The purpose of this study has been to investigate the possible effects of the normal joint cavity environment on chondrocytic differentiation of bone-marrow-derived mesenchymal stem cells (MSCs). Autologous bone marrow was aspirated from the iliac crest of male sheep. MSCs were purified, expanded, and labeled with the fluorescent dye PKH26. Labeled MSCs were then grown on a three-dimensional porous scaffold of poly (L-lactic-co-glycolic acid) in vitro and implanted into the joint cavity by a surgical procedure. At 4 or 8 weeks after implantation, the implants were removed for histochemical and immunohistochemical analysis. The cells labeled with red fluorescent PKH26 in the implants expressed type II collagen and synthesized sulfated proteoglycans. However, the osteoblast-specific marker, osteocalcin, was not detected by immunohistochemistry indicating that the implanted MSCs had not differentiated into osteoblasts by being directly exposed to the normal joint cavity. To investigate the possible factors involved in chondrocytic differentiation of MSCs further, we co-cultured sheep MSCs with the main components of the normal joint cavity, viz., synovial fluid or synovial cells, in vitro. After 1 or 2 weeks of co-culture, the MSCs in both co-culture systems expressed markers of chondrogenesis. These results suggest that synovial fluid and synovium from normal joint cavity are important for the chondrocytic differentiation of adult bone-marrow-derived MSCs.
BACKGROUND: The goal of this study was to evaluate the effects of resistance training on subjects with COPD. METHODS: We performed a systematic search in MEDLINE, PubMed, Embase, CINAHL, Elsevier ScienceDirect, EBM Reviews, Cochrane Central Register of Controlled Trials, and ClinicalTrials.gov and also of leading respiratory journals for randomized controlled trials on COPD treatment for > 4 weeks with resistance training compared with non-exercise control or with combined resistance and endurance training compared with endurance training alone. Data from these studies were pooled to calculate odds ratio and weighted mean differences (WMDs) with 95% CI. RESULTS: Eighteen trials with 750 subjects with advanced COPD met the inclusion criteria. There were 2 primary and 5 secondary outcomes. Compared with non-exercise control, resistance training led to significant improvements in the dyspnea domain of the Chronic Respiratory Disease Questionnaire (WMD of 0.59, 95% CI 0.26 -0.93, I2 ؍ 0%, P < .001), skeletal muscle strength, and percent-of-predicted FEV 1 (WMD of 6.88%, 95% CI 0.41-13.35%, I2 ؍ 0%, P ؍ .04). The combination of resistance and endurance training significantly improved the St George Respiratory Questionnaire total score (WMD of ؊7.44, 95% CI ؊12.62 to ؊2.25, I2 ؍ 0%, P ؍ .005), each domain score, and skeletal muscle strength. There were no significant differences in 6-min walk distance, 6-min pegboard and ring test, maximum exercise work load, and maximum oxygen consumption between the 2 groups. There were no reports of adverse events related to resistancetraining intervention. CONCLUSIONS: Resistance training can be successfully performed alone or in conjunction with endurance training without increased adverse events during pulmonary rehabilitation in COPD.
Polygonatum cyrtonema lectin (PCL), a mannose/sialic acid-binding lectin isolated from the rhizomes of Polygonatum cyrtonema Hua, has been reported to possess remarkable anti-tumour effects via inducing apoptosis and autophagy. The aim of this study was to investigate the molecular mechanisms mediating PCL-induced apoptosis and autophagy in A549 cells. Herein, we found that the treatment of A549 cells with PCL caused a remarkable generation of reactive oxygen species (ROS) and ROS scavenger N-acetyl-cysteine (NAC) inhibited PCL-induced apoptosis and autophagy. In addition, PCL treatment activated mitogen-activated protein kinase (MAPK) members extracellular signal-regulated kinase (ERK), JNK and p38, JNK inhibitor and p38 inhibitor partially reduced PCL-induced apoptosis and autophagy. Moreover, PCL administration activated NF-κB survival pathway in A549 cells, NF-κB inhibitor Bay11-7082 promoted PCL-induced apoptosis. Importantly, we found PCL may bind to the cell surface in a mannose-specific manner, and was then internalized and accumulated primarily onto the mitochondria. These findings may provide a new perspective of PCL as a potential anti-tumour drug targeting apoptosis and autophagy pathways for future cancer therapeutics.
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