Yazan: admin Tarih: Åžub 25th, 2010 | Kategori::
Paraoxonase
Turk Kardiyol Dern Ars. 2009 Oct;37(7):473-8.
Taşkiran P, Cam SF, Sekuri C, Tüzün N, Alioğlu E, Altintaş 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 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>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.
Yazan: admin Tarih: Åžub 25th, 2010 | Kategori::
Multiple sclerosis
Akcali A, Pehlivan S, Pehlivan M, Sever T, Akgul P, Neyal M.
Department of Neurology, Gaziantep University School of Medicine, Gaziantep, Turkey.
Summary Dysregulation in the expression of pro- and anti-inflammatory cytokines is one of the milestones in multiple sclerosis (MS) development and progression. Tumour necrosis factor (TNF-alpha), a proinflammatory cytokine is believed to play an important role in MS pathogenesis. The objective of this study is to investigate the association between TNF-alpha promoter region (TNF-alpha-238, -308 and -857) and susceptibility to MS and clinical course of the disease. Eighty-six relapsing remitting MS patients and 150 sex-, age- and ethnic-matched controls were enrolled in the study. Genotyping was performed by PCR-RFLP method. We observed a statistically significant increase in TNF-alpha 857 CC genotype in MS patients than controls (P < 0.001) while TNF-alpha 857 CT genotype showed a significant negative correlation with MS patients (P = 0.033). No differences in the distribution of the TNF-alpha-238 and -308 alleles were observed. None of the three polymorphisms (-238, -308 and -857) did not show relation with disease duration, Expanded Disability Status Scale or age of onset. On the other hand, significant difference of TNF -857 CC genotype was identified with the low disease index (P = 0.025). Although the study group is small, the results indicate that TNF-alpha 857 CC genotype may cause susceptibility to MS in the Turkish population.
Yazan: admin Tarih: Åžub 25th, 2010 | Kategori::
Chronic periodontitis
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 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.
