Purpose of review This review will examine the recent scientific literature surrounding high-fat-diet (HFD)-induced alterations in gut microbiota and subsequent development of obesity and chronic disease risk. Recent findings Excessive consumption of HFDs has undoubtedly contributed to the obesity epidemic. However, the mechanisms responsible for this relationship are likely to be more complex than the simple concept of energy balance. In fact, emerging literature has implicated HFD-induced alterations in gut microbiota in the obesity epidemic. HFD consumption generally leads to a decrease in Bacteroidetes and an increase in Firmicutes, alterations that have been associated with obesity and subsequent development of chronic diseases. Potential mechanisms for this effect include 1) an improved capacity for energy harvest and storage and, 2) enhanced gut permeability and inflammation. We highlight the most important recent advances linking HFD-induced dysbiosis to obesity, explore the possible mechanisms for this effect, examine the implications for disease development, and evaluate the possibility of therapeutic targeting of the gut microbiome to reduce obesity. Summary A better understanding of the mechanisms linking HFD to alterations in gut microbiota is necessary to allow for the regulation of dysbiosis and ensuing promotion of anti-obesity effects.

Background: 5-Aminosalicylates remain important in the treatment of ulcerative colitis, but it is uncertain if the various preparations currently available are equivalent given the different delivery systems that exist. Generic prescription of mesalazine (mesalamine) is therefore inappropriate. Ipocol has recently become available as an alternative to Asacol-MR. Aim: To compare the two agents in a controlled trial using a non-inferiority design. Methods: Eighty-eight ulcerative colitis patients with a mild to moderate clinical relapse were randomized to one of the two drugs at a daily dose of 2.4 g for 8 weeks.

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peptides derived from the patient's mismatched-HLA molecules that can be presented by shared HLA. Methods: A Dutch multicenter cohort of 685 patients was retrospectively studied. PIRCHE numbers were determined either presented on HLA class-I (PIRCHE-I) or class-II (PIRCHE-II) for patients receiving a single HLA-mismatched (9/10) unrelated donor transplant (N = 249), using unambiguous high-resolution HLA-A,-B,-C,-DRB1 and-DQB1 typings. Patients were divided into three equal-sized groups according to their PIRCHE numbers (low, medium, and high). The clinical outcome of these groups was compared to a reference group of HLA-matched transplantations (N = 436). The primary endpoints were OS and non-relapse mortality (NRM). Findings: The group transplanted with low PIRCHE-I and-II had an OS (HR 1.33, P = .13) and an NRM (HR .90, P = .69) comparable with the 10/10 HLA-matched group. The medium with high PIRCHE-I or-II had significantly increased risks of mortality (HR 1.44, P = .009) and NRM (HR 1.47, P = .02). Moreover, PIRCHE numbers also dissected HLA mismatches into those with a significantly increased or comparable risk of progression-free survival and acute graft-versus-host disease as HLA-matched transplantations, whereas there were no differences in progression risk when comparing the PIRCHE groups with HLA-matched transplantations. Interpretation: This study suggests that the permissibility of HLA-mismatched transplantations may be predicted by PIRCHE numbers. In future, PIRCHE may provide a novel method for selection of HLA-mismatched donors.