ABSTRACT

         Background and objectives: Globally, about one third of the population has been infected with Hepatitis B virus (HBV) and more than 400 million people have become chronically infected. Nearly, 20-25% of all carriers develop serious liver diseases such as cirrhosis, chronic hepatitis and hepatocellular carcinoma (HCC). According to the World Health Organization, HBV infection causes more than one million deaths every year. Co-infection with Human Immunodeficiency virus (HIV) and HBV is common, since both viruses have the same routes of transmission. Approximately 10 -15% of HIV-infected individuals develop chronic hepatitis B. The risk of liver diseases-related deaths is also higher in the co-infected patients. According to previous studies, mutation of the pre-core (PC) and basal-core promoter (BCP) regions may play an important role in development of HBV-related HCC and severe liver disease. The aim of this study was to investigate mutations in the BCP, PC and core regions of HBV in HIV-positive patients.

          Methods: DNA was extracted using commercial kits to determine the BCP, PC/core mutations in 124 HIV/HBV co-infected patients (32.4% female and 67.6% male). Polymerase chain reaction (PCR) was performed using specific primers. The positive PCR products were subjected to automated sequencing. Then, nucleotide sequences were aligned with the standard hepatitis B sequence [Gene bank, accession number: AB033559] for mutation detection and analysis.

          Results: In this study, three patients (8.1%) were HBeAg-positive and all of them were HBsAg-positive. The mean of CD4 cell count was 120 cells/mL. The mean age of the patients was 36.16 years. The important pathological mutations in HBV patients including 1752A (73%), 1773C (70.3%), 1753C (10.8%), 1896A (8.1%) and 1762T/1764A (2.7%) were detected in this study.

         Conclusion: Identification of mutations in co-infected patients is of greater importance compared to mono-infected patients, because it can be useful for prediction of HCC-related mutations. Co-infection with HIV has important effects on the natural history of HBV infection, and creates different mutational patterns compared to mono-infected patients.

           Keywords: HBV, HIV, Mutation.

ABSTRACT
           Esophageal cancer (EC) is one of the most common types of cancer, especially in Asia. Esophageal squamous cell cancer (ESCC) is the most important histological subtype of EC, which accounts for 90% of all EC cases worldwide. ESCC is highly prevalent in Turkey, Iran, Kazakhstan and northern and central parts of China. Selenium is an essential micronutrient that is required for cellular functioning and synthesis of several selenoproteins. It also modulates the antioxidant defense system, cell cycle and apoptosis. This article reviews the most important molecular mechanisms of EC and investigates the association between selenium level and incidence of EC in high-risk areas.
           Keywords: Esophageal cancer, selenium, selenoprotein.

Background: Leptin and adiponectin, two members of the adipokine family, play roles in increasing lipid metabolism and inhibiting lipogenesis. Reduced levels of these cytokines are associated with obesity and insulin resistance. This study aimed to determine the serum levels of leptin and adiponectin in type-2 diabetic patients with and without metabolic syndrome compared to a control group.
Methods: Three groups of individuals participated in this study: 47 type-2 diabetic patients with metabolic syndrome (DM+MetS), 25 type-2 diabetic patients without metabolic syndrome (DM-MetS), and 40 individuals with no history of diabetes or metabolic syndrome (Control group). Fasting blood samples were collected, and serum levels of fasting blood sugar, cholesterol, triglycerides, HDL-cholesterol, and LDL-cholesterol were measured using the enzymatic method. Blood pressure, height, and weight were recorded using stadiometers, while leptin and adiponectin levels were determined via enzyme-linked immunosorbent assay.
Results: A significant difference was observed between the DM+MetS group and the DM-MetS group in serum leptin (p = 0.004) and adiponectin (p < 0.001) levels. In patients with type-2 diabetes and metabolic syndrome, serum leptin (p = 0.530) and adiponectin (p < 0.001) levels were lower compared to the control group.
Conclusion: A decrease in the serum levels of key adipokines, such as leptin and adiponectin, in type-2 diabetic patients may serve as a predictor of metabolic syndrome.