Coronary artery disease (CAD) and its complications are the major causes of death in the world. Although statins have been used to lower lipid levels in CAD patients, this goal can not be attained in 1/3 of the patients. The objective of this study was to investigate whether common variations in HMG-CoA Reductase(HMGCR) and Apolipoprotein E (ApoE) genes involved in lipid and statin metabolism modify the effect of statins on serum lipid and lipoprotein concentrations in CAD patients.A hundred  CAD patients were enrolled into the study. At the beginning of the study biochemical measurements were performed to determine the baseline levels performed. Patients were treated with 40 mg atorvastatin for 2 months and biochemical measurements were repeated. According to the post-treatment, LDL-c levels,  patients were divided into 2 groups as non-responders and responders, respectively. The information regarding the risk factors such as smoking, alcohol consumption etc. were also obtained. DNA was isolated from peripheral blood. The presence of rs17244841 ve rs17238540 mutations in HMGCR and ε2, ε3 and ε4 variants of ApoE were determined by using RT-PCR. Results were evaluated statistically. HMGCR mutatations were mostly found in responders and ε4 variant of ApoE was mostly found in non-responders. It was also found that presence of HMGCR mutations causes a significant reduction in total cholesterol and LDL-c levels. Also presence of ε2 variant of ApoE causes a statistically significant increase in trigliseride levels. Our findings should be investigated with other researchers to clarify the mechanism.

Obstructive sleep apnea syndrome (OSAS) is a highly prevalent disorder which results in markedly reduced (hypopnea) or absent (apnea) airflow at the nose/mouth. Since vitamin D deficiency has found in an association with some disorders it is thought to be related with OSAS progression. The aim of this study is to investigate the association between VDR, VDBP mutations, vitamin D level and some environmental risk factors with OSAS. Fifty individuals who were diagnosed as OSAS were selected as patients, 50 healthy volunteers without any disease were selected as controls. FokI (rs2228570) and BsmI (rs1544410) mutations in VDR; rs4588 and rs7041 mutations in VDBP were investigated with quantitative real-time polymerase chain reaction (qPCR). Other risk factors were also investigated. Results were evaluated statistically. Statistically significant differences were observed according to the baseline characteristics between the groups, When groups were compared with each other, CA genotype in rs4588, CC genotype in rs2228570 and AA genotype in rs1544410 mutations were found statistically significant in patients whereas TC genotype in rs2228570 and GA genotype in rs1544410 mutations were found statistically significant in controls. When the relation between risk factors and genotypes were investigated, statistically significant associations were detected for body mass index (BMI), waist circumference, Apnea-Hypopnea Index (AHI), excessive daytime sleepiness (EDS), vitamin D and triglyceride levels. VDR and VDBP mutations were found highly related with OSAS. Possible tracking of these mutations and risk factors may help to understand the metabolism as well as the progression of the disease.

Aim of the Study: Interferon-beta (IFNβ), multiple sclerosis (MS) drug for years, does not have therapeutic effects on each patient. Yet, a considerable portion has experienced no therapeutic response to IFNβ. Therefore, it is necessary to determine disease-specific biomarkers that affect drug response. Here, we aimed to determine the effects of interleukin 10 (IL10) and 23 (IL23A), as well as forkhead box P3 (FOXP3) genes on MS after IFNβ therapy.Materials and Methods: Peripheral blood mononuclear cells (PBMCs) of 42 MS patients were isolated to obtain CD4+ and CD25+ T cells. Both cell types were characterised by flow cytometry. To determine optimum drug concentration of IFNβ, cytotoxicity assays were assessed on each cell type for 4, 16, 24 and 48 hours respectively. Then, cells were cultured in the presence of 500 IU/mL of IFNβ. cDNA synthesis was performed after mRNA extraction. RT-PCR was performed to measure gene expressions of IL10, IL23A and FOXP3. Results were evaluated statistically.Results: It was found that the cytotoxic effect of IFNβ was more efficient as the exposure time was expanded regardless of drug concentration. Moreover, CD25+ T lymphocytes were more resistant to IFNβ. IL23A was down-regulated, whereas FOXP3 was up-regulated at 48 hours in CD4+ T cells. For CD25+ T cells, the graded increase in FOXP3 was obtained while IL10 expression was gradually decreased throughout the drug intake. Conclusion:Although a considerable change in expression was obtained, the longterm IFNβ effect on both genes and cells should be determined by follow-up at least a year. What's knownIFNβ reduces the number of episodes and slows down the progression of disability in MS patients. However, the expected therapeutic response has not been experienced in the majority How to cite this article:

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Koroner arter hastalığı (KAH), koroner arterlerdeki yapısal ve fonksiyonel değişikler sonucu iskemi veya plak rüptürü görülebilen ve endotelyal fonksiyon bozukluğuyla yakından ilişkili olduğu bilinen oldukça yaygın bir hastalıktır (1). Dünya Sağlık Örgütü, 2004 yılında kardiyovasküler hastalıklar sonucu 17,1 milyon olan ölüm oranının, 2030 yılında 23,4 milyon olacağını öngörmektedir (2). Hastalığın tedavisinde 90'lardan bu yana kullanılan en yaygın tedavi yöntemi ise hastalara stent takılmasıdır. Perkütan koroner girişim (PKG) sırasında stentlerin kullanımın yaygınlaşması, temeli gecikmiş endotel oluşumuna dayanan stent restenozunu ve stent trombozunu önlemeye yö