Considering the more favourable outcomes of graft failures, knee joint stability and knee joint function in double-bundle reconstruction, we concluded that arthroscopic double-bundle reconstruction should be considered as the primary treatment in ACL reconstruction.

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Erectile dysfunction (ED) is a major health issue among men with diabetes, and ED induced by diabetes mellitus (DMED) is particularly difficult to treat. Therefore, novel therapeutic approaches for the treatment of DMED are urgently needed. Exosomes, nanosized particles involved in many physiological and pathological processes, may become a promising tool for DMED treatment. In this study, we investigated the therapeutic effect of exosomes derived from corpus cavernosum smooth muscle cells (CCSMC‐EXOs) on erectile function in a rat model of diabetes and compared their effect with that of exosomes derived from mesenchymal stem cells (MSC‐EXOs). We incubated labelled CCSMC‐EXOs and MSC‐EXOs with CCSMCs and then observed uptake of the exosomes at different time points using laser confocal microscopy. CCSMC‐EXOs were more easily taken up by CCSMCs. The peak concentration and retention time of labelled CCSMC‐EXOs and MSC‐EXOs in the corpus cavernosum of DMED rats after intracavernous injection were compared by in vivo imaging techniques. Intracavernous injection of CCSMC‐EXOs was associated with a relatively high peak concentration and long retention time. Our data showed that CCSMC‐EXOs could improve erectile function in DMED rats. Meanwhile, CCSMC‐EXOs could exert antifibrotic effects by increasing the smooth muscle content and reducing collagen deposition. CCSMC‐EXOs also increased the expression of eNOS and nNOS, followed by increased levels of NO and cGMP. These findings initially identify the possible role of CCSMC‐EXOs in ameliorating DMED through inhibiting corporal fibrosis and modulating the NO/cGMP signalling pathway, providing a theoretical basis for a breakthrough in the treatment of DMED.

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The loss of airway epithelial integrity contributes significantly to asthma pathogenesis. Evidence suggests that vitamin D plays an important role in the prevention and treatment of asthma. However, its role in airway epithelial barrier function remains uncertain. We have previously demonstrated impaired epithelial junctions in a model of toluene diisocyanate (TDI)-induced asthma. In the present study, we hypothesized that 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] may prevent TDI-induced epithelial barrier disruption. Male BALB/c mice were dermally sensitized and then challenged with TDI. The mice were then administered 1,25(OH)2D3 intraperitoneally prior to challenge with TDI. For in vitro experiments, 16HBE bronchial epithelial cells were cultured and stimulated with TDI-human serum albumin (HSA). The results revealed that the mice treated with 1,25(OH)2D3 displayed decreased airway hyperresponsiveness (AHR), suppressed neutrophil and eosinophil infiltration into the airways, as well as an increased E-cadherin and zonula occludens-1 (ZO-1) expression at the cell-cell contact sites. In vitro, exposure of the cells to TDI-HSA induced a rapid decline in transepithelial electrical resistance (TER) and an increase in cell permeability, followed by a decrease in occludin expression and the redistribution of E-cadherin, accompanied by a significant upregulation in the levels of phosphorylated extracellular signal-regulated kinase (ERK)1/2. These effects were all partly reversed by treatment with either 1,25(OH)2D3 or an ERK1/2 inhibitor. In conclusion, the findings of our study demonstrate that 1,25(OH)2D3 prevents TDI-induced epithelial barrier disruption, and that the ERK1/2 pathway may play a role in this process.

ObjectiveCurrent medical practice for the treatment of articular cartilage lesions remains a clinical challenge due to the limited self-repair ability of articular cartilage. Both experimental and clinical researches show that moderate exercise can improve articular cartilage repair process. However, optimal timing of moderate exercise is unclear. We aimed to evaluate the effect of timing of moderate treadmill exercise on repair of full-thickness defects of articular cartilage.DesignFull-thickness cartilage defects were drilled in the patellar groove of bilateral femoral condyles in a total of 40 male SD rats before they were randomly assigned into four even groups. In sedentary control (SED) group, no exercise was given; in 2-week (2W), 4-week (4W) and 8-week groups, moderate treadmill exercise was initiated respectively two, four and eight weeks after operation. Half of the animals were sacrificed at week 10 after operation and half at week 14 after operation. Femoral condyles were harvested for gross observation and histochemical measurement by O'Driscoll scoring system. Collagen type II was detected by immunohistochemistry and mRNA expressions of aggrecan and collagen type II cartilage by RT-PCR.ResultsBoth 10 and 14 weeks post-operation, the best results were observed in 4W group and the worst results appeared in 2W group. The histochemistry scores and the expressions of collagen type II and aggrecan were significantly higher in 4W group than that in other three groups (P<0.05).ConclusionsModerate exercise at a selected timing (approximately 4 weeks) after injury can significantly promote the healing of cartilage defects but may hamper the repair process if performed too early while delayed intervention by moderate exercise may reduce its benefits in repair of the defects.