Systematic and meta-based evaluation of the relationship between the built environment and physical activity behaviors among older adults.

Objectives: Existing assertions about the relationship between various factors of the built environment and physical activity behaviors are inconsistent and warrant further exploration and analysis. Methods: This study systematically searched PubMed, Embase, Web of Science, Scopus, the Cochrane Library and Google Scholar for the effect of the built environment on the physical activity behaviors of older adults. R software was used to calculate the meta-estimated odds ratio with a 95% confidence interval. Simultaneously, the quality of included studies was evaluated using an observational study quality evaluation standard recommended by American health care quality and research institutions. Results: A total of 16 original researches were included in this meta-analysis and eight factors of the built environment were evaluated. These factors which ranked from high to low according to their impact were traffic safety (OR = 1.58, 95% CI [1.14-2.20]), destination accessibility (OR = 1.24, 95% CI [1.06-1.44]), aesthetics of sports venues (OR = 1.21, 95% CI [1.07-1.37]), virescence of sports venues (OR = 1.14, 95% CI [1.06-1.23]), building density (OR = 1.07, 95% CI [1.02-1.13]). Additionally, it seemed that there was no potential association between mixed land use (OR = 1.01, 95% CI [0.92-1.10]), the quality of pedestrian facilities (OR = 1.00, 95% CI [0.92-1.08]) or commercial facilities (OR = 0.94, 95% CI [0.88-1.00]) and physical activity behaviors of older adults. Conclusions: The built environment has been found to exhibit a significant relationship with the physical activity behaviors of older adults. It is proposed that factors such as traffic safety, destination accessibility, aesthetics of sports venues, virescence of sports venues, and building density be given more consideration when aiming to promote physical activity levels among older adults.

A predicting model of child-bearing-aged women' spontaneous abortion by co-infections of TORCH and reproductive tract.

To develop a predicting model of child-bearing-aged women' spontaneous abortion (SA) by co-infections of TORCH and reproductive tract, in order to provide a reference tool for accurately predicting the risk of SA and guide the early prevention, diagnosis and treatment of SA. A prospective cohort study was designed based on 218 958 child-bearing-aged women following up in Hebei province in China from 2010 to 2017. Multivariable logistic regression analysis was used to select candidate predictive variables. Fisher's discriminant analysis was performed to build a predictive model, and the validity of the model was evaluated. The incidence rate of SA was 2.4%. Multivariable logistic regression analysis showed that age (OR = 3.507), adverse pregnancy history (OR = 1.509), co-infections status of Candida and HBsAg (ORCandida positive×HBsAg negative  = 4.091, ORCandida negative×HBsAg positive  = 3.327, and ORCandida positive×HBsAg positive  = 13.762), and co-infections status of HBsAg, Rubella (IgG) and CMV (IgG) (ORHBs-Ag negative×Rubella (IgG) negative×CMV (IgG) positive  = 1.789, ORHBs-Ag positive×Rubella (IgG) positive×CMV (IgG) negative  = 3.809, and ORHBsAg positive×Rubella (IgG) positive×CMV (IgG) positive  = 11.919) were the independent predictors of SA. The total discriminant rate reached 91%, with 82% of the sensitivity and 91% of the specificity. The predicting model of child-bearing-aged women' SA by co-infections status has a good performance. The co-infection status of TORCH and reproductive tract are suggested to be considered in pre-pregnancy physical examination.

Expression profiles of SLC39A/ZIP7, ZIP8 and ZIP14 in response to exercise-induced skeletal muscle damage.

BACKGROUND: Zinc transporters are thought to facilitate the mobilization of zinc (Zn) and the role of Zn as a signaling mediator during cellular events. Little is known about the response of Zn movement and zinc transporters during muscle proliferation and differentiation processes after damage. METHODS: After rats were subjected to one 90-min session of downhill running to cause muscle damage, the gastrocnemius muscles were harvested to assess the expression of zinc transporters SLC39A/ZIP7, ZIP8, ZIP14 and myogenic regulatory factors at the 0 h, 6 h, 12 h, 1 d, 2 d, 3 d, 1 w and 2 w time points after exercise. RESULTS: SLC39A/ZIP7, ZIP8 and ZIP14 had translocated to different compartments of the cell following damage, and they exhibited differential expression profiles after eccentric exercise. The results regarding the myogenetic regulators showed that nf-κb was upregulated 2 d after exercise, and STAT3 and Akt1 mRNA levels were mostly expressed 2 w after exercise. The upregulation of phosphatidylinositol 3-kinase, catalytic subunit gamma (pik3cg), erk1 and erk2 mostly occurred at the early stage (6 h or 12 h) after exercise. In addition, we found that zip7, zip8 and zip14 expression was moderately correlated with certain markers of muscle regeneration. CONCLUSION: The zinc transporters SLC39A/ZIP7, ZIP8 and ZIP14 have differential expression profiles upon eccentric exercise, and they might regulate muscle proliferation or differentiation processes through different cellular pathways after exercise-induced muscle damage.

Eccentric exercise results in a prolonged increase in interleukin-6 and tumor necrosis factor-α levels in rat skeletal muscle.

Interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) are well-known cytokines with pro-inflammatory capabilities, and have been shown to be involved in adaptation to exercise as multifaceted myokines. However, the precise role of IL-6 and TNF-α during exercise-induced skeletal muscle injury and subsequent repair processes is not fully understood. In this study, IL-6 and TNF-α were examined in soleus muscles at the gene and protein levels using in situ hybridization and immunohistochemical staining, respectively, and serum levels of IL-6 and TNF-α were determined before and after a 90-min downhill running session in rats. There were no changes in serum levels of IL-6 and TNF-α after exercise, but IL-6 and TNF-α mRNA increased and maintained high expression in muscles for 1-2 weeks after exercise. IL-6 and TNF-a mRNAs were identified in both the cytoplasm and the nuclei of myocytes, as well as in invading inflammatory cells. IL-6 and TNF-α protein mainly distributed in cytoplasm unevenly and had a prolonged expression until 2 weeks after eccentric exercise. Our results demonstrate that there is increased IL-6 and TNF-α expression in skeletal muscle that is induced by eccentric exercise and that the high expression of IL-6 and TNF-α in the long-term phase after eccentric exercise may be more involved in the subsequent recovery of damaged muscle.

Aging of the immune system causes reductions in muscle stem cell populations, promotes their shift to a fibrogenic phenotype, and modulates sarcopenia.

Aging is associated with diminished muscle mass, reductions in muscle stem cell functions, and increased muscle fibrosis. The immune system, especially macrophages, can have important roles in modulating muscle growth and regeneration, suggesting that the immune system may also have significant influences on muscle aging. Moreover, the immune system experiences changes in function during senescence, suggesting that regulatory interaction between muscle cells and the immune system may also change during aging. In this study, we performed bone marrow transplantations between age-mismatched donor and recipient mice to test the influence of the age of the immune system on muscle aging. Transplantation of young bone marrow cells into old recipients prevented sarcopenia and prevented age-related change in muscle fiber phenotype. Transplantation of old bone marrow cells into young animals reduced satellite cell numbers and promoted satellite cells to switch toward a fibrogenic phenotype. We also demonstrated that conditioned media from young, but not old, bone marrow cells promoted myoblast proliferation in vitro, and we found that factors released by young bone marrow cells were more supportive of myotube differentiation in vitro. Together, our results demonstrate that aging of bone marrow cells promotes the age-related reduction of satellite cell number and function and contributes to sarcopenia.-Wang, Y., Wehling-Henricks, M., Welc, S. S., Fisher, A. L., Zuo, Q., Tidball, J. G. Aging of the immune system causes reductions in muscle stem cell populations, promotes their shift to a fibrogenic phenotype, and modulates sarcopenia.

Response of macrophages in rat skeletal muscle after eccentric exercise.

PURPOSE: Macrophages are known to be important for healing numerous injured tissues depending on their functional phenotypes in response to different stimuli. The objective of this study was to reveal macrophage phenotypic changes involved in exercise-induced skeletal muscle injury and regeneration. METHODS: Adult male Sprague-Dawley rats experienced one session of downhill running (16° decline, 16 m/min) for 90 min. After exercise the blood and soleus muscles were collected at 0 h, 6 h, 12 h, 1 d, 2 d, 3 d, 1 w and 2 w after exercise, separately. RESULTS: It was showed that CD68+ M1 macrophages mainly infiltrated into muscle necrotic sites at 1-3 d, while CD163+ M2 macrophages were present in muscles from 0 h to 2 weeks after exercise. Using transmission electron microscopy, we observed activated satellite cells 1 d after exercise. Th1-associated transcripts of iNOS and Ccl2 were inhibited post exercise, while COX-2 mRNA was dramatically increased 12 h after running (p < 0.01). M2 phenotype marker Arg-1 increased 12 h and 3 d (p < 0.05, p < 0.01) after exercise, and Clec10a and Mrc2 were up-regulated in muscles 12 h following exercise (p < 0.05, p < 0.05). CONCLUSION: The data demonstrate the dynamic patterns of macrophage phenotype in skeletal muscle upon eccentric exercise stimuli, and M1 and M2 phenotypes perform different functions during exercise-induced skeletal muscle injury and recovery.

MicroRNAs in the regeneration of skeletal muscle.

MicroRNAs (miRNAs) have emerged as critical regulators of numerous biological processes by modulating gene expression at the post-transcriptional level. The discovery of miRNAs as new and important regulators of gene expression is expected to broaden our biological understanding of the regulatory mechanism in muscle by adding another dimension of regulation to the diversity and complexity of gene-regulatory networks. Exercise-induced skeletal muscle injury and repair have always been among the highlights of research in sports medicine. However, many mechanism problems that occur during regeneration and repair in the aftermath of skeletal muscle injury remain unsolved. It has become increasingly clear that the regeneration of skeletal muscle development involve regulation by miRNAs. In the last few years the field has seen a rapid expansion of our knowledge of miRNAs in the regeneration of skeletal muscle. This study reviews the miRNAs related with regeneration of skeletal muscle, and discuss the regulation of their expression in muscles, and emerging themes of miRNA regulation.