Diabetes Mellitus is characterized by chronic hyperglycemia and associated with an increased production of reactive oxygen species (ROS). Oxidative stress is the result of accumulation of free radicals in tissues which specially affects beta cells in pancreas. Glutathione S-transferases (GSTs) are a family of antioxidant enzymes that include several classes of GSTs. These enzymes have important roles in decreasing of ROS species and act as a kind of antioxidant defense. To investigate the association between GSTs polymorphism with type 2 diabetes mellitus (T2DM), we investigated the frequency of GSTM1, T1 and P1 genotypes in patients with T2DM and controls. The genotypes of GSTT1, M1 and P1 were determined in 171 clinically documented T2DM patients and 169 normal cases (as controls) by multiplex polymerase chain reaction and PCR-RFLP. In diabetic patients, the frequency of GSTM1-null genotype was significantly (OR = 1.74; 95 % CI = 1.13-2.69, P = 0.016) higher than that in control. However, the frequency of GSTT1 (OR = 1.29; 95 % CI = 0.07-2.14, P = 0.367) and GSTP1 (OR = 0.83; 95 % CI = 0.53-1.30, P = 0.389) genotypes were not significantly different comparing both groups. Also, the frequency of both GSTT1-null and GSTM1-null genotypes in patients (19.88 %) was significantly higher compared to controls with the same genotypes (11.83 %, P = 0.022). Our results indicated that GSTM1 and GSTT1 genotypes might be involved in the pathogenesis of T2DM in south Iranian population.

BACKGROUND: Colorectal cancer (CRC), is the third most common cancer type. MicroRNAs and their roles in cancer progression have gained considerable attention in the scientifi c community. miR-485-3p has been identifi ed to be abnormally expressed in different types of cancer, but its expression level, biological function, and underlying pathways are still unclear in CRC. Targeting Protein for Xenopus kinesin-like protein 2 (TPX2) is a nuclear protein which plays vital roles in cancer progression and mitotic spindle assembly. TPX2 is overexpressed in various malignancies and has been predicted as an indirect target of miR-485-3p. This study aims to investigate the miR-485-3p and TPX2 expression level, their potential correlation, and underlying molecules like P53 and P21 in forty-one pairs of colorectal cancer tissues compared to matched non-cancerous ones. MATERIALS AND METHODS: We used forty-one pairs of CRC fresh tissue samples and their adjacent normal ones for RNA extraction. After cDNA synthesis, the expression level of miR-485-3p, TPX2, P53 and P21 were determined by Real-time PCR. RESULTS AND CONCLUSIONS: The results revealed that miR-485-3p was signifi cantly downregulated and TPX2 was highly upregulated in CRC tissues. Moreover, miR-485-3p was negatively correlated with TPX2 expression and positively correlated with P21 expression. We present miR-485-3p as a suppressor for colorectal cancer (Tab. 2, Fig. 8, Ref.

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Background: Single-nucleotide polymorphism (SNP) rs2476601 within protein tyrosine phosphatase non-receptor type 22 gene (PTPN22) has been shown to be a risk factor for different autoimmune diseases. This study explored the association of 1858 C/T SNP with rheumatoid arthritis (RA) and celiac disease (CD) in a region covering southwest of Iran. Methods: Totally, 52 patients with CD, 120 patients with RA, and 120 healthy subjects were selected. The samples were genotyped for the rs2476601 in PTPN22 gene using the tetra-amplification refractory mutation system polymerase chain reaction. Results: The frequency of +1858T risk allele was significantly increased in both RA (P=0.021, OR=2.56, 95%CI=1.19-5.47) and CD (P=0.002, OR=3.87, 95%CI=1.68-8.95) patients, as compared to the control group. However, no association was found between the +1858C/T PTPN22 gene SNP and the anticyclic citrullinated peptide and rheumatoid factor positivity in RA patients. Conclusions: PTPN22 gene could play a crucial role in people's susceptibility to certain autoimmune diseases.

ABSTRACT. Phenylketonuria (PKU) is a heterogeneous and autosomal recessive metabolic disorder that is mainly caused by mutations in the hepatic phenylalanine hydroxylase (PAH) gene. This study was designed to identify PAH mutations within exons 6, 7, and 10-12 in PKU patients from southwest Iran. Forty Iranian patients with clinical and biochemically confirmed PKU were enrolled. The exons were sequenced directly and 13 different mutations were identified including I224T, S231P, R176X, c.592_613del22, R243X, R252W, R261Q, Y356X, V388M, IVS10-11G>A, IVS11+1G>C, IVS11-2A>G, and Q375R, which were associated with 23 genotypes. A novel sequence variant, Q375R (c.1124A>G), was detected in exon 11. In one patient, a typical genotype with more than two mutations (R243X/S231P/ S231P) was found. Seven different polymorphisms and three new variants were also detected in intron regions of PAH. A high mutation spectrum was predicted in the southwestern region of Iran due to its ethnic heterogeneity, especially the Khuzestan Province. The detection PAH mutations in southwest Iran of 13 different mutations, corresponding to a mutation detection rate of 53.75%, confirmed this phenomenon.

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Introduction:Genetic and environmental factors are involved in the incidence of schizophrenia and bipolar disorder. Many reports confirm that several common genes are connected with these two psychotic disorders. Several neurotransmitters may be involved in the molecular mechanisms of schizophrenia and bipolar disorder. We aimed to estimate the role of two talent genes: DAOA in neurotransmission of glutamate and COMT in neurotransmission of dopamine to guide the treatment of schizophrenia and bipolar disorder.Methods:Blood samples (n=100 for schizophrenia, n=100 for bipolar I disorder and n=127 for case control) were collected from individuals unrelated in the southwest of Iran. The SNPs (rs947267 and rs3918342 for DAOA gene/rs165599 and rs4680 for COMT gene) were genotyped using the PCR-RFLP method. Our finding was studied by logistic regression and Mantel-Haenszel Chi-square tests.Results:We observed an association in rs3918342, rs165599 and rs4680 single nucleotide polymorphisms and schizophrenia and bipolar I disorder. In addition, our data demonstrated that the rs947267 was related to bipolar I disorder but there was no association between this SNP and schizophrenia.Conclusion:In conclusion, this result supports the hypothesis that variations in DAOA and COMT genes may play a role in schizophrenia and bipolar disorder.

Background: There is a great deal of interest in using adipose tissue-derived mesenchymal stem cells (AT-MSCs) for clinical applications. However, the important limitations of clinical application of stem cells are the small number of cells and their differentiation into undesirable lineage in vitro. To overcome this problem, various growth factors are studied extensively. Objectives: The current study aimed at using 3 different doses of epidermal growth factor (EGF), glial cell line-derived neurotrophic (GDNF), and leukemia inhibitory factor (LIF) to culture AT-MSCs and evaluating their effects on proliferation, viability, differentiation potential, and maintenance of the stemness state of cells. Methods: The current experimental study was conducted on 8 -10 male NMRI (Naval medical research institute) mice provided from research center and experimental animal house of Jundishapur University of Ahvaz, Iran, from September 2016 to April 2017. AT-MSCs were isolated from mice adipose tissue. The cells were cultured with three different doses of EGF, LIF, and GDNF. The morphology and cell proliferation of the AT-MSCs were studied on the days 5, 7, and 11 by an inverted microscope and MTT assay, respectively. To evaluate the stemness state of the cells, Oct4 expression was measured using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Also, differentiation potential of AT-MSCs toward adipogenic and osteogenic lineages was assessed. All tests were done in triplicate.