shRNA-mediated downregulation of α-N-Acetylgalactosaminidase inhibits migration and invasion of cancer cell lines

Objective(s): Extracellular matrix (ECM) is composed of many kinds of glycoproteins containing glycosaminoglycans (GAGs) moiety. The research was conducted based on the N-Acetylgalactosamine (GalNAc) degradation of ECM components by α-N-acetylgalactosaminidase (Nagalase) which facilitates migration and invasion of cancer cells. This study aims to investigate the effects of Naga-shRNA downregulation on migration and invasion of cancer cell lines. Materials and Methods: In this study, MCF-7 cell line (human mammary carcinoma cell line) and A2780 (human ovarian carcinoma cell line) were used. The level of normalized Naga expression and Nagalase protein were evaluated by quantitative polymerase chain reaction and enzyme-linked immunosorbent assay/western blotting, respectively. Migration and invasion were determined using transwell assays, and statistical analysis was carried out by ANOVA test. Results: Response to transduction by shRNA compared to the control group, migrative and invasive properties of the transfected cells were significantly inhibited. Conclusion: These results indicate that Nagalase may have an important role in migration and invasion of cancer cells and can be considered as a candidate for further studies

Mutations in the coding regions of the hepatocyte nuclear factor 4 alpha in Iranian families with maturity onset diabetes of the young

Hepatocyte nuclear factor 4α (HNF4α) is a nuclear receptor involved in glucose homeostasis and is required for normal β cell function. Mutations in the HNF4α gene are associated with maturity onset diabetes of the young type 1 (MODY1). The aim of the present study was to determine the prevalence and nature of mutations in HNF4α gene in Iranian patients with a clinical diagnosis of MODY and their family members. Twelve families including 30 patients with clinically MODY diagnosis and 21 members of their family were examined using PCR-RFLP method and in case of mutation confirmed by sequencing techniques. Fifty age and sex matched subjects with normal fasting blood sugar (FBS) and Glucose tolerance test (GTT) were constituted the control group and investigated in the similar pattern. Single mutation of V255M in the HNF4α gene was detected. This known mutation was found in 8 of 30 patients and 3 of 21 individuals in relatives. Fifty healthy control subjects did not show any mutation. Here, it is indicated that the prevalence of HNF4α mutation among Iranian patients with clinical MODY is considerable. This mutation was present in 26.6% of our patients, but nothing was found in control group. In the family members, 3 subjects with the age of ≤25 years old carried this mutation. Therefore, holding this mutation in this range of age could be a predisposing factor for developing diabetes in future

The frequency of HBeAg and relation with serum level of aminotransferase in chronic hepatitis B

زمینه و هدف: ویروس هپاتیت B (HBV) شایع ترین علت بیماری کبدی حاد و مزمن در جهان به شمار می رود. در افراد ناقل HBV می بایست وضعیت تکثیر ویروسی با استفاده از مارکرهای مناسب از جمله HbeAg مورد بررسی قرار گیرد تا در صورت مثبت بودن و همچنین بالا بودن آنزیم های کبدی افراد مبتلا به هپاتیت مزمن شناسایی شده و سپس تحت درمان قرار گیرند. لذا این مطالعه با هدف تعیین فراوانی مارکر HBeAg و ارتباط آن با سطح ترانس آمینازهای کبدی در افراد HBsAg مثبت انجام گرفت. روش بررسی: در این مطالعه توصیفی – تحلیلی 144 فرد آلوده به ویروس هپاتیت B در مراجعین به بیمارستان امام رضا(ع) شهر مشهد در سال 1385 انتخاب و سپس در سرم این افراد، HBeAg و آنزیم های کبدی با روش الایزا و تست های بیوشیمیایی اندازه گیری شدند. داده ها با استفاده از آزمون های آماری من ویتنی و کای دو تجزیه و تحلیل شد. یافته ها: فراوانی افراد 94 نفر مذکر و 50 نفر مونث بود. این افراد در محدوده سنی 85-2 با میانگین 3/2±4/37 سال قرار داشتند. 18 (26 نفر) دارای HBeAg در سرم بودند. میانگین آنزیم آسپارتات آمینو ترانسفراز (AST) در گروه HBeAg مثبت IU/L 83 و در گروه HBeAg منفی IU/L 2/56 بود (01/0

Molecular mechanisms regulating immune responses in thromboangiitis obliterans: a comprehensive review

Thromboangiitis obliterans (TAO) is a thrombotic-occlusive as well as an inflammatory peripheral vascular disease with unknown etiology. Recent evidence has supported the immunopathogenesis of the disease, however, the factors contributing to the altered immune function and vascular tissue inflammation are still unclear. This review was intended to collate the more current knowledge on the regulatory molecules involved in TAO from an immunoreactive perspective. The homeostasis of the immune system as well as a variety of progenitor cell populations appear to be affected during TAO and these alterations are associated with intrinsic signaling defects that are directing to an improved understanding of the crosstalk between angiogenesis and the immune system, as well as the potential of new co-targeting strategies applying both immunotherapy and angiogenic therapy