The Application Progress of Nonthermal Plasma Technology in the Modification of Bone Implant Materials.

With the accelerating trend of global aging, bone damage caused by orthopedic diseases, such as osteoporosis and fractures, has become a shared international event. Traffic accidents, high-altitude falls, and other incidents are increasing daily, and the demand for bone implant treatment is also growing. Although extensive research has been conducted in the past decade to develop medical implants for bone regeneration and healing of body tissues, due to their low biocompatibility, weak bone integration ability, and high postoperative infection rates, pure titanium alloys, such as Ti-6A1-4V and Ti-6A1-7Nb, although widely used in clinical practice, have poor induction of phosphate deposition and wear resistance, and Ti-Zr alloy exhibits a lack of mechanical stability and processing complexity. In contrast, the Ti-Ni alloy exhibits toxicity and low thermal conductivity. Nonthermal plasma (NTP) has aroused widespread interest in synthesizing and modifying implanted materials. More and more researchers are using plasma to modify target catalysts such as changing the dispersion of active sites, adjusting electronic properties, enhancing metal carrier interactions, and changing their morphology. NTP provides an alternative option for catalysts in the modification processes of oxidation, reduction, etching, coating, and doping, especially for materials that cannot tolerate thermodynamic or thermosensitive reactions. This review will focus on applying NTP technology in bone implant material modification and analyze the overall performance of three common types of bone implant materials, including metals, ceramics, and polymers. The challenges faced by NTP material modification are also discussed.

Effects of transcranial magnetic stimulation on axonal regeneration in the corticospinal tract of female rats with spinal cord injury.

BACKGROUND: This study investigates the potential of transcranial magnetic stimulation (TMS) to enhance spinal cord axon regeneration by modulating corticospinal pathways and improving motor nerve function recovery in rats with spinal cord injury (SCI). NEW METHOD: TMS is a non-invasive neuromodulation technique that generates a magnetic field to activate neurons in the brain, leading to depolarization and modulation of cortical activity. Initially utilized for brain physiology research, TMS has evolved into a diagnostic and prognostic tool in clinical settings, with increasing interest in its therapeutic applications. However, its potential for treating motor dysfunction in SCI has been underexplored. RESULTS: The TMS intervention group exhibited significant improvements compared to the control group across behavioral assessments, neurophysiological measurements, pathological analysis, and immunological markers. COMPARISON WITH EXISTING METHODS: Unlike most studies that focus on localized spinal cord injury or muscle treatments, this study leverages the non-invasive, painless, and highly penetrating nature of TMS to focus on the corticospinal tracts, exploring its therapeutic potential for SCI. CONCLUSIONS: TMS enhances motor function recovery in rats with SCI by restoring corticospinal pathway integrity and promoting axonal regeneration. These findings highlight TMS as a promising therapeutic option for SCI patients with currently limited treatment alternatives.

The effect of repetitive magnetic stimulation on neuronal apoptosis and PI3K/Akt protein expression in rats with incomplete spinal cord injury.

The pathological and physiological process of spinal cord injury is complex, and there is currently no effective treatment method. Magnetic stimulation is an emerging electromagnetic therapy method in recent years, and studies have shown its potential to reduce cell apoptosis. This study used an improved Allen's method to replicate an incomplete spinal cord injury rat model, and repetitive magnetic stimulation intervention was performed on the rats for 21 days. The research plan consists of two parts. The first part aims to observe the effects of rMS on motor function and neuronal cell apoptosis in rats. The BBB score results indicate that rMS promotes the recovery of motor function in rats; H&E staining showed that rMS improved spinal cord structural damage and inflammatory infiltration; TUNEL and NeuN staining suggest that rMS can reduce cell apoptosis and promote neuronal cell survival. The second part aims to explore the mechanism of action of rMS. Immunofluorescence staining showed that after rMS intervention, the positive counts of PI3K and Akt increased, while the positive counts of Caspase-3 decreased. Western blot showed that after rMS intervention, the expression of p-PI3K/PI3K, p-Akt/Akt, and Bcl-2 increased, while the expression of Bax and Caspase-3 decreased. In summary, rMS can significantly reduce cell apoptosis in the damaged spinal cord and promote neuronal cell survival. Its mechanism of action may be related to promoting the expression of PI3K/Akt pathway proteins, upregulating the anti apoptotic protein Bcl-2, downregulating the pro apoptotic protein Bax, and thereby inhibiting the expression of apoptotic protein Caspase-3.

Polydopamine-Functionalized Strontium Alginate/Hydroxyapatite Composite Microhydrogel Loaded with Vascular Endothelial Growth Factor Promotes Bone Formation and Angiogenesis.

Critical-size bone defects are a common and intractable clinical problem that typically requires filling in with surgical implants to facilitate bone regeneration. Considering the limitations of autologous bone and allogeneic bone in clinical applications, such as secondary damage or immunogenicity, injectable microhydrogels with osteogenic and angiogenic effects have received considerable attention. Herein, polydopamine (PDA)-functionalized strontium alginate/nanohydroxyapatite (Sr-Alg/nHA) composite microhydrogels loaded with vascular endothelial growth factor (VEGF) were prepared using microfluidic technology. This composite microhydrogel released strontium ions stably for at least 42 days to promote bone formation. The PDA coating can release VEGF in a controlled manner, effectively promote angiogenesis around bone defects, and provide nutritional support for new bone formation. In in vitro experiments, the composite microhydrogels had good biocompatibility. The PDA coating greatly improves cell adhesion on the composite microhydrogel and provides good controlled release of VEGF. Therefore, this composite microhydrogel effectively promotes osteogenic differentiation and vascularization. In in vivo experiments, composite microhydrogels were injected into critical-size bone defects in the skull of rats, and they were shown by microcomputed tomography and tissue sections to be effective in promoting bone regeneration. These findings demonstrated that this novel microhydrogel effectively promotes bone formation and angiogenesis at the site of bone defects.

Body Weight Support Treadmill Training Combined With Sciatic Nerve Electrical Stimulation Ameliorating Motor Function by Enhancing PI3K/Akt Proteins Expression via BDNF/TrkB Signaling Pathway in Rats with Spinal Cord Injury.

OBJECTIVE: To investigate the effects of body weight support treadmill training (BWSTT) and sciatic nerve electrical stimulation (SNES) on motor function recovery in spinal cord injury (SCI) rats and its possible mechanism. METHODS: Modified Allen's method was utilized for T10 incomplete SCI. The Basso-Beattie-Bresnahan (BBB) score and modified Tarlov score were applied to assess motor function. Pathologic alterations of the spinal cord and muscles were observed by hematoxylin and eosin (HE) staining. The positive staining region of collagen fibers was assessed with Masson staining. Immunofluorescence was applied to count the positive cells of brain-derived neurotrophic factor (BDNF) and tropomyosin-related kinase B (TrkB). BDNF, TrkB, phosphatidylinositol-3-kinase (PI3K), and protein kinase B (Akt) relative mRNA and protein expressions were evaluated by reverse transcription polymerase chain reaction (RT-PCR) and Western blotting. RESULTS: On the 21st day of the intervention, the motor scores in SNES and BWSTT + SNES groups were higher than that in SCI group (P < 0.05). Compared with SCI group, mRNA and protein expressions of BDNF/TrkB and PI3K/Akt were more significant on the 21st day of the intervention in SNES and BWSTT + SNES groups (P < 0.05), but there was no difference in BWSTT group (P > 0.05). CONCLUSIONS: This experiment demonstrated that BWSTT combined with SNES contributed to alleviating spinal cord tissue injury, delaying muscle atrophy and improving locomotion. One of the possible mechanisms may be related to the regulation of the BDNF/TrkB signaling pathway, which changes the expression of PI3K/Akt protein. Furthermore, it was discovered that the ultra-early BWSTT may not be conducive to recovery.

Analyzing the Effect of Badminton on Physical Health and Emotion Recognition on the account of Smart Sensors.

Emotional ability is an important symbol of human intelligence. Human's understanding of emotions, from subjective consciousness to continuous or discrete emotional dimensions, and then to physiological separability, has shown a trend of gradually diverging from psychological research to the field of intelligent human-computer interaction. This article is aimed at studying the effects of smart sensor-based emotion recognition technology and badminton on physical health. It proposes a method of using smart sensor technology to recognize badminton movements and emotions during the movement. And the impact of emotion recognition based on smart sensors and badminton sports on physical health is carried out in this article. Experimental results show that the emotion recognition technology based on smart sensors can well recognize the changes in people's emotions during badminton sports, and the accuracy of emotion recognition is higher than 70%. At the same time, experiments show that badminton can greatly improve people's physical fitness and strengthen people's physique.

Effect of TREM2 on Release of Inflammatory Factor from LPS-stimulated Microglia and Its Possible Mechanism.

OBJECTIVE: This study aims to explore the effect of triggering a receptor expressed on myeloid cells 2 (TREM2) in lipopolysaccharide (LPS)-stimulated primary microglia cells and its mechanisms. METHODS: We isolated mouse primary microglia cells in this study. The levels of TREM2, IL-6, and TNF-α in peripheral blood of SCI patients were examined by ELISA assay. The qRT-PCR and western blotting assays were performed to investigate the effects of TREM2 in LPS-induced primary microglia cells. RESULTS: The levels of TREM2, IL-6, and TNF-α significantly increased in peripheral blood of SCI patients and in LPS-stimulated primary microglia cells. Down-regulation of TREM2 significantly reduced the expression of p-NF-κB and the production of IL-6 and TNF-α. In addition, PDTC (a NF-κB inhibitor) treatment inhibited TREM2 overexpression induced-production of IL-6 and TNF-α. CONCLUSIONS: Downregulating the expression of TREM2 can inhibit the release of inflammatory factors from LPS-stimulated microglia by inhibiting NF-κB signaling pathway activity, which may be beneficial for the treatment of SCI.

Anti-inflammatory effects of isoalantolactone on LPS-stimulated BV2 microglia cells through activating GSK-3ß-Nrf2 signaling pathway.

Isoalantolactone (ISO) is a sesquiterpene lactone isolated from Inula helenium that has been known to exhibit anti-inflammatory effect. Nevertheless, the effects of ISO on neuroinflammation have not been explored. BV2 microglia cells were pretreated with ISO and then stimulated with LPS. ISO attenuated the production of inflammatory mediators, such as TNF-α, IL-1ß, NO, and PGE2 in LPS-stimulated BV2 microglia cells. ISO suppressed the LPS-induced NF-κB activation in a concentration-dependent manner. The expression of Nrf2 and HO-1 were increased by the treatment of ISO. Inhibition of Nrf2 by siRNA could reverse the anti-inflammatory effects of ISO, as confirmed by the reversed inflammatory mediator production. Furthermore, ISO increased the level of phosphorylated GSK-3ß, the upstream molecule of Nrf2. In conclusion, these results indicated that ISO might exhibit its anti-inflammatory effects through activating GSK-3ß-Nrf2 signaling pathway.

The transplantation of human urine stem cells combined with chondroitinase ABC promotes brain-derived neurotrophic factor and nerve growth factor following spinal cord injury in rats.

Cells based on therapies are currently gaining momentum in neural tissue engineering to treat spinal cord injury (SCI). The present study aimed to evaluate the effects of the concomitant use of human urine stem cells (hUSCs) and chondroitinase ABC (ChABC) on functional improvement and to explore the expressions of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF). The SCI model was induced by a falling heavy object. hUSCs were cultured and transplanted into the impaired spinal cord with ChABC administration. The Basso, Beattie and Bresnahan (BBB) scores were valued, and real time PCR, immunofluorescence and Western blot were used to detect the expression of BDNF and NGF. We found that rats receiving both hUSCs and ChABC treatment demonstrated the best functional recovery. In addition, the mRNA and protein expressions of the BDNF and NGF expressions were found to be effectively higher in the combined treatment group than these in the other groups. In conclusion, hUSCs transplantation combined with ChABC administration promotes motor functional recovery in SCI rats, which may be associated with BDNF and NGF regulation.

SIRT3 is a novel prognostic biomarker for esophageal squamous cell carcinoma.

Sirtuin-3 (SIRT3) protein is a member of Sirtuins family. It functions as a critical mitochondrial deacetylase, which is involved in a variety of diseases, such as cancer, cardiovascular disease and diabetes. However, its role in esophageal squamous cell carcinoma (ESCC) has never been investigated before. With the help of immunohistochemistry, we studied the clinical significance of SIRT3 expression in ESCC. The receiver operating characteristic method was used to define the SIRT3 IRS cutoff value. The correlations between SIRT3 expression and clinicopathological variables were assessed using Pearson's χ (2) test. To evaluate the clinical significance of SIRT3 expression, Kaplan-Meier analysis was used to compare postoperative survival between different SIRT3 expression groups of ESCC patients. High expression of SIRT3 in ESCC tissues was more frequently observed than corresponding adjacent non-malignant esophageal mucosa tissues. No correlations were found between SIRT3 expression and clinical parameters. Multivariate analysis revealed that SIRT3 expression was an independent prognostic factor in ESCC (HR 1.454, P = 0.034). Increased SIRT3 expression suggests unfavorable prognosis for ESCC patients. Further studies are warranted.