The prevention effect of pulsed electromagnetic fields treatment on senile osteoporosis in vivo via improving the inflammatory bone microenvironment.

This study aimed to assess PEMF in a rat model of senile osteoporosis and its relationship with NLRP3-mediated low-grade inflammation in the bone marrow microenvironment. A total of 24 Sprague Dawley (SD) rats were included in this study. Sixteen of them were 24-month natural-aged male SD rats, which were randomly distributed into the Aged group and the PEMF group (n = 8 per group). The remaining 8 3-month -old rats were used as the Young positive control group (n = 8). Rats in the PEMF group received 12 weeks of PEMF with 40 min/day, five days per week, while the other rats received placebo PEMF intervention. Bone mineral density/microarchitecture, serum levels of CTX-1 and P1CP, and NLRP3-related signaling genes and proteins in rat bone marrow were then analyzed. The 12-week of PEMF showed significant mitigation of aging-induced bone loss and bone microarchitecture deterioration, i.e. PEMF increased the bone mineral density of the proximal femur and L5 vertebral body and improved parameters of the proximal tibia and L4 vertebral body. Further analysis showed that PEMF reversed aging-induced bone turnover, specifically, decreased serum CTX-1 and elevated serum P1CP. Furthermore, PEMF also dramatically inhibited NLRP3-mediated low-grade inflammation in the bone marrow, i.e. PEMF inhibited the levels of NLRP3, proCaspase1, cleaved Caspase1, IL-1ß, and GSDMD-N. The study demonstrated that PEMF could mitigate the aging-induced bone loss and reverses the deterioration of bone microarchitecture probably through inhibiting NLRP3-mediated low-grade chronic inflammation to improve the inflammatory bone microenvironment in aged rats.

A robust performance evaluation method based on interval evidential reasoning approach under uncertainty.

Performance evaluation (PE) is an important part of equipment health management. If the monitoring information of the equipment is interfered, the evaluation results may be erroneous. A robust performance evaluation (RPE) method is proposed to solve this problem. The performance evaluation results are obtained by distinguishing the cases of single evidence with interference and two evidence with interference, and a robustness measurement based on interval similarity is proposed. To improve the accuracy of the evaluation results, the referential values in the IER evaluation model are optimized. The robustness thresholds of the input indexes are obtained under the satisfaction of the robustness constraints. If the interference value of the input index is within the thresholds, the deviation between the evaluation results using monitoring information with interference and those using monitoring information without interference is small. Finally, the proposed method is applied to a type of electric servo mechanism performance evaluation, and the case shows the validity of the RPE method.

A New Evidential Reasoning Rule Considering Interval Uncertainty and Perturbation.

The evidential reasoning (ER) rule has been widely applied in the multiple attribute decision making (MADM), which makes the decision-making process transparent and credible by using a belief structure. To improve the ability of the ER rule in dealing with the interval uncertainty, a new interval ER (IER) rule is proposed in this article. The interval uncertainty is described as the interval grade in the new frame of discernment (FoD) to model the local ignorance. It is proved that the IER rule is a generalization of the ER rule. To study the influence of perturbation on the IER rule, the perturbation is first introduced to the belief structure, and the perturbation analysis (PA) is conducted for the IER rule. An optimization model is established to estimate the perturbation threshold, which can measure the effectiveness of the inference result under perturbation. Two numerical examples and a case study are carried out, respectively, to show the implementation process of the proposed IER rule and validate its effectiveness in different decision-making scenarios.

Treadmill training mitigates bone deterioration via inhibiting NLRP3/Caspase1/IL-1ß signaling in aged rats.

INTRODUCTION: Although aerobic physical exercise may improve osteoporosis during ageing, the underlying mechanism of the favorable effects remains unclear. The aim of this study was to examine the localized and generalized proinflammatory indicators and the adaptive skeletal responses to treadmill training in aged rats to explore the potential mechanisms by which treadmill training impacts bone deterioration in a natural aged rat model. MATERIALS AND METHODS: A total of 24 Sprague Dawley (SD) rats were included in this study. Sixteen of all these animals were twenty-four months natural aged male SD rats, which were distributed into two groups (n = 8/group): AC group with sham treadmill training, and AT group with 8 weeks treadmill training. The remaining 8 were six months male SD rats matched subline and supplier, which were used as the adult control group with sham treadmill training (YC group, n = 8). The serum, bone marrow, fresh femur, tibia, and lumbar spine were harvested for molecular biological analysis, bone mineral density (BMD) testing, and micro-CT analysis after 8 weeks of treadmill training. RESULTS: After 8 weeks of intervention, the results showed that treadmill training increased BMD and inhibited deterioration of bone microarchitecture of hind limb bones. Further analysis showed that treadmill training increased serum P1CP concentration and decreased serum CTX-1level. Interestingly, treadmill training down-regulated the protein expressions of proinflammatory indicators, including NLRP3, proCaspase1, cleaved Caspase1, IL-1ß, and GSDMD-N, and the mRNA levels of NLRP3, Caspase1, and IL-1ß of the bone marrow. In addition, treadmill training also inhibited serum TNF-α and IL-1ß concentration. However, 8 weeks of treadmill training did not increase BMD and bone microarchitecture in the lumbar spine. CONCLUSION: Treadmill training mitigates the ageing-induced bone loss and reverses the deterioration of bone microarchitecture in hind limbs probably through inhibiting NLRP3/Caspase1/IL-1ß signaling to attenuate low-grade inflammation and improve the inflammatory bone microenvironment.

Effect of the Pulsed Electromagnetic Field Treatment in a Rat Model of Senile Osteoporosis In Vivo.

This study assessed the effects of pulsed electromagnetic fields (PEMF) in a rat model of senile osteoporosis and the underlying molecular events. 24-month-old male Sprague-Dawley (SD) rats were randomly divided into control and PEMF groups (n = 8 per group) using a random digit table, while 3-month-old male SD rats were set as the young-age control group. Rats in the PEMF group were treated by PEMF for 40 min/day for 5 days/week. Bone mineral density/microarchitecture, level of serum bone-specific alkaline phosphatase (BALP), tartrate-resistant acid phosphatase 5b (TRACP5b), and Wnt/ß-catenin signaling genes in rat bone marrow cells were then analyzed. The 12-week PEMF intervention showed a significant effect on inhibition of age-induced bone density loss and deterioration of trabecular bone structures in the PEMF group rats versus control rats, that is, the treatment enhanced bone mineral density of the proximal femoral metaphysis and the fifth lumbar (L5) vertebral body and improved the proximal tibia and L4 vertebral body parameters using bone histomorphometry analysis. Furthermore, the BALP level in the bones was significantly increased, but the TRACP5b level was reduced in the PEMF group of rats versus control rats. PEMF also dramatically upregulated expression of Wnt3a, LRP5, ß-catenin, and Runx2 but downregulated PPAR-γ expression in the aged rats. The results demonstrated that PEMF could prevent bone loss and architectural deterioration due to the improvement of bone marrow mesenchymal stromal cell differentiation and proliferation abilities and activating the Wnt signaling pathway. Future clinical studies are needed to validate these findings. © 2022 Bioelectromagnetics Society.