Recent advances in peptic ulcer bleeding

Peptic ulcer bleeding remains a common cause of hospital admission, morbidity and mortality. Data published since 2006 illustrate that assessment, endoscopic and pharmacological management, and follow-up strategies can be refined to improve the overall prognosis of peptic ulcer bleeding

Pathophysiological mechanisms linking obesity and esophageal adenocarcinoma

In recent decades there has been a dramatic rise in the incidence of esophageal adenocarcinoma (EAC) in the developed world. Over approximately the same period there has also been an increase in the prevalence of obesity. Obesity, especially visceral obesity, is an important independent risk factor for the development of gastro-esophageal reflux disease, Barrett’s esophagus and EAC. Although the simplest explanation is that this mediated by the mechanical effects of abdominal obesity promoting gastro-esophageal reflux, the epidemiological data suggest that the EAC-promoting effects are independent of reflux. Several, not mutually exclusive, mechanisms have been implicated, which may have different effects at various points along the reflux-Barrett’s-cancer pathway. These mechanisms include a reduction in the prevalence of Helicobacter pylori infection enhancing gastric acidity and possibly appetite by increasing gastric ghrelin secretion, induction of both low-grade systemic inflammation by factors secreted by adipose tissue and the metabolic syndrome with insulin-resistance. Obesity is associated with enhanced secretion of leptin and decreased secretion of adiponectin from adipose tissue and both increased leptin and decreased adiponectin have been shown to be independent risk factors for progression to EAC. Leptin and adiponectin have a set of mutually antagonistic actions on Barrett’s cells which appear to influence the progression of malignant behaviour. At present no drugs are of proven benefit to prevent obesity associated EAC. Roux-en-Y reconstruction is the preferred bariatric surgical option for weight loss in patients with reflux. Statins and aspirin may have chemopreventative effects and are indicated for their circulatory benefits

Appendix 1. Individual abstract-level data for abstracts presented at the BSG meeting in 1995 and 2005.

<p>The dataset shows the extraction of data related to individual abstracts presented at the BSG meetings in 1995 and 2005. Classification of abstracts by type of study and topic area and details of subsequent peer-reviewed publications are shown.</p

Appendix 2. Unadjusted odds ratios (OR) for subsequent publication of abstracts presented to the British Society of Gastroenterology in 2005 compared to 1995.

<p>Table showing odds ratios for the subsequent publication in peer-reviewed journals of abstracts presented at the BSG meeting in 2005 compared to those presented at the 1995 meetings. Results are shown by classification of abstract by study type, main area of study and discipline for fundamental (life) sciences.</p

Activation of Akt is increased in the dysplasia-carcinoma sequence in Barrett's oesophagus and contributes to increased proliferation and inhibition of apoptosis: a histopathological and functional study-2

<p><b>Copyright information:</b></p><p>Taken from "Activation of Akt is increased in the dysplasia-carcinoma sequence in Barrett's oesophagus and contributes to increased proliferation and inhibition of apoptosis: a histopathological and functional study"</p><p>http://www.biomedcentral.com/1471-2407/7/97</p><p>BMC Cancer 2007;7():97-97.</p><p>Published online 8 Jun 2007</p><p>PMCID:PMC1899509.</p><p></p>an anti-Ob-R antibody, primary antibody binding was recognised using a donkey-FITC conjugated ant-rabbit antibody and fluorescence microscopy (). No staining was detected in the absence of anti-Ob-R antibody () (× 63 magnification). Leptin increased cell numbers in OE33 cells (serum-starved OE33 cells were treated with increasing concentrations of leptin and relative cell numbers assessed after 24 hours using the MTT colourmetric assay, results expressed as mean ± SEM, N = 3, *< 0.05 vs basal

Activation of Akt is increased in the dysplasia-carcinoma sequence in Barrett's oesophagus and contributes to increased proliferation and inhibition of apoptosis: a histopathological and functional study-4

<p><b>Copyright information:</b></p><p>Taken from "Activation of Akt is increased in the dysplasia-carcinoma sequence in Barrett's oesophagus and contributes to increased proliferation and inhibition of apoptosis: a histopathological and functional study"</p><p>http://www.biomedcentral.com/1471-2407/7/97</p><p>BMC Cancer 2007;7():97-97.</p><p>Published online 8 Jun 2007</p><p>PMCID:PMC1899509.</p><p></p> caspase-3 activity in cell lysates (). Where indicated cells were pretreated with the PI3-kinase inhibitor LY294002 (10 μM) for 60 minutes before any stimulation. Nucleosomes results are expressed as (A– A) values, which represent relative nuclesome concentrations, compared to untreated control cells. Caspase-3 activity is expresses as percentage of untreated control activity. Results expressed as mean ± SEM, N = 3, * < 0.05 vs untreated control, ** < 0.05 vs acid or leptin alone, *** < 0.05 vs stimulus in the absence of LY29400