Stem cells for pancreatitis 425 Gastric injury and bacterial overgrowth 433 The effect of visceral fat on SMA configuration 451 Antiplatelet agents in ulcerative colitis 459 Differentiation of BMSCs into intestinal ce 466 GERDOFF ® efficacy in patients with GERD

Background: In-stent-restenosis is a case restricting the benefits of percutaneous-transluminal coronary angioplasty (PTCA). PCSK9 controls LDLR levels, and variations in PCSK9, ApoE and ApoER genes may affect the development of restenosis. The aim of this study was to assess the effects of genetic variants on restenosis risk after PTCA.Methods and Results: The study groups include 109 CAD-patients with restenosis (S-CAD) and 82 CAD-patients without restenosis (open-stent,OS-CAD). SNPs were analyzed by RT- PCR. PCSK9 levels were detected via ELISA method. The distributions of ApoE Epsilon, APOER (rs5174), PCSK9 rs2182833 and rs11206510 polymorphisms were found similar between study groups while the frequency of the PCSK9 E670G G allele in S-CAD group was found significantly higher than OS-CAD patients (p= 0.015). No difference was found between study groups in terms of the serum levels of PCSK9. LDL-C was found lower and HDL-C was found higher in OS-CAD group comparing with S-CAD group (p=0.042, p=0.008, respectively). Frequencies of Type 2 DM and hyperlipidemia were also found higher in S-CAD group than OS-CAD group (p=0.007, p=0.001, respectively) while EF% was found lower in S-CAD group than OS-CAD group (p=0.007).Conclusions: Our findings indicate that although ApoE Epsilon, APOER (rs5174), PCSK9 rs2182833, rs11206510 and E670G polymorphisms has no effect on serum PCSK9 levels, PCSK9-rs505151G-allele and hyperlipidemia may be risk factors in the development of restenosis.

Background/aim: Abnormal immune response occurs in individuals who have alleles associated with innate and adaptive immune mechanisms that predispose to inflammatory bowel disease (IBD). Interleukin-1 receptor-associated kinase 4 (IRAK-4) involved in the pathway produces cytokines that initiate and maintain inflammation through Toll-like receptors and interleukin-1 receptors on the membranes of innate immune cells are stimulated with antigens. It was aimed to investigate whether IRAK-4 rs3794262 and rs4251481 polymorphisms predispose to IBD and the possible effects of these polymorphisms by examining these gene polymorphisms with the clinic and prognostic parameters of IBD. Material and methods: Real-time PCR technique was used to detect IRAK-4 polymorphisms in 107 patients with IBD and 103 healthy controls. Results: As a result of experimental studies, the frequency of occurrence of rs4251481 polymorphism related AG genotype (P = 0.029) and G allele (P = 0.005) was found to increase statistically in patients compared to controls. In the control group, the rs4251481 AA genotype rate of incidence increased compared with the patient group (P = 0.005). Conclusion: Consequently, this is the first study in terms of both polymorphisms on IBD. These results suggest that rs4251481 AG genotype and G allele are associated with increased IBD risk in patients.

Aim: Inflammatory bowel disease has two major types: Crohn's disease and ulcerative colitis that occur in the gastrointestinal tract with unknown etiology. COX-2 has important role on carcinogenesis process including colon cancer supporting the tumor growth. COX-2 was also known due to its ability to change homeostasis on colonic mucosa in inflammatory cells on patients who have inflammatory bowel disease. In this study, we have aimed to find a linkage between inflammatory bowel disease and COX-2 in a Turkish population. Methods:A total of 106 patients,42 with Crohn's disease and 64 with ulcerative colitis and 121 healthy control subjects were included the study. Gene variants of COX-2-765G→C and COX-2-1195A→G were analyzed by polymerase chain reaction and restriction fragment length polymorphism techniques. Results: The results demonstrated that COX-2-1195A→G gene variants AA carriers were statistically found in high level on patients with both ulcerative colitis (p=0.001) and Crohn's disease (p=0.008). In contrast, AG genotype and G carriers were statistically found higher in control group (Crohn's disease, p=0.005 for AG and p= 0.008 for G; ulcerative colitis, p=0.001 for AG and p=0.001 for G). Conclusion: In this research, we have observed important and questionable results between inflammatory bowel disease and COX-2, especially COX-2-1195A→G gene variants AA carriers in a Turkish population. Researches need to focus on their local roles on inflammatory bowel disease pathogenesis with large sample size.

Given the prevalence and annual incidence of cancer, head and neck cancer is affecting more than 600,000 people each year. In this research, it was decided to investigate that which genes are involved and how MPO, NQO1, SOD2 enzyme levels effective to develop of head and neck cancer and for the first time at the tissue level. 35 tumor tissues in all head and neck anatomy and their surrounding tissue (70 in total) were enclosed the research that received surgery. Determination of the apoptosis genes expression levels (Mtch1, Akt1, Caspase3, Caspase9, Bcl2, Mdm2, mTOR) were determined by RT-PCR techniques and the same patients' sample used for ROS associated oxidant-antioxidant system by using MPO, NQO1, SOD2 enzyme levels using ELISA method. According to statistical results, caspase 9 gene was found statistically high expressed in early stage in contrast to late stage (p=0,013). Level of SOD2, NQO1 and MPO was determined and only MPO level was found significantly important on tumor tissues p=0,008).  Specially, our findings for high expression of Cas9 on early stage were thought to be the target for treatment with its well-known initiator role of the apoptosis. Our results suggest that the higher level of MPO in tumor tissues and indicates that it has some role on pathology of head and neck cancers. We believe that, our research will lead the proposal in-vivo studies and will open new areas on therapeutic targets.