The metabolic effects of habitual leg shaking: A randomized crossover trial.

AIMS: The adverse effects of sedentary behavior on obesity and chronic diseases are well established. However, the prevalence of sedentary behavior has increased, with only a minority of individuals meeting the recommended physical activity guidelines. This study aimed to investigate whether habitual leg shaking, a behavior traditionally considered unfavorable, could serve as an effective strategy to improve energy metabolism. MATERIALS AND METHODS: A randomized crossover study was conducted, involving 15 participants (mean [SD] age, 25.4 [3.6]; mean [SD] body mass index, 22 [3]; 7 women [46.7%]). The study design involved a randomized sequence of sitting and leg shaking conditions, with each condition lasting for 20 min. Energy expenditure, respiratory rate, oxygen saturation, and other relevant variables were measured during each condition. RESULTS: Compared to sitting, leg shaking significantly increased total energy expenditure [1.088 kj/min, 95% confidence interval, 0.69-1.487 kj/min], primarily through elevated carbohydrate oxidation. The average metabolic equivalent during leg shaking exhibited a significant increase from 1.5 to 1.8. Leg shaking also raised respiratory rate, minute ventilation, and blood oxygen saturation levels, while having no obvious impact on heart rate or blood pressure. Electromyography data confirmed predominant activation of lower leg muscles and without increased muscle fatigue. Intriguingly, a significant correlation was observed between the increased energy expenditure and both the frequency of leg shaking and the muscle mass of the legs. CONCLUSIONS: Our study provides evidence that habitual leg shaking can boost overall energy expenditure by approximately 16.3%. This simple and feasible approach offers a convenient way to enhance physical activity levels.

New hope for cancer treatment: exploring the distinction between normal adult stem cells and cancer stem cells.

For decades, intensive studies have attempted to identify the mechanisms underlying malignant tumor growth. Despite significant progress, most therapeutic approaches fail to eliminate all tumor cells. The remaining tumor cells often result in recurrence and metastasis. Recently, the idea of a cancer stem cell was proposed to explain of the origin of cancer cells. According to this hypothesis, a small fraction of tumor cells have the capacity for self-renewal, with unlimited slow proliferation potential. They are often resistant to chemotherapy and radiation and thus are responsible for continuously supplying new cancer cells, which themselves may have a limited life span. In recent years, accumulating experimental evidence supports this hypothesis and provides new possibilities to conquer cancer. This review will focus on the distinction between normal adult stem cells and cancer stem cells and identifies possible key targets for effective therapies of cancer.

NANOG has a role in mesenchymal stem cells' immunomodulatory effect.

It is well known that terminally differentiated cells derived from mesenchymal stem cells (MSCs) will lose the immunomodulation capacity. NANOG is known to be a core transcription factor in the maintenance of stem cell specific features or stemness. To evaluate whether NANOG was involved in the immunomodulation effects of MSCs, MSCs' immunomodulation capacity on lymphocyte activation and proliferation before or after endogenous NANOG interference was investigated. We found that MSCs' inhibitory effects on lymphocyte activation and proliferation was significantly weakened after NANOG knockdown. In addition, NANOG RNAi and chromatin immunoprecipitation experiments showed that NANOG suppressed the expression and secretion of DKK-1, transforming growth factor-beta1 (TGF-ß1), TGF-ß2, and TGF-ß3, which are all important factors mediating MSCs' immunomodulation capacity. Based on these data, we propose that NANOG plays an important role in maintaining the immunomodulation functions of MSCs by regulating the expression and secretion of TGF-ß1, TGF-ß2, TGF-ß3, and DKK-1.

Inhibition of hepatic stellate cells proliferation by mesenchymal stem cells and the possible mechanisms.

AIM: During fibrosis, hepatic stellate cells (HSCs) undergo a complex activation process characterized by increased proliferation and extracellular matrix deposition. Previous studies have suggested that mesenchymal stem cells (MSCs) may ameliorate fibrogenesis and represent a promising strategy for cell therapy. However, the underlying mechanisms are not fully understood. METHODS: Hepatic stellate cells were treated with or without MSCs. Then cell proliferation and cell cycle were analyzed. Production of soluble factors by MSCs and its relation with cell proliferation suppression was evaluated by transwell co-culture and RNA interference. Effects of MSCs on the gene expression of collagen were also evaluated. RESULTS: MSCs induced G(0)/G(1) arrest of HSCs growth partly through secreting soluble factors TGF-beta3 and HGF, which resulted in up-regulation of p21(Cip1) and p27(Kip1) expression and down-regulation of cyclinD1. MSCs inhibited the phosphorylation of extracellular signal-regulated kinase (ERK) 1/2 and reduced gene expression of collagen type I and III. MSCs did not reverse the proliferation and collagen type I gene expression of HSCs provoked by PDGF. CONCLUSIONS: The growth inhibition of HSCs induced by MSCs through an arrest in the G(0)/G(1) phase of the cell cycle is partially mediated by secretion of TGF-beta3 and HGF. MSCs inhibit HSCs activation through decreasing phosphorylation of extracellular signal-regulated kinase (ERK) 1/2. These results further support MSCs may be used as a novel therapy for treating fibrotic diseases in human.