A Cross-Sectional Review of Reporting Variation in Postoperative Bowel Dysfunction After Rectal Cancer Surgery.

Background: Postoperative bowel dysfunction affects quality of life after sphincter-preserving rectal cancer surgery, but the extent of the problem is not clearly defined because of inconsistent outcome measures used to characterize the condition.

Objective: The purpose of this study was to assess variation in the reporting of postoperative bowel dysfunction and to make recommendations for standardization in future studies. If possible, a quantitative synthesis of bowel dysfunction symptoms was planned.

Systematic Review and Meta-analysis of Prophylactic Mesh During Primary Stoma Formation to Prevent Parastomal Hernia.

Background: Implantation of mesh at the time of stoma formation may reduce the rate of parastomal hernia. Until recently, the evidence has been limited to only a few small randomized controlled trials.

Objective: We present an updated systematic review and meta-analysis to assess the effect of mesh prophylaxis on rates of parastomal hernia.

Cytoplasmic plaque formation in hemidesmosome development is dependent on SoxF transcription factor function.

Hemidesmosomes are composed of intricate networks of proteins, that are an essential attachment apparatus for the integrity of epithelial tissue. Disruption leads to blistering diseases such as epidermolysis bullosa. Members of the Sox gene family show dynamic and diverse expression patterns during development and mutation analyses in humans and mice provide evidence that they play a remarkable variety of roles in development and human disease.

Methylation of CLDN6, FBN2, RBP1, RBP4, TFPI2, and TMEFF2 in esophageal squamous cell carcinoma.

In the development and progression of cancer, tumor suppressor genes may be silenced by mechanisms such as methylation. Thus the discovery of new genes silenced by methylation may uncover new tumor suppressor genes, and improve our understanding of cancer biology. In this study we investigated the methylation of 19 genes in esophageal squamous cell carcinoma.

Similarity of aberrant DNA methylation in Barrett's esophagus and esophageal adenocarcinoma.

Background: Barrett's esophagus (BE) is the metaplastic replacement of squamous with columnar epithelium in the esophagus, as a result of reflux. It is the major risk factor for the development of esophageal adenocarcinoma (EAC). Methylation of CpG dinucleotides of normally unmethylated genes is associated with silencing of their expression, and is common in EAC.

Methylation of TIMP3 in esophageal squamous cell carcinoma.

Aim: To measure the frequency of DNA methylation of the tissue inhibitor of metalloproteinase 3 (TIMP3) promoter and relate this to any change of gene expression in esophageal squamous cell carcinoma in patients from a region of high incidence in China.

Methods: Cancer cell lines were treated with or without the demethylating reagent 5-aza-2'-deoxycytidine. Methylation of the TIMP3 promoter was assessed in three regions by melt curve analysis and its expression was assessed by real-time RT-PCR.

Effect of disrupted SOX18 transcription factor function on tumor growth, vascularization, and endothelial development.

Background: The growth of solid tumors depends on establishing blood supply; thus, inhibiting tumor angiogenesis has been a long-term goal in cancer therapy. The SOX18 transcription factor is a key regulator of murine and human blood vessel formation.

Methods: We established allograft melanoma tumors in wild-type mice, Sox18-null mice, and mice expressing a dominant-negative form of Sox18 (Sox18RaOp) (n = 4 per group) and measured tumor growth and microvessel density by immunohistochemical analysis with antibodies to the endothelial marker CD31 and the pericyte marker NG2.

Metallothionien 3 expression is frequently down-regulated in oesophageal squamous cell carcinoma by DNA methylation.

Background: Metallothionein 3 (MT3) inhibits growth in a variety of cell types. We measured MT3 gene expression by RT-PCR, and DNA methylation in the MT3 promoter by combined bisulphite restriction analysis, in four oesophageal cancer cell lines and the resected oesophagus from 64 patients with oesophageal squamous cell carcinoma (SCC).

Results: MT3 expression was not detected in one of the four oesophageal cell lines.

Assessment of an electronic voting system within the tutorial setting: a randomised controlled trial [ISRCTN54535861].

Background: Electronic voting systems have been used in various educational settings with little measurement of the educational impact on students. The goal of this study was to measure the effects of the inclusion of an electronic voting system within a small group tutorial.

Method: A prospective randomised controlled trial was run at the Royal Adelaide Hospital, a teaching hospital in Adelaide, Australia.

Regulation of the Wnt signalling component PAR1A by the Peutz-Jeghers syndrome kinase LKB1.

Loss-of-function mutations in the LKB1 (STK11) serine-threonine kinase gene cause Peutz-Jeghers syndrome, which is associated with inherited susceptibility to colorectal and other cancers. No downstream targets of LKB1 kinase activity have been identified. Here we show that LKB1 can direct the phosphorylation of the serine-threonine kinase PAR1A.

The regulation of glycogen synthase kinase-3 nuclear export by Frat/GBP.

Previous studies have shown that nuclear levels of glycogen synthase kinase-3 (GSK-3) are dynamically regulated and may affect access of GSK-3 to its substrates. In this study we show that the GSK-3-binding protein Frat/GBP regulates the nuclear export of GSK-3. We show that Frat/GBP contains a nuclear export sequence that promotes its own nuclear export and that of associated GSK-3.

Identification of the Axin and Frat binding region of glycogen synthase kinase-3.

Glycogen synthase kinase-3 (GSK-3) is a key component of several signaling pathways including those regulated by Wnt and insulin ligands. Specificity in GSK-3 signaling is thought to involve interactions with scaffold proteins that localize GSK-3 regulators and substrates. This report shows that GSK-3 forms a low affinity homodimer that is disrupted by binding to Axin and Frat.