Objectives: The coronavirus disease 2019 (COVID-19) pandemic continues to pose profound challenges on society. Governments around the world have managed to mitigate its spread through strategies including social distancing; however, this may result in the adoption of sedentary lifestyle. This study aimed to investigate: 1) physical activity (PA) levels, sedentary behavior (SB) and sleep among young adults during COVID-19 epidemic, and 2) the change in these behaviors before and during the pandemic. Methods: A total of 631 young adults (38.8% males) participated in the cross-sectional study and completed an online survey that included five components: general information, COVID-19 related issues, PA, SB, and sleep. For longitudinal study, PA, SB, and sleep data collected from 70 participants before and during COVID-19 pandemic were analyzed. Results: Participants reported engaging in low PA, high SB and long sleep duration during COVID-19 pandemic. Females had greater concern for COVID-19 related issues and engaged in more prevention strategies than males. Moreover, a significant decline in PA while increase in both times spent in SB and sleep were determined after COVID-19 outbreak. Conclusion: The results of this study demonstrated a sedentary lifestyle in young adults in responses to social distancing during the COVID-19 pandemic, which will assist health policy makers and practitioners in the development of population specific health education and behavior interventions during this pandemic and for other future events.

Objective The aim of this study was to assess gut microbiota modifications after exercise in humans and animal models with obesity or type 2 diabetes and their role in exercise‐induced weight loss. Methods A systematic search of six databases was conducted on July 31, 2021. The extracted data on body fat or body weight from human and animal studies were analyzed using random‐effects meta‐analysis. Results A total of 28 studies were included, with all studies reporting exercise‐induced gut microbiota modifications; however, the modified taxa varied among studies. Proteobacteria was the only taxa reported to be altered by exercise in more than one human and one animal study. Taxa belonging to Firmicutes were the most responsive to exercise in humans and mice, whereas Proteobacteria taxa were the most responsive to exercise in rats. A meta‐analysis was conducted to examine the weight‐lowering effect of exercise based on data subgrouped by altered or unaltered α‐diversity or β‐diversity. The association between the weight‐lowering effect of exercise and altered β‐diversity was observed in humans with obesity but not in animals. Conclusions These findings suggest that gut microbiota modifications contribute to exercise‐induced weight loss in obesity; however, their precise contributions, especially those of taxon‐level variations, remain to be investigated.

Despite well-known systemic immune reactions in peripheral trauma, little is known about their roles in posttraumatic neurological disorders, such as anxiety, sickness, and cognitive impairment. Leukocyte invasion of the brain, a common denominator of systemic inflammation, is involved in neurological disorders that occur in peripheral inflammatory diseases, whereas the influences of peripheral leukocytes on the brain after peripheral trauma remain largely unclear. In this study, we found that leukocytes, largely macrophages, transiently invaded the brain of zebrafish larvae after peripheral trauma through vasculature-independent migration, which was a part of the systemic inflammation and was mediated by interleukin-1b (il1b). Notably, myeloid cells in the brain that consist of microglia and invading macrophages were implicated in posttraumatic anxiety-like behaviors, such as hyperactivity (restlessness) and thigmotaxis (avoidance), while a reduction in systemic inflammation or myeloid cells can rescue these behaviors. In addition, invading leukocytes together with microglia were found to be responsible for the clearance of apoptotic cells in the brain; however, they also removed the nonapoptotic cells, which suggested that phagocytes have dual roles in the brain after peripheral trauma. More importantly, a category of conserved proteins between zebrafish and humans or rodents that has been featured in systemic inflammation and neurological disorders was determined in the zebrafish brain after peripheral trauma, which supported that zebrafish is a translational model of posttraumatic neurological disorders. These findings depicted leukocyte invasion of the brain during systemic inflammation after peripheral trauma and its influences on the brain through il1b-dependent mechanisms.

The purpose of this study was to determine if acute intake of glutamine modulates homeostatic, hematologic, immune, and inflammatory responses to exhaustive exercise in the heat. Thirteen healthy, untrained young men participated in this randomized, double-blind, placebo-controlled, crossover study. They served as their own control and completed 2 trials of treadmill exercise at 40% maximal oxygen uptake to exhaustion in a hot environment (temperature, 38.0 ± 1.0 °C; relative humidity, 60.0% ± 5.0%; oxygen, 20.8%) following placebo (PLA) and glutamine (GLN) consumption. Heart rate, gastrointestinal temperature, forehead temperature, the rating of perceived exertion, and body weight were measured. Blood samples were collected before and after exercise. After exhaustive exercise in the heat (PLA vs. GLN: 42.0 ± 9.5 vs. 39.6 ± 7.8 min, p > 0.05), significant changes in homeostatic, hematologic, and immune parameters (elevated natural killer (NK) cells and neutrophils, and reduced CD4+/CD8+ ratio and CD19+ lymphocytes) were found in the control group owing to the time effect (p < 0.05). Moreover, a condition × time interaction effect was observed for the absolute count of CD3+ (F = 4.26, p < 0.05) and CD3+CD8+ T lymphocytes (F = 4.27, p < 0.05), which were elevated following acute glutamine intervention. While a potential interaction effect was also observed for the absolute count of CD3+CD4+ T lymphocytes (F = 3.21, p = 0.08), no condition or interaction effects were found for any other outcome measures. The results of this study suggest that acute glutamine ingestion evokes CD3+ and CD3+CD8+ T lymphocytosis but does not modulate neutrophil and NK cell leukocytosis and immune disturbances after exhaustive exercise in the heat.

Despite the well-described discrepancy between some of the macroautophagy/autophagy-related genes (ATGs) in the regulation of hematopoiesis, the varying essentiality of core ATGs in vertebrate definitive hematopoiesis remains largely unclear. Here, we employed zebrafish (Danio rerio) to compare the function of six core atgs from the core autophagy machineries, which included atg13, beclin1 (becn1), atg9a, atg2a, atg5, and atg3, in vertebrate definitive hematopoiesis via CRISPR-Cas9 ribonucleoprotein targeting. Zebrafish embryos with various atg mutations showed autophagic deficiency throughout the body, including hematopoietic cells. The atgs mutations unsurprisingly caused distinctive hematopoietic abnormalities in zebrafish. Notably, becn1 or atg9a mutation resulted in hematopoietic stem cells (HSCs) expansion during the development of the embryo into a larva, which can be attributed to the proteomic changes in metabolism, HSCs regulators, and apoptosis. Besides, atg3 mutation lowered the leukocytes in developing zebrafish embryos. Intriguingly, a synergistic effect on HSCs expansion was identified in atg13+becn1 and atg9a+atg2a or atg3 double mutations, in which atg13 mutation and atg2a or atg3 mutation exacerbated and mitigated the HSCs expansion in becn1 and atg9a mutations, respectively. In addition, the myeloid cell type-specific effects of various atgs were also determined between neutrophils and macrophages. Of these, a skewed ratio of neutrophils versus macrophages was found in atg13 mutation, while both of them were reduced in atg3 mutation. These findings demonstrated the distinct roles of atgs and their interplays in zebrafish definitive hematopoiesis, thereby suggested that the vertebrate definitive hematopoiesis is regulated in an atgs-dependent manner.

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METHODS:Parents or guardians of children with T1D (< 18 years) filled out an online survey. Anthropometric characteristics, PA, play and sport and sedentary time were collected before and after the introduction of restrictions. Moreover, we investigated the medical-related factors. RESULTS: a total of 280 children and adolescents (mean age was 11.8±3.3 years; 58.5% M) were included in the analysis. Before and after the introduction of restrictions, we reported a significant decline in participation in sport activities (-2.1±2.1 h/week) and a reduction in time spent in outdoor plays (-73.9±93.6 min/day). Moreover, we reported a significant increase in sedentary time (+144.7±147.8 min/day). Finally, an increase in mean glycaemic values (-25.4±33.4 mg/dL) and insulin delivery (in 71.8% of patients) were also recorded. CONCLUSIONS: a decline in participation in sport activities and a significant increase of sedentary time can influence the management of T1D in children and adolescents, influencing the risk of acute and long-term complications. Online exercise programs may be useful to maintain both the health and wellbeing of youth with T1D.

PTEN-induced putative kinase 1 (PINK1) is a well-characterized regulator of mitochondrial quality control through mitophagy and its mutations are associated with recessive Parkinson’s disease. However, little is known about its functions in normal and malignant hematopoiesis in vertebrates. Here we aim to unravel the roles of PINK1 in definitive hematopoiesis and its underlying mechanisms using zebrafish (Danio rerio). In this study, we utilized CRISPR/Cas9 system to generate pink1 knockout zebrafish model and PINK1-deficient leukemia cell line. We found that pink1 deficiency activated autophagy in hematopoietic cells and promoted definitive hematopoiesis in zebrafish embryos, which can be alleviated by canonical autophagy inhibition. Further, the proteomic and metabolic analysis revealed an elevated expression of cell proliferation markers and enhanced respiration in pink1-deficient zebrafish embryos. On the other hand, PINK1 deficiency also induced autophagy and cell proliferation in human leukemic cells. Therefore, our findings demonstrated that PINK1 functions as a negative regulator of normal and malignant hematopoiesis through the autophagy-mediated pathway.