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Background and objective: Serotonin plays an important role in the pathophysiology of aggressive behavior. Low serotonin levels and altered functions of serotonin receptors affect suicidal behavior. TPH-1, TPH-2 and SLC6A4 genes have important roles in serotonin production and degradation pathways. In this study, polymorphic variants of the TPH-1, TPH-2 and SLC6A4 genes, rs1800532, rs7305115, rs6355 and rs1386494, were investigated in 100 completed suicides and 100 healthy individuals. Materials and methods: After DNA isolation, a new polymerase chain reaction technology KASP TM (Competitive allele-specific polymerase chain reaction method), was used in the genotyping of the selected gene variants. Results: No statistically significant difference was found for the genotype and individual allele frequencies of the polymorphic variants between suicide and control groups, as well as between men and women in suicide cases. However, we observed non-significant tendencies of increased minor alleles in suicidal men for all TPH SNPs. Conclusions: More molecular genetic research studies are needed to understand the pathophysiology of suicide and to reveal its relationship with gender.

Abstract Introduction Behçet syndrome (BS) is a chronic, multisystemic inflammatory condition with unanswered questions regarding its pathogenesis and rational therapeutics. A microarray‐based comparative transcriptomic analysis was performed to elucidate the molecular mechanisms of BS and identify any potential therapeutic targets. Methods Twenty‐nine BS patients (B) and 15 age and sex‐matched control subjects (C) were recruited. Patients were grouped as mucocutaneous (M), ocular (O), and vascular (V) according to their clinical phenotypes. GeneChip Human Genome U133 Plus 2.0 arrays were used for expression profiling on peripheral blood samples of the patients and the control subjects. Following documentation of the differentially expressed gene (DEG) sets, the data were further evaluated with bioinformatics analysis, visualization, and enrichment tools. Validation of the microarray data was performed using quantitative reverse transcriptase polymerase chain reaction. Results When p ≤ 0.05 and fold change ≥2.0 were chosen, the following numbers of DEGs were obtained; B versus C: 28, M versus C: 20, O versus C: 8, V versus C: 555, M versus O: 6, M versus V: 324, O versus V: 142. Venn diagram analysis indicated only two genes, CLEC12A and IFI27, in the intersection of M versus C ∩ O versus C ∩ V versus C. Another noteworthy gene appeared as CLC in the DEG sets. Cluster analyses successfully clustered distinct clinical phenotypes of BS. While innate immunity‐related processes were enriched in the M group, adaptive immunity‐specific processes were significantly enriched in the O and V groups. Conclusions Distinct clinical phenotypes of BS patients displayed distinct expression profiles. In Turkish BS patients, expression differences regarding the genes CLEC12A, IFI27, and CLC seemed to be operative in the disease pathogenesis. Based on these findings, future research should consider the immunogenetic heterogeneity of BS clinical phenotypes. Two anti‐inflammatory genes, namely CLEC12A and CLC, may be valuable as therapeutic targets and may also help design an experimental model in BS.

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Background: Acute myeloid leukaemia(AML) is a disease of the haematopoietic stem cells. Beta-catenin, a key element of the Wnt signalling, which is particularly active in various cancers. Our aim of this study was to determine beta-catenin gene expression levels in AML patients. Then, it is planned to compare the genes between AML grouped according to beta-catenin gene expression levels by DNA microarray. When the gene group identified in this way is combined with the genes in the control group, the aim is to determine the genes that are associated with beta-catenin in AML. Methods: In this study, beta-catenin gene expression levels were determined in 19 AML patients and 3 controls by qRT-PCR. Transcriptome analysis was performed on AML grouped according to beta-catenin expression levels. Differentially expressed genes(DEGs) were identified and investigated with using DAVID, GO, KEGG and STRING. Results: The transcriptome profiles of our AML samples showed different molecular signature profiles according on their beta-catenin levels(high-low). A total of 20 genes have been identified as hub genes. Among these, TTK, HJURP, KIF14 and BTF3, RPL17, RSL1D1 were found to be associated with poor survival and suggested to be associated with beta-catenin in AML. Furthermore, for the first time in our study, the ELOV6 gene, which is the most highly up-regulated gene in human AML samples, was correlated with a poor prognosis via beta-catenin high levels. Conclusion: It is suggested that the identification of beta-catenin-related gene profiles in AML may help to select new therapeutic targets for the treatment of AML.

Introduction: Pluripotent stem cells have been used by various researchers to differentiate and characterize endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) for the clinical treatment of vascular injuries. Studies continue to differentiate and characterize the cells with higher vascularization potential and low risk of malignant transformation to the recipient. Unlike previous studies, this research aimed to differentiate induced pluripotent stem (iPS) cells into endothelial progenitor cells (EPCs) and VSMCs using a step-wise technique. This was achieved by elucidating the spatio-temporal expressions of the stage-specific genes and proteins during the differentiation process. The presence of highly expressed oncogenes in iPS cells was also investigated during the differentiation period. Methods: Induced PS cells were differentiated into lateral mesoderm cells (Flk1+). The Flk1+ populations were isolated on day 5.5 of the mesodermal differentiation period. Flk1+ cells were further differentiated into EPCs and VSMCs using VEGF165 and platelet-derived growth factor-BB (PDGF-BB), respectively, and then characterized using gene expression levels, immunocytochemistry (ICC), and western blot (WB) methods. During the differentiation steps, the expression levels of the marker genes and proto-oncogenic Myc and Klf4 genes were simultaneously studied. Results: The optimal time for the isolation of Flk1+ cells was on day 5.5. EPCs and VSMCs were differentiated from Flk1+ cells and characterized with EPC-specific markers, including Kdr, Pecam1, CD133, Cdh5, Efnb2, Vcam1; and VSMC-specific markers, including Acta2, Cnn1, Des, and Myh11. Differentiated cells were validated based on their temporal gene expressions, protein synthesis, and localization at certain time points. Significant decreases in Myc and Klf4 gene expression levels were observed during the EPCs and VSMC differentiation period. Conclusion: EPCs and VSMCs were successfully differentiated from iPS cells and characterized by gene expression levels, ICC, and WB. We observed significant decreases in oncogene expression levels in the differentiated EPCs and VSMCs. In terms of safety, the described methodology provided a better safety margin. EPCs and VSMC obtained using this method may be good candidates for transplantation and vascular regeneration.