DESIGN: A meta-analysis was conducted to determine the potential impact of blood flow restriction on patients with knee injuries. PubMed, EBSCO, and Web of Science databases were searched for eligible studies from January 2000 until January 2020. The mean differences of the data were analyzed using Revman 5.3 software with a 95% confidence interval.
RESULTS: Nine studies fulfilled the inclusion criteria. These studies involved 179 patients who received L-BFR, 96 patients who underwent high-load resistance training, and another 94 patients who underwent low-load resistance training. The analysis of pooled data showed that patients in both the L-BFR (standardized mean difference, 0.83 [0.53, 1.14], P < 0.01) and high-load resistance training (standardized mean difference, -0.09 [-0.43, 0.24], P = 0.58) groups experienced an increase in muscle strength after the training. In addition, pain score was significantly reduced in the L-BFR group compared with the other two groups (standardized mean difference, -0.61 [-1.19, -0.03], P = 0.04).
CONCLUSIONS: Muscle strength increased after L-BFR and high-load resistance training compared with low-load resistance training. Furthermore, pain score was significantly reduced after L-BFR. Hence, L-BFR is a potential intervention to be applied in rehabilitation of knee injuries.
MATERIALS AND METHODS: The lentivirus transfection method was used to establish ARC-overexpressing BMSCs. The CCK-8 method was used to detect cell proliferation. The BD Pharmingen™ APC Annexin V Apoptosis Detection kit was used to detect cell apoptosis. The osteogenic capacity was investigated by OCN immunofluorescence staining, ALP analysis, ARS assays, and RT-PCR analysis. Cells were seeded into calcium phosphate cement (CPC) scaffolds and then inserted subcutaneously into nude mice and the defect area of the rat calvarium. Histological analysis was conducted to evaluate the in vivo cell apoptosis and new bone formation of the ARC-overexpressing BMSCs. RNA-seq was used to detect the possible mechanism of the effect of ARC on BMSCs.
RESULTS: ARC promoted BMSC proliferation and inhibited cell apoptosis. ARC enhanced BMSC osteogenic differentiation in vitro. An in vivo study revealed that ARC can inhibit BMSC apoptosis and increase new bone formation. ARC regulates BMSCs mainly by activating the Fgf-2/PI3K/Akt pathway.
CONCLUSIONS: The present study suggests that ARC is a powerful agent for promoting bone regeneration of BMSCs and provides a promising method for bone tissue engineering.
RESULTS: The results showed that lipid content of cell dry weight in Snf-β knockout strain was increased by 32 % (from 19 to 25 %). However, in Snf-β overexpressing strain, lipid content of cell dry weight was decreased about 25 % (from 19 to 14.2 %) compared to the control strain. Total fatty acid analysis revealed that the expression of the Snf-β gene did not significantly affect the fatty acid composition of the strains. However, GLA content in biomass was increased from 2.5 % in control strain to 3.3 % in Snf-β knockout strain due to increased lipid accumulation and decreased to 1.83 % in Snf-β overexpressing strain. AMPK is known to inactivate acetyl-CoA carboxylase (ACC) which catalyzes the rate-limiting step in lipid synthesis. Snf-β manipulation also altered the expression level of the ACC1 gene which may indicate that Snf-β control lipid metabolism by regulating ACC1 gene.
CONCLUSIONS: Our results suggested that Snf-β gene plays an important role in regulating lipid accumulation in M. circinelloides WJ11. Moreover, it will be interesting to evaluate the potential of other key subunits of AMPK related to lipid metabolism. Better insight can show us the way to manipulate these subunits effectively for upscaling the lipid production. Up to our knowledge, it is the first study to investigate the role of Snf-β in lipid accumulation in M. circinelloides.