Background: We have previously demonstrated a negative relationship between the prevalence of Helicobacter pylori and gastro‐oesophageal reflux disease (GERD). Aim: To study the effects of H. pylori infection on the severity of GERD. Methods: Ethnic Chinese patients with frequent heartburn and/or endoscopic oesophagitis were studied. Endoscopic examination was performed to assess the severity of oesophagitis (modified Savary–Miller grading) and the presence of hiatus hernia. Biopsies were taken for rapid urease testing and confirmation of Barrett’s oesophagus. Risk factors which may affect the severity of oesophagitis (age, sex, smoking, drinking, diabetes mellitus, hiatus hernia, H. pylori status and body mass index) were evaluated by a multiple regression model. The cagA status of H. pylori infected GERD and age‐and‐sex matched controls were determined by Western blot. Age‐and‐sex matched non‐reflux patients were recruited as controls for comparison. Results: Two hundred and twenty‐five patients with GERD were studied, of whom 77 (34%) were infected with H. pylori. Oesophagitis and Barrett’s oesophagus were found in 140 patients (62%) and six patients (3%), respectively. H. pylori infected patients had significantly less severe oesophagitis compared to the uninfected group (P=0.022). All patients with Barrett’s oesophagus were uninfected. Factors that predicted severe oesophagitis included age over 60 years (P < 0.001) and hiatus hernia (P < 0.001). H. pylori infection was the only factor that showed a negative correlation with severe oesophagitis (P=0.011). The prevalence of the cagA positive strain in endoscopy‐negative GERD, erosive oesophagitis and control subjects was 70, 76 and 78%, respectively (P=0.75). Conclusions: H. pylori infection is associated with milder GERD.

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The discovery of the novel KIF5B-ALK variant further consolidated the role of aberrant ALK signaling in lung carcinogenesis.

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Prader-Willi syndrome (PWS) is a chromosomal disorder characterized by the presence of hyperghrelinemia, hyperphagia, and obesity. The optimal treatment for PWS patient remains controversial. Here, we present our experience of treating PWS with laparoscopic mini-gastric bypass (LMGBP) and laparoscopic sleeve gastrectomy (LSG). Three patients with genetic diagnosis of PWS and body mass index (BMI) greater than 40 kg/m(2) were referred for bariatric surgery. All of them had completed 2-year postoperative follow-up. Body weight, BMI, and ghrelin levels were recorded before and after surgery. They were two females and one male. Their age ranged from 15 to 23 years old, and the mean BMI was 46.7 kg/m(2) (range 44-50). Two patients underwent LSG and one patient underwent LMGBP. After a median follow-up of 33 months (range 24-36 months), mean weight loss and percentage of excessive weight loss at 2 years were 32.5 kg (24.9-38.3 kg) and 63.2 % (range 50.5-86.2 %), respectively. The mean fasting active ghrelin level decreased from 1,134.2 pg/ml preoperatively to 519.8 pg/ml 1 year after surgery. No major complication was observed. Iron deficiency anemia was observed in the patient who underwent LMGBP. Significant reduction of body weight and level of serum ghrelin can be achieved with minimal morbidity by LSG or LMGBP in patients with PWS.

Colorectal cancer is the third most common cancer in the world and liver is the most frequent site of distant metastasis with poor prognosis. The aim of this study is to investigate microRNAs leading to liver metastasis. We applied microarray analysis and quantitative PCR to identify and validate dysregulated miRNAs in liver metastases when compared to primary CRCs. Functional significance and the underlying molecular mechanism of selected miRNA was demonstrated by a series of in vitro and in vivo assays. Our microarray analysis and subsequent quantitative PCR validation revealed that miR-885-5p was strongly up-regulated in liver metastases and in CRC cell-lines derived from distant metastases. Overexpression of miR-885-5p significantly induced cell migration, cell invasion, formation of stress fibre in vitro and development of liver and lung metastases in vivo. MiR-885-5p induced metastatic potential of CRC by repressing cytoplasmic polyadenylation element binding protein 2 transcription through directly binding to two binding sites on its 3′ untranslated region, and consequently led to up-regulation of TWIST1 and hence epithelial-mesenchymal transition. Our findings demonstrated the overexpression of miR-885-5p in liver metastasis and its roles in inducing CRC metastasis, potentiating development of miR-885-5p inhibitor to treat advanced CRC in the future.

• No significant changes were observed in fat-fraction, T2* and volume of brown adipose tissue after bariatric surgery. • Non-alcoholic fatty liver disease was resolved after surgery. • Abdominal white fat and liver fat were significantly reduced 6 months after surgery and become stable between 6 and 12 months while pancreatic fat was significantly reduced between 0 and 12 months.

Initiatives are required to improve awareness of younger people with regard to lifestyle risk factors for CRC, especially since this group stand to benefit most from risk reduction. Those with a lower educational level also had poor awareness but felt that the NHS should not prescribe exercise and lifestyle change; targeting this group would need to take this into account.