肚皮舞操与产褥操对产妇后期体形的影响

目的探讨产后肚皮舞操与产褥操对产妇体形及盆底肌张力恢复的效果。方法对102例志愿参与的顺产产妇,于产后第2天开始进行产褥操锻炼,每1～2天增加1节,共七节,到全部掌握。产后4周末,随机将产妇分为产褥操组和肚皮舞操组。于产后8周末、16周末随访产妇的腰围、臀围、腹部皮褶、体质量指数和盆底肌张力恢复指标。结果两组产妇8周末体形客观状态和盆底肌张力指标比较,差异无统计学意义(P>0.05),而两组产妇16周末体形客观状态和盆底肌张力恢复指标比较,差异有统计学意义(P<0.05)。结论产后后期肚皮舞操比产褥操能更好的恢复产妇的体形和盆底肌张力。     

Core muscle functional strength training for reducing the risk of low back pain in military recruits: An open-label randomized controlled trial

Background: Core muscle functional strength training(CMFST) has been reported to reduce injuries to the lower extremity. However, no study has confirmed whether CMFST can reduce the risk of low back pain(LBP).Objective: This study identified the effects of CMFST on the incidence of LBP in military recruits.Design, setting, participants and intervention: We performed a prospective, open-label, randomized, controlled study in a population of young healthy male naval recruits from a Chinese basic c...     

The Effect of a 2-Year Intervention Consisting of Diet,Physical Exercise,Cognitive Training,and Monitoring of Vascular Risk on Chronic Morbidity—the FINGER Randomized Controlled Trial

Objective

To verify whether a multidomain intervention lowers the risk of developing new chronic diseases in older adults.

Differential Effects of Dietary versus Exercise Intervention on Intrahepatic MAIT Cells and Histological Features of NAFLD

Background: Mucosal-associated invariant T (MAIT) cells promote inflammation in obesity and are implicated in the progression of non-alcoholic fatty liver disease (NAFLD). However, as the intrahepatic MAIT cell response to lifestyle intervention in NAFLD has not been investigated, this work aimed to examine circulating and intrahepatic MAIT cell populations in patients with NAFLD, after either 12 weeks of dietary intervention (DI) or aerobic exercise intervention (EI). Methods: Multicolour flow cytometry was used to immunophenotype circulating and intrahepatic MAIT cells and measure MAIT cell expression (median fluorescence intensity, MFI) of the activation marker CD69 and apoptotic marker CD95. Liver histology, clinical parameters, and MAIT cell populations were assessed at baseline (T0) and following completion (T1) of DI or EI. Results: Forty-five patients completed the study. DI participants showed decreased median (interquartile range) expression of the activation marker CD69 on circulating MAIT cells (T0: 104 (134) versus T1 27 (114) MFI; p = 0.0353) and improvements in histological steatosis grade post-intervention. EI participants showed increased expression of the apoptotic marker CD95, both in circulating (T0: 1549 (888) versus T1: 2563 (1371) MFI; p = 0.0043) and intrahepatic MAIT cells (T0: 2724 (862) versus T1: 3117 (1622) MFI; p = 0.0269). Moreover, the percentage of intrahepatic MAIT cells significantly decreased after EI (T0: 11.1 (14.4) versus T1: 5.3 (9.3)%; p = 0.0029), in conjunction with significant improvements in fibrosis stage and hepatocyte ballooning. Conclusions: These data demonstrate independent benefits from dietary and exercise intervention and suggest a role for intrahepatic MAIT cells in the observed histological improvements in NAFLD.     

Resistance Exercise Training Improves Metabolic and Inflammatory Control in Adipose and Muscle Tissues in Mice Fed a High-Fat Diet

This study investigates whether ladder climbing (LC), as a model of resistance exercise, can reverse whole-body and skeletal muscle deleterious metabolic and inflammatory effects of high-fat (HF) diet-induced obesity in mice. To accomplish this, Swiss mice were fed for 17 weeks either standard chow (SC) or an HF diet and then randomly assigned to remain sedentary or to undergo 8 weeks of LC training with progressive increases in resistance weight. Prior to beginning the exercise intervention, HF-fed animals displayed a 47% increase in body weight (BW) and impaired ability to clear blood glucose during an insulin tolerance test (ITT) when compared to SC animals. However, 8 weeks of LC significantly reduced BW, adipocyte size, as well as glycemia under fasting and during the ITT in HF-fed rats. LC also increased the phosphorylation of Akt_Ser473 and AMPK_Thr172 and reduced tumor necrosis factor-alpha (TNF-α) and interleukin 1 beta (IL1-β) contents in the quadriceps muscles of HF-fed mice. Additionally, LC reduced the gene expression of inflammatory markers and attenuated HF-diet-induced NADPH oxidase subunit gp91phox in skeletal muscles. LC training was effective in reducing adiposity and the content of inflammatory mediators in skeletal muscle and improved whole-body glycemic control in mice fed an HF diet.     

How Diet and Physical Activity Modulate Gut Microbiota: Evidence,and Perspectives

Gut microbiota plays a significant role in the maintenance of physiological homeostasis, contributing to human health. Nevertheless, some factors (sex, age, lifestyle, physical activity, drug-based therapies, diet, etc.) affect its composition and functionality, linked to pathologies and immunological diseases. Concerning diet, it interacts with microorganisms, leading to beneficial or detrimental outcomes for the health of host. On the other hand, physical activity is known to be useful for preventing and, sometimes, treating several diseases of cardiovascular, neuroendocrine, respiratory, and muscular systems. This paper focuses on diet and physical activity presenting the current knowledge about how different diets (Western, ketogenic, vegan, gluten free, Mediterranean) as well as different types of exercise (intensive, endurance, aerobic) could shape gut microbiota.     

Effects of Internet-Based Nutrition and Exercise Interventions on the Prevention and Treatment of Sarcopenia in the Elderly

Effective nutrition and exercise interventions may improve sarcopenia in the elderly. The purpose of our study was to investigate the effectiveness of Internet-based nutrition and exercise interventions in the elderly with sarcopenia. Participants were divided into 4 groups: control, nutrition, exercise, and comprehensive (nutrition plus exercise) groups; there was at least 50 participants in each group. Our trial lasted 12 weeks. We conducted dietary and exercise interventions through an app and collected feedback from the participants every three weeks. Information on the diet, skeletal muscle mass, and muscle function was collected before and after the interventions. The comprehensive group had higher high-quality protein intake than the control (p = 0.017) and exercise (p = 0.012) groups. After the interventions, we obtained differences in skeletal muscle mass, skeletal muscle mass/height², skeletal muscle mass/weight, muscle mass/BMI, and skeletal muscle mass/body fat percentage (p < 0.05). Changes in average daily energy and total daily protein intakes were not significantly different; however, there was an overall improvement in the intervention groups relative to baseline data. There were no changes in the average daily time of moderate physical activity. The Internet was an effective tool of nutrition intervention in the elderly with sarcopenia. The Internet-based nutrition intervention improved high-quality protein intake and skeletal muscle mass in the elderly with sarcopenia.     

力竭运动致大鼠心肌损伤及S100A4蛋白表达变化

目的观察S100A4蛋白在力竭运动损伤心肌组织中的表达变化,探讨S100A4蛋白对力竭运动损伤心肌组织的作用。方法 W istar大鼠12只,随机分为对照组和力竭运动组,大鼠进行力竭训练10d后,取血及心肌组织,用光镜和电镜对心肌进行组织学观察;采用蛋白免疫印迹(western-b lot)法和免疫组织化学法检测心肌蛋白表达。结果力竭运动组大鼠心肌组织苏木精-伊红(HE)染色可见大鼠心肌和血管内皮细胞空泡变性和心肌间质水肿等;电镜可见血管内皮细胞发生典型细胞凋亡特征;W estern-b lot结果表明,对照组心肌中S100A4蛋白弱表达,而力竭运动组S100A4蛋白表达量升高;免疫组化结果显示,与对照组比较,力竭运动组心肌中S100A4蛋白表达升高1.68倍,且在心肌和血管内皮细胞中均有表达。结论力竭运动造成大鼠心肌损伤,S100A4蛋白在损伤心肌中表达升高。     

临床带教老师要注重培养护生的“慎独”修养

本文从“慎独”修养的含义、“慎独”在护理工作中的重要性出发，就如何培养和锻炼实习 护生阐述了自己的观点，临床带教老师应通过言传身教，使实习护生提高认识，刻意追求，努力达到 “慎独”。     

Primary cilia in satellite cells are the mechanical sensors for muscle hypertrophy

Skeletal muscle atrophy is commonly associated with aging, immobilization, muscle unloading, and congenital myopathies. Generation of mature muscle cells from skeletal muscle satellite cells (SCs) is pivotal in repairing muscle tissue. Exercise therapy promotes muscle hypertrophy and strength. Primary cilium is implicated as the mechanical sensor in some mammalian cells, but its role in skeletal muscle cells remains vague. To determine mechanical sensors for exercise-induced muscle hypertrophy, we established three SC-specific cilium dysfunctional mouse models—Myogenic factor 5 (Myf5)-Arf-like Protein 3 (Arl3)^−/−, Paired box protein Pax-7 (Pax7)-Intraflagellar transport protein 88 homolog (Ift88)^−/−, and Pax7-Arl3^−/−—by specifically deleting a ciliary protein ARL3 in MYF5-expressing SCs, or IFT88 in PAX7-expressing SCs, or ARL3 in PAX7-expressing SCs, respectively. We show that the Myf5-Arl3^−/− mice develop grossly the same as WT mice. Intriguingly, mechanical stimulation-induced muscle hypertrophy or myoblast differentiation is abrogated in Myf5-Arl3^−/− and Pax7-Arl3^−/− mice or primary isolated Myf5-Arl3^−/− and Pax7-Ift88^−/− myoblasts, likely due to defective cilia-mediated Hedgehog (Hh) signaling. Collectively, we demonstrate SC cilia serve as mechanical sensors and promote exercise-induced muscle hypertrophy via Hh signaling pathway.

Exercise is considered as the primary intervention to improve muscle strength and to counteract muscle atrophy. While physical exercise training is considered a suitable intervention to improve muscle strength and endurance in healthy individuals, some people are resistant to the beneficial effects of exercise (1–3). It has been debated whether exercise is beneficial or harmful for patients with myopathic disorders (4) and type 2 diabetes (5). This so-called “exercise resistance” is considered congenital, and one recently identified causative factor involved in exercise resistance is hepatokine selenoprotein P (2, 6).Primary cilia have a mechanosensory function in bone cells (7), renal cells (8), and airway smooth muscle cells exert a role in sensing oscillatory fluid flow and transducing extracellular mechano-chemical signals into intracellular biochemical responses (9). Intriguingly, low muscle tone is a clinical feature often present in congenital ciliopathies with unclear underlying mechanisms (10). Arf-like Protein 3 (ARL3) is a highly conserved ciliary protein across ciliated organisms. ARL3, a regulator of intraflagellar transport in primary cilia, has been reported involving with various ciliary signaling functions (11, 12) and maintaining cell division polarity (13). Arl3 mutations cause Joubert syndrome (14, 15). Arl3^−/− knockout does not affect cilia structure but compromises ciliary function (16).Cells utilize primary cilia to convert environmental cues, mechanical or chemical, into various cellular signaling essential for development (17–21). During skeletal muscle development, Hedgehog (Hh) signaling helps to initiate the myogenic program (22). In myoblast cells, Fu et al. (23) showed that primary cilia are assembled during the initial stages of myogenic differentiation but disappear as cells progress through myogenesis. The ablation of primary cilia suppresses Hh signaling and myogenic differentiation while enhancing proliferation. However, there are still significant gaps in our understanding of how exercise and mechanical signals activate the Hh signaling pathway. In the present study, we hypothesize that primary cilia in satellite cells (SCs) transduce mechanical stimulation through activation of Hh signaling and promote muscle hypertrophy induced by exercise.Hypertrophy of skeletal muscle is a complex biological process that involves multiple cell types, including SCs, fibro-adipogenic precursors, endothelial cells, fibroblasts, pericytes, and immune cells. Removing cilia from fibro-adipogenic precursors can reduce intramuscular adipogenesis and increase myofibril size during muscle healing (24). SCs play an essential role in muscle hypertrophy and exercise adaptation (25, 26), especially in young mice (27). Mechanical signals can interrupt SC suppression in a skeletal muscle loss model induced by ovariectomy. Diminished SC number and elevated adipogenic gene expression in muscle caused by ovariectomy are averted by mechanical stimulation (28). Experiments in vitro indicate that mechanical stimulation enhances the fusion of SCs (29). SCs are a heterogeneous population of stem cells and committed progenitors (30). Paired box protein Pax-7 (Pax7) is a traditional marker of SCs and acts at different levels in a nonhierarchical regulatory network controlling SC-mediated muscle hypertrophy (31). A major target gene of Pax7 is Myogenic factor 5 (Myf5), and loss of Pax7 significantly decreases Myf5 expression in myoblasts (32). However, Myf5 is present in Pax3/Pax7 double mutants, indicating Myf5 activation occurs independently of Pax3/Pax7 (33). Furthermore, 10% of Pax7-expressing satellite cells have never expressed Myf5 (30). Parise et al. (34) observed an approximately sixfold increase in the number of Myf5-expressing cells by 48 h following exercise, which remained elevated until at least 96 h after exercise. We established three mouse models of Myf5-Arl3^−/−, Pax7-Intraflagellar transport protein 88 homolog (Ift88^−/−), and Pax7-Arl3^−/− to investigate the SC during mechanical stimulation and exercise. In the present study, we provide exciting evidence that SC cilia act as the key mechanical sensor for exercise-induced hypertrophy.