Obesity is a well-known primary risk factor for osteoarthritis (OA). In recent decades, the biomechanicsbased theoretical paradigm for the pathogenesis of obesity-associated OA has been gradually but fundamentally modified. This modification is a result of accumulating evidence that biological factors also contribute to the etiology of the disease. The gut microbiota is a complicated ecosystem that profoundly influences the health of the host and can be modulated by the combined effects of environmental stimuli and genetic factors. Recently, enteric dysbacteriosis has been identified as a causal factor in the initiation and propagation of obesity-associated OA in animal models. Gut microbes and their components, microbe-associated lipid metabolites, and OA interact at both systemic and local levels through mechanisms that involve interplay with the innate immune system. However, the demonstration of causality in humans will require further studies. Nonetheless, probiotics, prebiotics, dietary habits and exercise, which aid the restoration of a healthy microbial community, are potential therapeutic approaches in the treatment of obesity-associated OA.

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Autism spectrum disorder (ASD) is a complex and heterogeneous neurodevelopmental disorder characterized by stereotyped behaviors, specific interests, and impaired social and communication skills. Synapses are fundamental structures for transmitting information between neurons. It has been reported that synaptic deficits, such as the increased or decreased density of synapses, may contribute to the onset of ASD, which affects the synaptic function and neuronal circuits. Therefore, targeting the recovery of the synaptic normal structure and function may be a promising therapeutic strategy to alleviate ASD symptoms. Exercise intervention has been shown to regulate the structural plasticity of synapses and improve ASD symptoms, but the underlying molecular mechanisms require further exploration. In this review, we highlight the characteristics of synaptic structural alterations in the context of ASD and the beneficial effects of an exercise intervention on improving ASD symptoms. Finally, we explore the possible molecular mechanisms of improving ASD symptoms through exercise intervention from the perspective of regulating synaptic structural plasticity, which contributes to further optimizing the related strategies of exercise intervention promoting ASD rehabilitation in future.

Objective Objective: To study the changes of mitochondrial autophagy-related genes and autophagosome after skeletal muscle blunt trauma, to reveal the changes of mitochondrial adaptive repair process after skeletal muscle blunt trauma, and to elucidate the mechanism of blunt trauma repair process. Methods Methods: Sixty - four male Wistar rats were randomly divided into control group and blunt trauma group三 (divided into 12h group, 2d group, 5d group, 7d group, 10d group, 15d group and 30d group) according to the time of extraction. The expression of HIF-1α, AMPKα2, BNIP3 and NIX protein in skeletal muscle hypoxia and autophagy-related factors were measured by Western-Blot. QRT-PCR was performed to analyze the expression levels of HIF-1α, AMPKα2, BNIP3 and NIX. The ultrastructure and autophagic formation at different time points were observed by transmission electron microscopy (TEM). Results Results: The expression of HIF-1α and AMPKα2 protein reached the peak at 12h and 2d, and the expression of HIF-1α was significantly higher than that of the control group (P <0.05). The expression of AMPKα2 was significantly higher at 5 days after injury (P <0.05), and reached the normal level at 10 days. BNIP3 began to decline after 5 days, but still higher than normal at 10 days after treatment. NIX expression peak appeared at 12h and 2d after injury, with high-express to 7d. The expression of HIF-1α and AMPKα2 mRNA was significantly higher than that of the control group (P <0.01), but decreased until 5d (P <0.05), then decreased to normal level. The mRNA expression of BNIP3 and NIX was basically the same as their protein performance. A number of autophagosomes were observed at 12 h after injury, and the number of autophagosomes increased gradually at 2-7 d. After 10 days, the number of autophagosomes decreased compared with that of 12 h-7 d after blunt. And after 15 days, the number of autophagosites decreased gradually. Conclusions Conclusion: The changes of early stage metabolic regulator AMPKα2 and hypoxia-sensitive factor HIF-1αafter skeletal muscle blunt trauma indicated that  an energy crisis occurred in the skeletal muscle after injury, and the hypoxic environment was formed. The mitochondrial autophagy, the expression of BNIP3 and NIX showed that mitochondrial autophagy was activated and hypoxia induced mitochondrial autophagy at early skeletal muscle contusion peroid. Hypoxia-induced mitochondrial autophagy could remove the damaged mitochondria, maintain mitochondrial quality and provide raw materials for new mitochondria generation, facilitate the rapid recovery of damaged skeletal muscle, which may be a compensatory mechanism of the body response to injury.

Objective To examine the effect of voluntary wheel-running exercise on cartilage morphology of knee osteoarthritis(KOA) in obese mice induced by high-fat diet,and explore the protective role of 4 weeks voluntary wheel-running exercise on KOA,finally providing effective experimental evidence for clinical treatment of knee osteoarthritis. Methods C57BL/6J mice were randomly assigned to the C-Sed group,C-Ex group,HF-Sed group and HF-Ex group.The control groups were fed a control diet(13.5% kcal from fat),and the high-fat groups were fed a high-fat diet(60% kcal from fat).After feeding 8 weeks different diets,the exercise groups were starting running.In order to examine the effect of voluntary wheel-running exercise on cartilage morphology of KOA,the joint of knee were harvested to be fixed,decalcified and embedded in paraffin,and the four-micrometer-thick sections were stained with both HE and toluidine blue . Results After feeding twelve weeks different diets,the body mass of the high-fat diet group mice has a significant increase,which demonstrates that high-fat diet could successfully induce the mice obese.From the results of HE and toluidine blue,in comparison to the C-Sed group,the surface of the knee articular cartilage in the HF-Sed group was not intact and smooth,and the thickness of articular cartilage has a significant decrease（p<0.001）;contrary to the HF-Sed group,the surface of the knee articular cartilage in HF-Ex group was slightly smooth,and there was significant increase in cartilage thickness. Conclusions Four weeks voluntary wheel-running exercise can increase cartilage thickness ,decrease the Mankin’s score and delay the degeneration of knee cartilage in obese mice.To conclude,the short-term wheel-running exercise protects against obesity-induced KOA.