse%20A%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Menevse A</strong></a>.</div>
<p class="affiliation">Department of Medical Biology and Genetics, Gazi University Faculty of Medicine, Besevler, Ankara, Turkey. erkan_yurtcu@yahoo.com</p>
<p class="abstract">Obesity is a complex disease caused by both genetics and environmental factors. Melanocortin-4 receptor (MC4R) (MIM 155541) gene polymorphisms were reported to be the cause of monogenic obesity in humans. We studied three polymorphisms (Val50Met, Val103Ile, and Ser58Cys) and a mutation (Asn274Ser) of the MC4R gene in 203 obese patients and in 110 healthy subjects in the Turkish population. A high incidence of Val103Ile and Val50Met polymorphisms as well as the Asn274Ser mutation was found in the obese patients, whereas no significant correlation was found regarding the Ser58Cys polymorphism. We conclude that there is a concordance between the polymorphisms (Val103Ile, Val50Met, Ser58Cys) that were first studied in the Turkish population with obesity.</p>
</dd>
]]></content:encoded>
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		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>FcγRIIIa-V/F 158 polymorphism in Turkish children with asthma bronchiale and allergic rhinitis</title>
		<link>http://polymorphisms.info/cancer-kanser/kategorisiz/fc%ce%b3riiia-vf-158-polymorphism-in-turkish-children-with-asthma-bronchiale-and-allergic-rhinitis.html</link>
		<comments>http://polymorphisms.info/cancer-kanser/kategorisiz/fc%ce%b3riiia-vf-158-polymorphism-in-turkish-children-with-asthma-bronchiale-and-allergic-rhinitis.html#comments</comments>
		<pubDate>Wed, 22 Apr 2009 10:28:13 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Kategorilenmemiş]]></category>
		<category><![CDATA[aegean university]]></category>
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		<category><![CDATA[asthma bronchiale]]></category>
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		<category><![CDATA[fc receptors]]></category>
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		<category><![CDATA[immune regulation]]></category>
		<category><![CDATA[izmir bornova]]></category>
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		<category><![CDATA[Molecular]]></category>
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		<category><![CDATA[pediatric allergy]]></category>
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		<category><![CDATA[Zeyrek]]></category>

		<guid isPermaLink="false">http://polymorphisms.info/?p=220</guid>
		<description><![CDATA[
Dost Zeyrek 1 , Remziye Tanac 1 , Serdar Altinoz 1 , Afig Berdeli 2 , Figen Gulen 1 , Huseyin Koksoy 1 and Esen Demir 1 
  1 Department of Pediatric Allergy and Pulmonology, Aegean University ,   2 Molecular Research Laboratory, Aegean University, Izmir, Turkey 
Correspondence to Dost Zeyrek, Department of Pediatric Allergy [...]]]></description>
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<div class="author-info"><span class="name"><span class="forenames">Dost</span> <span class="surname">Zeyrek</span> <sup>1</sup> </span>, <span class="name"><span class="forenames">Remziye</span> <span class="surname">Tanac</span> <sup>1</sup> </span>, <span class="name"><span class="forenames">Serdar</span> <span class="surname">Altinoz</span> <sup>1</sup> </span>, <span class="name"><span class="forenames">Afig</span> <span class="surname">Berdeli</span> <sup>2</sup> </span>, <span class="name"><span class="forenames">Figen</span> <span class="surname">Gulen</span> <sup>1</sup> </span>, <span class="name"><span class="forenames">Huseyin</span> <span class="surname">Koksoy</span> <sup>1</sup> </span>and <span class="name"><span class="forenames">Esen</span> <span class="surname">Demir</span> <sup>1</sup> </span></p>
<div class="addresses"><span class="address"><a class="invisible-anchor" name="a1"><span style="color: #336699;"> </span></a><span id="a1"> <span class="number"><sup>1</sup> </span>Department of Pediatric Allergy and Pulmonology, Aegean University</span> , <a class="invisible-anchor" name="a2"><span style="color: #336699;"> </span></a><span id="a2"> <span class="number"><sup>2</sup> </span>Molecular Research Laboratory, Aegean University, Izmir, Turkey</span> </span></div>
<div class="correspondence-address"><span class="correspondence-label">Correspondence to </span>Dost Zeyrek, Department of Pediatric Allergy and Pulmonology, Aegean University, Cocuk Klinigi Izmir, Bornova 35100, Izmir, Turkey<br />
Tel.: +903903500<br />
E-mail: <a class="externallink" href="mailto:dost.zeyrek@ege.edu.tr"><span style="color: #336699;">dost.zeyrek@ege.edu.tr</span></a></div>
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<div class="bpg40copyright">Copyright 2008 The Authors Journal compilation 2008 Blackwell Munksgaard</div>
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<div class="keyword-title">KEYWORDS</div>
<div class="keywords">FcRγIIIa gene polymorphism • bronchial asthma • allergic rhinitis • children</div>
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<div id="abstract" class="abstract-content">
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<div class="bp_abstractinfo">Zeyrek D, Tanac R, Altinoz S, Berdeli A, Gulen F, Koksoy H, Demir E. FcγRIIIa-V/F 158 polymorphism in Turkish children with asthma bronchiale and allergic rhinitis.<br />
Pediatr Allergy Immunol 2008: 19: 20–24.<br />
© 2008 The Authors<br />
Journal compilation © 2008 Blackwell Munksgaard</div>
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<h1 id="Abstract" class="abstract-title">ABSTRACT</h1>
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<p class="para">Fc receptors (FcR) play an important role in immune regulation. This might be linked to the variability in immune response, therefore relating to the pathogenesis of atopic diseases. The aim of the present study was to evaluate the Fc<span class="i"><em>γ</em></span>RIIIa gene polymorphism in Turkish children with asthma and allergic rhinitis. The study included 364 atopic children (184 bronchial asthma, 180 allergic rhinitis) and 234 healthy subjects as the control group, aged between 5 to 16 years. Patients were recruited from outpatient clinics of allergy and general pediatric care. Plasma IgE concentrations were measured by immunoassays and skin prick test was done in children with atopic diseases. The Fc<span class="i"><em>γ</em></span>RIIIa gene polymorphism was determined using the polymerase chain reaction method. Distribution of V158V genotype was significantly different among patient groups compared to controls (for asthmatic children OR: 5.33, 95% CI: 2.80–10.23, p &lt; 0.001; for allergic rhinitis OR: 3.25, 95% CI: 1.75–6.07, p = 0.001). Distribution of 158 V allele was significantly different among asthmatic children (OR: 2.20, 95% CI: 1.65–2.92, p &lt; 0.001) and allergic rhinitis patients (OR: 1.77, 95% CI: 1.32–2.35, p &lt; 0.001) compared to healthy controls. Our study shows that the V158V genotype in Fc<span class="i"><em>γ</em></span>RIIIa gene polymorphism may be a genetic risk factor for the development of atopic diseases.</p>
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<div class="dates"><span class="history"></p>
<p class="para">Accepted 13 January 2007</p>
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<div class="doi-title">DIGITAL OBJECT IDENTIFIER (DOI)</div>
<p><span class="doi">10.1111/j.1399-3038.2007.00553.x</span> <a href="http://www3.interscience.wiley.com/doiinfo.html" target="_new"><span style="color: #336699;">About DOI</span></a></div>
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