No abstract

MYC is an oncogene responsible for excessive cell growth in cancer, enabling transcriptional activation of genes involved in cell cycle regulation, metabolism, and apoptosis, and is usually overexpressed in gastric cancer (GC). By using siRNA and Next-Generation Sequencing (NGS), we identified MYC-regulated differentially expressed Genes (DEGs) in three Brazilian gastric cancer cell lines representing the histological subtypes of GC (diffuse, intestinal, and metastasis). The DEGs were picked using Sailfish software, followed by Gene Set Enrichment Analysis (GSEA) and Kyoto Encyclopedia of Gene and Genome (KEGG) pathway analysis using KEGG. We found 11 significantly enriched gene sets by using enrichment score (ES), False Discovery Rate (FDR), and nominal P-values. We identified a total of 5.471 DEGs with correlation over (80%). In diffuse-type and in metastatic GC cell lines, MYC-silencing caused DEGs downregulation, while the intestinal-type GC cells presented overall DEGs upregulation after MYC siRNA depletion. We were able to detect 11 significant gene sets when comparing our samples to the hallmark collection of gene expression, enriched mostly for the following hallmarks: proliferation, pathway, signaling, metabolic, and DNA damage response. When we analyzed our DEGs considering KEGG metabolic pathways, we found 12 common branches covering a wide range of biological functions, and three of them were common to all three cell lines: ubiquitin-mediated proteolysis, ribosomes, and system and epithelial cell signaling in Helicobacter pylori infection. The GC cell lines used in this study share 14 MYC-regulated genes, but their gene expression profile is different for each histological subtype of GC. Our results present a computational analysis of MYC-related signatures in GC, and we present evidence that GC cell lines representing distinct histological subtypes of this disease have different MYC-regulated expression profiles but share a common core of altered genes. This is an important step towards the understanding of MYC's role in gastric carcinogenesis and an indication of probable new drug targets in stomach cancer.

Objective: to determine, using a systematic review of meta-analysis studies, whether or not, remote alcohol and smoke are significant risk factors for late-onset Alzheimer's disease. Methods: using a meta-analysis statistics model, 12 case-control studies (6 for alcohol /6 for smoke) published on Medline from 1984 until 1999 which evaluated the interaction between those factors and Alzheimer's disease were investigated. Mantel-Haenszel adjusted odds ratio (OR) and 95% confidence intervals were calculated in stratified data. Epi Info statistical software was used to determine p-value with significant level at 0.05. Results: the studies showed that a prior history of alcohol abuse wasn't associated with late-onset of dementia due to Alzheimer's disease (OR=0.98; 95%CI 0.63 to 1.52; and p-value=0.996). And the other studies showed that a prior history of tabagism wasn't considered as a risk factor for AD (OR=0.70; 95%CI 0.57 to 0.85; and p-value= 0.0004). Conclusions: In this study alcoholism wasn't considered as a risk factor for AD .On the other hand , in people who had the smoke habit, chances of late-onset Alzheimer's development were reduced in 30%. In that case, tabagism was considered as a protector factor for AD.

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Interaction between Trypanosoma cruzi spheromastigotes (amastigotes) and mouse macrophages was studied. The spheromastigotes, isolated from the spleens of infected mice, were incorporated and digested by the macrophages. By use of horseradish peroxidase labeling of the macrophage lysosomes we showed that fusion of lysosomes with phagocytic vacuoles containing T. cruzi occurred. Parasites showing alterations indicative of digestion were seen inside the phagocytic vacuoles. Our results suggest that intracellular spheromastigotes of T. cruzi, isolated from the spleens of infected mice, are not able to induce a productive infection in mouse macrophages maintained in vitro.