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Objective: This study explored the nursing effect of anesthesia care integration combined with preventive nursing on older patients with perioperative lumbar disc herniation (LDH). Methods: Clinical data of 100 older patients with LDH who were admitted to our hospital between May 2017 and May 2022 were used, and there were no patients who had not had surgery between January and May 2020 because of the COVID-19 pandemic. Based on the different nursing methods, the patients were divided into control and observation groups, with 50 cases each. The control group received anesthesia care integration, whereas the observation group received anesthesia care integration combined with preventive nursing. Lumbar spine function, pain score, anesthesia recovery assessment, and nursing effects were compared between the two groups. Results: The scores of the anesthesia recovery assessment of the two groups were compared, and the vital signs of the observation group during recovery from anesthesia were significantly better than those of the control group (P<0.05). After nursing care, the Japanese Orthopaedic Association (JOA) score of the observation group was significantly higher than that of the control group; however, the numerical scale (NRS) score of the observation group was significantly lower than that of the control group (P<0.05). After nursing care, the physical comfort, emotional state, psychological support, self-care ability, and pain scores were higher in the observation group than in the control group; however, the NRS score of the observation group was significantly lower than that of the control group (P<0.05). Conclusion: Anesthesia care integration combined with preventive nursing has a positive effect on older patients with perioperative LDH, and it significantly improves lumbar spine function, reduces pain, shortens recovery time, and benefits physical and mental health.

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The aim of this study is to investigate the effect and mechanism of 17 ß-estradiol (E2) on oxidative stress in the osteoblasts. An oxidative stress-induced damage model was established using H2O2 in MC3T3-E1 cells, and H2O2-induced cells were treated with E2. The results indicated that E2 attenuated oxidative stress in H2O2- induced MC3T3-E1 cells. In addition, H2O2 upregulated the expression of miR-320-3p and downregulated that of RUNX2, but these changes were counteracted by E2. Thereafter, we verified the interactive relationship between miR-320-3p and RUNX2. Then, H2O2-induced MC3T3-E1 cells were transfected with miR-320-3p mimics or inhibitors and treated with E2. The results indicated that miR-320-3p inhibition suppressed H2O2- induced inflammation, apoptosis, and oxidative stress and promoted the osteogenic differentiation of MC3T3- E1 cells by regulating RUNX2, ALP, and OCN, and this effect was further strengthened by E2. In conclusion, the findings suggest that E2 alleviates oxidative damage in osteoblasts by regulating the miR-320/RUNX2 signaling.

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Chondrosarcoma is a bone tumor characterized by the secretion of a cartilage-like extracellular matrix. It has been proved to lack extracellular sensor primary cilia. This study aimed to illustrate a feasible therapeutic method for chondrosarcoma by regulating primary cilia assembly through inhibiting histone deacetylases 6 (HDAC6) activation. In order to detect the interaction between primary cilia and HDAC6 in human chondrosarcoma, Tubastatin A and small interfering RNA (siRNA) were used to inhibit the endogenous expression of HDAC6. Cell viability test and Transwell assay were applied to evaluate the effects of malignant biological properties. Primary cilia staining and related proteins were detected. The abnormal expression of HDAC6 and cilia intraflagellar transport protein 88 (IFT88) was found in chondrosarcoma tissues. The inhibition of HDAC6 could downregulate the proliferation of chondrosarcoma cells in a concentration- and time-dependent manner and suppress the invasion capacity of tumor cells. Besides, the downregulation of HDAC6 exhibited a negative effect on the proliferation of relevant proteins but a positive effect on the primary cilia-related expression of IFT88 and acetylated α-tubulin. Primary cilia restoration could be observed after HDAC6 siRNA transfection. The Aurora A-HDAC6 cascade was involved in regulating primary cilia resorption by affecting α-tubulin deacetylation and Tubastatin A could inhibit chondrosarcoma cell growth in vivo. These results indicate that restricting HDAC6 can restore primary cilia assembly accompanied with suppressed chondrosarcoma cell proliferation and invasion capacities. Thus, promoting primary cilia restoration by targeting HDAC6 may be a feasible potential therapeutic method for chondro-sarcoma treatment.

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PURPOSE: Our aim was to evaluate the association between the different degree of obesity and prosthetic joint infections (PJIs) after total hip replacement (THR) by performing a meta-analysis. METHODS: PubMed, Cochrane library and Embase databases up to May, 2014 were retrieved for identifying relevant studies. Relative risk (RR) and their 95 % confidence intervals (CIs) were used as effect sizes. RESULTS: A total of 15 articles were included in this meta-analysis. The overall analyses showed that the risk of PJIs in the BMI ≥ 30 group and in BMI ≥ 40 group were significantly higher than that in the BMI < 30 group. As well, the prospective pooled results showed that overweight and obesity could significantly increase the incidence of PJIs. CONCLUSIONS: Our meta-analysis indicates that all of obesity levels can significantly increase the risk of PJIs. However, further studies with more strict design are need in the future.

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Mechanical loading has been widely considered to be a crucial regulatory factor for growth plate development, but the exact mechanisms of this regulation are still not completely understood. In the growth plate, parathyroid hormone-related protein (PTHrP) regulates chondrocyte differentiation and longitudinal growth. Cyclic mechanical strain has been demonstrated to influence growth plate chondrocyte differentiation and metabolism, whereas the relationship between cyclic mechanical strain and PTHrP expression is not clear. The objective of this study was to investigate whether short-term cyclic tensile strain regulates PTHrP expression in postnatal growth plate chondrocytes in vitro and to explore whether the organization of cytoskeletal F-actin microfilaments is involved in this process. To this end, we obtained growth plate chondrocytes from 2-week-old Sprague-Dawley rats and sorted prehypertrophic and hypertrophic chondrocytes using immunomagnetic beads coated with anti-CD200 antibody. The sorted chondrocytes were subjected to cyclic tensile strain of varying magnitude and duration at a frequency of 0.5 Hz. We found that cyclic strain regulates PTHrP expression in a magnitude- and time-dependent manner. Incubation of chondrocytes with cytochalasin D, an actin microfilament-disrupting reagent, blocked the induction of PTHrP expression in response to strain. The results suggest that short-term cyclic tensile strain induces PTHrP expression in postnatal growth plate prehypertrophic and hypertrophic chondrocytes and that PTHrP expression by these chondrocytes may subsequently affect growth plate development. The results also support the idea that the organization of cytoskeletal F-actin microfilaments plays an important role in mechanotransduction.

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