Mitophagy is a vital form of autophagy for selective removal of dysfunctional or redundant mitochondria. Accumulating evidence implicates elimination of dysfunctional mitochondria as a powerful means employed by autophagy to keep the immune system in check. The process of mitophagy may restrict inflammatory cytokine secretion and directly regulate mitochondrial antigen presentation and immune cell homeostasis. In this review, we describe distinctive pathways of mammalian mitophagy and highlight recent advances relevant to its function in immunity. In addition, we further discuss the direct and indirect evidence linking mitophagy to inflammation and autoimmunity underlying the pathogenesis of autoimmune diseases including inflammatory bowel diseases (IBD), systemic lupus erythematosus (SLE) and primary biliary cirrhosis (PBC).

Background. Laboratory data suggests a reduction ofFaecalibacterium prausnitzii(F. prausnitzii) is confirmed both in fecal samples in inflammatory bowel disease (IBD) patients. Numerous observational studies have suspected dysbiosis, an imbalance between protective and harmful bacteria to be relevant to the etiology and pathogenesis of IBD.Methods. Medline, EMBASE, Pubmed, and others. were searched by 2 independent reviewers. Of 48 abstracts reviewed, 11 studies met our inclusion criteria (subjectN=1180). Meta-analysis was performed with Review Manager 5.2.Results. The bacterial count ofF. prausnitziiin IBD patients was significantly lower (6.7888±1.8875) log10 CFU/g feces than healthy controls (7.5791±1.5812) log10 CFU/g feces;P<0.0001. The Standardization Mean Difference ofF. prausnitziiin IBD patients was −0.94 (95% confidence interval [CI]: −1.07–−0.80). Subgroup analyses revealed a trend toward a greater effect for CD (SMD: −1.13, 95% CI: −1.32–−0.94) when compared to UC (SMD: −0.78, 95% CI: −0.97–−0.60).Conclusions. The abundance ofF. prausnitziiwas decreased in IBD patients compared with healthy controls. Furthermore, the reduction ofF. prausnitziiand misbalance of the intestinal microbiota are particularly higher in CD patients with ileal involvement.

Educators continue to search for better strategies for medical education. Although the unifying theme of reforms was “increasing interest in, attention to, and understanding of the knowledge base structures”, it is difficult to achieve all these aspects via a single type of instruction. We used related key words to search in Google Scholar and Pubmed. Related search results on this topic were selected for discussion. Despite the range of different methods used in medical education, students are still required to memorize much of what they are taught, especially for the basic sciences. Subjects like anatomy and pathology carry a high intrinsic cognitive load mainly because of the large volume of information that must be retained. For these subjects, decreasing cognitive load is not feasible and memorizing appears to be the only strategy, yet the cognitive load makes learning a challenge for many students. Cognitive load is further increased when inappropriate use of educational methods occurs, e.g., in problem based learning which demands clinical reasoning, a high level and complex cognitive skill. It is widely known that experts are more skilled at clinical reasoning than novices because of their accumulated experiences. These experiences are based on the formation of cognitive schemata. In this paper we describe the use of cognitive schemata, developed by experts as worked examples to facilitate medical students’ learning and to promote their clinical reasoning. We suggest that cognitive load theory can provide a useful framework for understanding the challenges and successes associated with education of medical professionals.

Inflammatory bowel disease (IBD) has increased in incidence and prevalence in Asian countries since the end of the 20^th century. Moreover, differences in the cause, phenotypes, and natural history of IBD between the East and West have been recognized. Therefore, the Asian Organization for Crohn's and Colitis and the Asia Pacific Association of Gastroenterology have established recommendations on medical management of IBD in Asia. Initially, the committee members drafted 40 recommendations, which were then assessed according to Grading of Recommendations Assessment, Development and Evaluation. 8 statements were rejected as this indicated that consensus had not been reached. The recommendations encompass pre‐treatment evaluation; medical management of active IBD; medical management of IBD in remission; management of IBD during the peri‐conception period and pregnancy; surveillance strategies for colitis‐associated cancer; monitoring side effects of thiopurines and methotrexate; and infections in IBD.

Antibiotic exposure in early life can lead to a significant change of the gut microbiota and may contribute to later onset of inflammatory bowel disease (IBD). However, the relationship between early-life antibiotic treatment and IBD is ambiguous, according to contradicting results of epidemiologic studies. In the present study, we demonstrated that low-dose penicillin pre-treatment had a unique protective effect against mouse colitis induced by dextran sodium sulfate (DSS). Low-dose penicillin also suppressed the expression of pro-inflammatory cytokine IL-17 in various intestinal tissues, and decreased the amount of Th17 cells in small-intestine lamina propria. Neither metronidazole nor enrofloxacin had a similar effect. We further confirmed that low-dose penicillin could cause specific changes of the gut microbiota, especially the eradication of segmented filamentous bacteria (SFB). Mice without SFB inoculation showed no disparity when treated with penicillin or water. Taken together, the results showed that low-dose penicillin can achieve a highly specific manipulation of sensitive bacteria and interfere with development of intestinal immune system in early life. The study may further indicate the possibility of achieving a favorable immune state among a certain group of patients with IBD, or other autoimmune diseases, by fine-tuning the gut microbiota.