Japan Gastroenterological Endoscopy Society (JGES) has compiled a set of guidelines for endoscopic management of non‐variceal upper gastrointestinal bleeding using evidence‐based methods. The major cause of non‐variceal upper gastrointestinal bleeding is peptic gastroduodenal ulcer bleeding. As a result, these guidelines mainly focus on peptic gastroduodenal ulcer bleeding, although bleeding from other causes is also overviewed. From the epidemiological aspect, in recent years in Japan, bleeding from drug‐related ulcers has become predominant in comparison with bleeding from Helicobacter pylori (HP)‐related ulcers, owing to an increase in the aging population and coverage of HP eradication therapy by national health insurance. As for treatment, endoscopic hemostasis, in which there are a variety of methods, is considered to be the first‐line treatment for bleeding from almost all causes. It is very important to precisely evaluate the severity of the patient's condition and stabilize the patient's vital signs with intensive care for successful endoscopic hemostasis. Additionally, use of antisecretory agents is recommended to prevent rebleeding after endoscopic hemostasis, especially for gastroduodenal ulcer bleeding. Eighteen statements with evidence and recommendation levels have been made by the JGES committee of these guidelines according to evidence obtained from clinical research studies. However, some of the statements that are supported by a low level of evidence must be confirmed by further clinical research.

Sarcopenia is a significant prognostic factor in metastatic renal cell carcinoma.

Background and aims: Endoscopic submucosal dissection (ESD) was developed in Japan and has been performed on many patients with early stage esophageal cancer; however quality of life in patients with postoperative stricture is drastically decreased and repeat, periodic endoscopic balloon dilatation (EBD) is usually required over long periods. In this study, we evaluate the efficacy of short period, low dose oral prednisolone in controlling post-procedural esophageal stricture. Patients and methods: In total, 33 patients who underwent semicircular or complete circular ESD for esophageal superficial squamous cell carcinoma were included in this study. They were divided into two groups: those who underwent large-circumference ESD with no preventative treatment for stricture (ESD alone group) and those who received systemic steroid treatment for stricture (oral prednisolone group). We compared the two groups in terms of stricture rate and total number of EBD sessions. The ESD alone group underwent no preventative treatment. The oral prednisolone group started with 30 mg/day prednisolone on the second day post-ESD, and continued with a gradually tapering prednisolone dose, finally discontinuing systemic steroid administration 3 weeks later. Results: The stricture rate after ESD was significantly lower in the oral prednisolone group (3 of 17 patients; 17.6 %) than in the ESD alone group (11 of 16 patients; 68.7 %) (P < 0.01). The number of EBD sessions was significantly lower in the oral prednisolone group than in the ESD alone group (median 4.6, range 2 – 10 vs. median 8.1, range 1 – 18; P < 0.01). Conclusion: Short period, low dose oral prednisolone showed promising results for the prevention of stricture after ESD for early stage esophageal cancers.

BackgroundPulmonary emphysema is characterized by alveolar destruction and persistent inflammation of the airways. Although IL-17A contributes to many chronic inflammatory diseases, it’s role in the inflammatory response of elastase-induced emphysema remains unclear.MethodsIn a model of elastase-induced pulmonary emphysema we examined the response of IL-17A-deficient mice, monitoring airway inflammation, static compliance, lung histology and levels of neutrophil-related chemokine and pro-inflammatory cytokines in bronchoalveolar lavage (BAL) fluid.ResultsWild-type mice developed emphysematous changes in the lung tissue on day 21 after elastase treatment, whereas emphysematous changes were decreased in IL-17A-deficient mice compared to wild-type mice. Neutrophilia in BAL fluid, seen in elastase-treated wild-type mice, was reduced in elastase-treated IL-17A-deficient mice on day 4, associated with decreased levels of KC, MIP-2 and IL-1 beta. Elastase-treated wild-type mice showed increased IL-17A levels as well as increased numbers of IL-17A+ CD4 T cells in the lung in the initial period following elastase treatment.ConclusionsThese data identify the important contribution of IL-17A in the development of elastase-induced pulmonary inflammation and emphysema. Targeting IL-17A in emphysema may be a potential therapeutic strategy for delaying disease progression.

Measurement of EBC biomarkers is a non-invasive and useful way to evaluate airway inflammation in patients with asthma.