Specifically, various single-nucleotide polymorphisms (SNPs) in a

Specifically, various single-nucleotide polymorphisms (SNPs) in apoptotic genes, CYT387 price such as FAS-1377 G/A SNP, have been associated

with cancer risk. FAS-1377 G/A SNP has been shown to alter FAS gene promoter transcriptional activity. Down-regulation of FAS and cell death resistance is key to many cancers, but an association between FAS-1377 G/A SNP and cancer risk is uncertain. Therefore, we conducted a meta-analysis of the current literature to clarify this relationship.\n\nMethodology/Principal Findings: From PubMed and Chinese language (CNKI and WanFang) databases, we located articles published up to March 5, 2013, obtaining 44 case-control studies from 41 different articles containing 17,858 cases and 24,311 controls based on search criteria for cancer susceptibility

related to the FAS gene -1377 G/A SNP. Odds ratios (ORs) and 95% confidence intervals (CI) revealed association strengths. Data show that the -1377 G allele was protective against cancer risk. Similar associations were detected in “source of control,” ethnicity and Selleckchem RG7112 cancer type subgroups. Lower cancer risk was found in both smokers with a GG+GA genotype and in nonsmokers with the GG+GA genotype, when compared to smokers and nonsmokers with the AA genotype. Males carrying the -1377G allele (GG+GA) had lower cancer incidence than those with the AA genotype. Individuals who carried both FAS-1377(GG+GA)/FASL-844(TT+TC) genotypes appeared to have lower risk of cancer than those who carried both FAS-1377 AA/FASL-844 CC genotypes.\n\nConclusions/Significance: The FAS-1377 G/A SNP may decrease cancer risk. Studies with larger samples

to study gene-environment GANT61 concentration interactions are warranted to understand the role of FAS gene polymorphisms, especially -1377 G/A SNP, in cancer risk.”
“Background: Rapid Response Teams aim to accelerate recognition and treatment of acutely unwell patients. Delays in delivery might undermine efficiency of the intervention. Our understanding of the causes of these delays is, as yet, incomplete.\n\nAim: To identify modifiable causes of delays in the treatment of critically ill patients outside intensive care with a focus on factors amenable to system design.\n\nMethods: Review of care records and direct observation with process mapping of care delivered to 17 acutely unwell patients attended by a Rapid Response Team in a District General Hospital in the United Kingdom. Delays were defined as processes with no added value for patient care.\n\nResults: Essential diagnostic and therapeutic procedures accounted for only 31% of time of care processes. Causes for delays could be classified into themes as (1) delays in call-out of the Rapid Response Team, (2) problems with team cohesion including poor communication and team efficiency and (3) lack of resources including lack of first line antibiotics, essential equipment, experienced staff and critical care beds.

Comments are closed.