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Background Out-of-bed mobilization is a significant component within the rehabilitation of people early after stroke. A top priority in acute stroke rehabilitation research is determining the optimal dose of out-of-bed mobilization exercises, such as frequency and timing. However, there is little evidence of the appropriate frequency out-of-bed mobilization for acute stroke patients. Aims The aim of the study described in this protocol is to investigate the effect of higher-frequency out-of-bed mobilization on the functional recovery of acute stroke patients. Methods This is a prospective randomized three-arm trial with the assessor blinded to the study intervention. 45 patients met the inclusion criteria will be randomly allocated to three groups, which are separately usual care (1 mobilization session/d), Frequency 1 group (2 mobilization sessions/d) and Frequency 2 group (4 mobilization sessions/d). Outcomes: The primary outcome is the modified Rankin Scale and the secondary outcomes are Rivermead Mobility Index, Fugl-Meyer (Lower Limb), Barthel Index and adverse events incidence. Outcomes will be measured at three time points. Summary: The proposed study will be beneficial for determining the frequency of out-of-bed mobilization, filling the gaps in the acute rehabilitation research field and optimising the recovery of people early after stroke. Trial registration: The proposed study has been registered at Chinese Clinical Trial on 11/03/2022, registry ID: ChiCTR2200057404.

We did this research to observe the effect of LIPUS on long bone fracture repair and caveolin-1, β-catenin signaling expression in the radius defects of rabbits, to explore its possible molecular mechanisms. 24 male New Zealand rabbits with bilateral radial bone defects were divided into 4 groups randomly, n = 6. The right side had daily LIPUS exposure for 20 minutes, while the left received sham treatment. After 7, 14, 21, 28 days, respectively, fracture healing was observed by X-ray imaging and Dual Energy X-ray Absorptiometry (DXA) scan, specimens were harvested for histology, immunohistochemistry, and gene expression analysis. We found that LIPUS brought forward endochondral ossification, increased the bone callus size without changes in Bone Mineral Density (BMD). The caveolin-1 expression increased first then decreased, while the β-catenin kept growing during the process. These demonstrated that caveolin-1 participated in fracture healing accelerated by LIPUS, which was speculated to play a dual role in β-catenin signaling expression.

We investigated the involvement of klotho in the inhibition of oxidative stress by sodium butyrate (NaB) in human nucleus pulposus cells (NPCs). NPCs were pretreated with different concentrations of NaB for 2 h before stimulation with tert-butyl hydroperoxide (TBHP). NaB alleviated TBHP-induced oxidative injury in the NPCs, as evident by the reduced accumulation of mitochondrial superoxide, intracellular reactive oxygen species, and malondialdehyde, and increased activities of superoxide dismutase and glutathione peroxidase. Flow cytometry and western blotting showed that TBHP-induced apoptosis of NPCs was inhibited by NaB. NaB also reduced the TBHP-induced release of proteases that degrade the extracellular matrix, including matrix metalloproteinases 3 and 13, and ADAMTS-4 (a disintegrin and metalloproteinase with thrombospondin motifs 4). Intriguingly, NaB significantly reversed TBHP-induced klotho suppression. However, the protective effects of NaB on NPCs were abolished by klotho-specific small interfering RNA (siRNA). TBHP stimulation had no obvious effects on total or nuclear expression of peroxisome proliferator-activated receptor γ (PPARγ), but significantly reduced PPARγ acetylation and transcriptional activity, which were restored by NaB. TBHP stimulation also promoted the nuclear translocation of histone deacetylase 3 (HDAC3) and enhanced the association between HDAC3 and PPARγ in the nucleus, but this interaction was substantially disrupted by NaB. siRNA-induced HDAC3 knockdown significantly increased PPARγ acetylation and transactivation, reversing the TBHP-induced suppression of klotho. Therefore, NaB alleviates TBHP-induced oxidative stress in human NPCs by elevating PPARγ-regulated klotho expression. HDAC3 may be a critical HDAC subtype that mediates the regulation of PPARγ activity by NaB under oxidative stress.

The present study was conducted to determine whether low intensity-pulsed ultrasound (LIPUS) could induce apoptosis of human hepatocellular carcinoma cells, SMMC-7721, and to define the mechanism of ultrasound-induced apoptosis, in vitro. MTT assay was used to measure cell proliferation. Apoptosis was investigated by multiple methods such as flow cytometry, DNA fragmentation, Ca(2+) mobilizations, pro- and anti-apoptotic protein expression, and light as well as ultramicroscopic morphology. The results provide evidence that LIPUS induced a dose-dependent effect on cell viability and apoptosis of SMMC-7721 cells. Specifically, exposure of cells to >0.5 W/cm(2) intensity significantly increased cell apoptosis, caused shifts in cell cycle phase, and induced structural changes. Ultrasound significantly increased intracellular Ca(2+) concentrations and modulated expression of caspase-3, Bcl-2 and Bax. The findings suggest that this novel technology can be used to induce SMMC-7721 apoptosis via the Ca(2+)/mitochondrial pathway and could potentially be of clinical use for the treatment of hepatocellular carcinoma (SMMC-7721 cell line) and other cancers.