A Geospatial database of gastric cancer patients and associated potential risk factors including lifestyle and air pollution.

OBJECTIVES: Gastric cancer (GC) is a multifactorial disease and the fifth most frequent diagnosed cancer worldwide. It accounts for one third of cancer-related mortalities. Geospatial analysis using geographical information systems (GIS) can provide an efficient solution to identify spatial disparities associated with GC. As such, GIS enables policymakers to control cancer in a better way and identify the regions where interventions are needed. This study aims to publish a comprehensive dataset, which was applied to conduct a spatial analysis of GC patients in the city of Mashhad, Iran. DATA DESCRIPTION: We provide a personal geodatabase, a Microsoft Access database that can store, query, and manage both spatial and non-spatial data, which contains four feature classes. "Male_Stomach_Cancer_Patients" and "Female_Stomach_Cancer_Patients" are point feature classes, which show the age and geographical location of 1156 GC cancer patients diagnosed between 2014 and 2017. "Air_Polution_Mashhad" is another point feature class that reveals the amount of six air pollutants, which was taken from Mashhad Environmental Pollutants Monitoring Center between 2017 and 2018. Finally, "Stomach_Cancer_and_Risk_Factors" is a polygon feature class of neighborhood division of Mashhad, consisting of contributor risk factors including dietary habits, smoking, alcohol use, body mass index and population by age groups for all 165 city neighborhoods.

Reduced Hepatic Carcinoembryonic Antigen-Related Cell Adhesion Molecule 1 Level in Obesity.

Impairment of insulin clearance is being increasingly recognized as a critical step in the development of insulin resistance and metabolic disease. The carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) promotes insulin clearance. Null deletion or liver-specific inactivation of Ceacam1 in mice causes a defect in insulin clearance, insulin resistance, steatohepatitis, and visceral obesity. Immunohistological analysis revealed reduction of hepatic CEACAM1 in obese subjects with fatty liver disease. Thus, we aimed to determine whether this occurs at the hepatocyte level in response to systemic extrahepatic factors and whether this holds across species. Northern and Western blot analyses demonstrate that CEACAM1 mRNA and protein levels are reduced in liver tissues of obese individuals compared to their lean age-matched counterparts. Furthermore, Western analysis reveals a comparable reduction of CEACAM1 protein in primary hepatocytes derived from the same obese subjects. Similar to humans, Ceacam1 mRNA level, assessed by quantitative RT-PCR analysis, is significantly reduced in the livers of obese Zucker (fa/fa, ZDF) and Koletsky (f/f) rats relative to their age-matched lean counterparts. These studies demonstrate that the reduction of hepatic CEACAM1 in obesity occurs at the level of hepatocytes and identify the reduction of hepatic CEACAM1 as a common denominator of obesity across multiple species.

Loss of Hepatic CEACAM1: A Unifying Mechanism Linking Insulin Resistance to Obesity and Non-Alcoholic Fatty Liver Disease.

The pathogenesis of human non-alcoholic fatty liver disease (NAFLD) remains unclear, in particular in the context of its relationship to insulin resistance and visceral obesity. Work on the carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) in mice has resolved some of the related questions. CEACAM1 promotes insulin clearance by enhancing the rate of uptake of the insulin-receptor complex. It also mediates a negative acute effect of insulin on fatty acid synthase activity. This positions CEACAM1 to coordinate the regulation of insulin and lipid metabolism. Fed a regular chow diet, global null mutation of Ceacam1 manifest hyperinsulinemia, insulin resistance, obesity, and steatohepatitis. They also develop spontaneous chicken-wire fibrosis, characteristic of non-alcoholic steatohepatitis. Reduction of hepatic CEACAM1 expression plays a significant role in the pathogenesis of diet-induced metabolic abnormalities, as bolstered by the protective effect of hepatic CEACAM1 gain-of-function against the metabolic response to dietary fat. Together, this emphasizes that loss of hepatic CEACAM1 links NAFLD to insulin resistance and obesity.

Impact of vitamin supplements on HAART related hematological abnormalities in HIV-infected patients.

BACKGROUND: The human immunodeficiency virus (HIV) is one of the most life- threatening human infections. The advent of highly active antiretroviral therapy (HAART) has dramatically changed the course of HIV infection and patients' quality of life. In addition to the benefits, HAART can have numerous side effects and toxicities. Therefore, we aimed to assess the impact of short-term vitamins treatment on hematological parameters of HIV infected patients receiving HAART. METHODS: This cross-sectional study was conducted on 100 confirmed HIV positive patients who referred to Shiraz HIV/AIDS research center in southwest of Iran. The first-line of HAART regimen contained Zidovudine, Lamivudine, and Efavirenz. The studied population received vitamin B12 weekly and folic acid daily for at least one month. RESULTS: After receiving HAART for at least 6 months with adherence above 90%, significant differences (p<0.05) were observed in MCV, MCH, HCT, TLC and RBC status compared to the baseline parameters. After one month of treatment, vitamins in four hematological parameters including TLC, MCV, RBC, and WBC showed significant differences compared to HAART parameters. CONCLUSION: Combined administration of B12 and folate supplements is a beneficial adjuster on hematologic status of HIV infected persons receiving HAART. However, future research with larger studied population and longer follow-up periods is required. Moreover, especial attention should be given to gender because the effect of vitamins was significantly different on some hematologic parameters between different genders.

Cardiovascular risk factors emerge after artificial selection for low aerobic capacity.

In humans, the strong statistical association between fitness and survival suggests a link between impaired oxygen metabolism and disease. We hypothesized that artificial selection of rats based on low and high intrinsic exercise capacity would yield models that also contrast for disease risk. After 11 generations, rats with low aerobic capacity scored high on cardiovascular risk factors that constitute the metabolic syndrome. The decrease in aerobic capacity was associated with decreases in the amounts of transcription factors required for mitochondrial biogenesis and in the amounts of oxidative enzymes in skeletal muscle. Impairment of mitochondrial function may link reduced fitness to cardiovascular and metabolic disease.

CEACAM1 regulates insulin clearance in liver.

We hypothesized that insulin stimulates phosphorylation of CEACAM1 which in turn leads to upregulation of receptor-mediated insulin endocytosis and degradation in the hepatocyte. We have generated transgenic mice over-expressing in liver a dominant-negative, phosphorylation-defective S503A-CEACAM1 mutant. Supporting our hypothesis, we found that S503A-CEACAM1 transgenic mice developed hyperinsulinemia resulting from impaired insulin clearance. The hyperinsulinemia caused secondary insulin resistance with impaired glucose tolerance and random, but not fasting, hyperglycemia. Transgenic mice developed visceral adiposity with increased amounts of plasma free fatty acids and plasma and hepatic triglycerides. These findings suggest a mechanism through which insulin signaling regulates insulin sensitivity by modulating hepatic insulin clearance.