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Atorvastatin-Induced Ingestion associated with Continual Subdural Hematoma Will be Partially Related to the particular Polarization involving Macrophages.
Aim This study set out to determine the effect of methylation on MALAT1 gene in primary colorectal lesions and tumors to gain further knowledge about the diagnostic and prognostic value of MALAT. Background Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is one of the long non-coding RNAs that plays an important role in invasion, cell proliferation, and metastasis of various cancers. However, there is insufficient information on the association between MALAT1 and the methylation process as well as its role in the development of colorectal cancer. Methods Methylation pattern of MALAT1 promoter was determined by Methylation-Specific Polymerase Chain Reaction (MSP) in 86 colorectal primary lesions, tumors, and normal specimens. MALAT1 methylation pattern was compared in tumor and polyp tissue. In order to obtain more accurate results, we investigated the association between MALAT1 promoter methylation pattern and clinicopathologic factors in patients. Results The results indicated that the MALAT1 promoter methylation pattern in the tumor tissue, primary lesion tissue, and normal was not significantly different (p=0.430). Comparison of the MALAT1 promoter methylation pattern between polyp types and tumor tissue groups was not significant either (p=0.437). Surprisingly, the methylation frequency of MALAT1 methylation was significantly higher in colon lesions than in their rectum lesion (p = 0.035). In addition, no significant hypermethylation of MALAT1 was observed between the other patients' clinicopathological data in both polyp 46/66 and tumor tissues 20/66. Conclusion This study dealt with determining the effect of methylation on MALAT1 gene in primary colorectal lesions and tumors to gain further knowledge about the diagnostic and prognostic value of MALAT. ©2019 RIGLD.Aim Given the high similarity of phenotypical and secretory properties of mesenchymal stem cells and fibroblasts, this study investigated the possibility of inducing EMT process by mesenchymal stem cells. Background Annually, more than 13% of deaths worldwide occur due to cancer. One of the main reasons for the high mortality rate is due to the metastasis of cancer stem cells. Induction of metastasis occurs during the EMT process, which can also be stimulated by fibroblast cells. Methods Mesenchymal stem cells (MSCs) were isolated and sub-cultured until passage 3 or 4. AGS cells were co-cultured with MSCs for 4 days. As the positive control group, AGS cells were treated with TGF-β (10ng/ml) for 48h. Finally, the mRNA expression level of Vimentin, β-catenin, Snail, and E-cadherin as the EMT pattern, were evaluated by RT-PCR technique. Results Our findings indicated that AGS cells' crosstalk with MSCs significantly upregulated fibroblast markers including Vimentin and Snail expression. However, no significant changes were identified for β-catenin gene expression. Additionally, AGS treatment with MSCs resulted in diminished E-cadherin in the targeted cells. Conclusion Based on the results, the AGS cells crosstalk with MSCs activates induction of epithelial mesenchymal transition, which is confirmed through the elevation of Vimentin and Snail expression and reduction of E-cadherin expression as a specific epithelial marker. However, it seems that MSc was not effective on Wnt/ β-catenin signal gastric cancer cell line. ©2019 RIGLD.Aim The main goal of this investigation was to provide an overview on H.pylori effect on gastric tissue via bioinformatics analysis of microarray-identified miRNAs and its target genes. Background MicroRNAs which control about 30 to 60% of gene expression in human body play a critical role in different cell growth stages. Expression modification of non-coding (NC) RNAs in H.pylori infections requires further investigations to provide better understanding of their roles in the body. https://www.selleckchem.com/products/CP-690550.html Methods GSE54397, the microRNA microarray dataset, was analyzed by GEO2R, the online GEO database for detection of differentially expressed microRNAs and lastly the potential target genes as well as their associated pathways. Results A total of 244 miRNAs were detected as differentially expressed (p2) in non-cancerous tissue of gastric with H.pylori infection in comparison with tissues without H.pylori infection. The findings indicated that hub microRNAs and target genes of up-regulated network are KIF9, DCTN3, and CA5BP1 along with hsa-miR-519d, hsa-miR-573, hsa-miR-646, hsa-miR-92a-1, hsa-miR-186, and hsa-miR-892a, respectively. For the down-regulated network, genes of RABGAP1, HSPB11 and microRNAs of hsa-miR-620, hsa-miR-19b-2, hsa-miR-555, and hsa-let-7f-2 were hubs. Most of the up-regulated microRNAs are involved in gastric cancer development while there is no evidence for the down-regulated ones. Yet, all of the hub down-regulated miRNAs are reported to have associations with different kinds of cancer. Conclusion The introduced hub miRNAs and genes may serve as feasible markers in the mechanisms of H.pylori infection for different kinds of gastric diseases, in particular gastric cancer. However, their role requires further investigations. ©2019 RIGLD.Aim We used mixture cure mode to separately investigate the risk factors for long-term and short-term survival of colorectal cancer patients. Background Colorectal cancer (CRC) is the second most common cancer worldwide. In cancer studies, patients' survival is the most important indicator of patients' status. Classical methods in analyzing the survival data usually apply Cox proportional hazard regression. Methods The study was performed on 1121 patients diagnosed with colorectal cancer. Mixture cure model with Weibull distribution and logit link function was fitted to data. Results Odds of long-term survival for rectum cancer patients were lower than for colon cancer patients (OR=0.29(0.09, 0.9)). Also, patients with the advanced stage of the disease had lower odds of long-term survival compared to early-stage patients (OR=0.24(0.06, 0.86)).In the short-term, the hazard of death for people with normal BMI was lower than the underweight group (HR=0.4(0.21, 0.76)). The short-term hazard of death for rectum cancer was about half of the short-term hazard for colon cancer (HR=0.
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