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This retrospective study investigates the effectiveness of a nursing intervention based on Orem's self-care model of nursing with elderly patients with femoral head necrosis who underwent total hip arthroplasty. Postoperative outcomes in the intervention and control groups were assessed by the visual analog scale (VAS), Barthel index, and Harris Hip Score (HHS). Participants in the intervention group had significantly better outcomes in terms of VAS, Barthel index, and HHS. The occurrence of pneumonia was significantly different between the groups. Those who underwent Orem's self-care model of nursing intervention were highly satisfied with their status postoperatively compared with the control group. [ABSTRACT FROM AUTHOR]

Vascular endothelial cell functions affect lower extremity arteriosclerosis obliterans (LEASO), while alpha-2-macroglobulin (A2M) and CCCTC-binding factor (CTCF) are closely related to the function of such cells. This paper aims to identify the influences of CTCF on vascular endothelial cells in LEASO by regulating A2M. A rat model of LEASO was established to measure intima-media ratio, blood lipid, and inflammatory factor levels. By constructing LEASO cell models, cell viability and apoptosis were assayed, while autophagy-related proteins, CTCF and A2M levels in femoral artery tissues and HUVECs were determined. The transcriptional regulation of CTCF on A2M was verified. In LEASO rat models, femoral artery lumen was narrowed and endothelial cells were disordered; levels of total cholesterol, IL-1, and TNF-α enhanced, and HDL-C decreased, with strong expression of A2M and low expression of CTCF. The viability of ox-LDL-treated HUVECs was decreased, together with higher apoptosis, lower LC3II/I expression, and higher p62 expression, which were reversed by sh-A2M transfection. Overexpression of CTCF inhibited A2M transcription, promoted the viability and autophagy of HUVECs, and decreased apoptosis. Collectively, CTCF improves the function of vascular endothelial cells in LEASO by inhibiting A2M transcription.

Background: Osteonecrosis of the femoral head (ONFH) is an ischemic disease characterized by the impairment of angiogenesis. We have previously elucidated the role of tsRNAs and BMSC exosomes in ONFH, but whether tsRNA-modified BMSC exosomes promote angiogenesis in ONFH remains unclear., Methods: The expression of angiogenesis-related tsRNA in plasma exosomes from ONFH patients was examined by q-PCR. The function of tsRNA in HUVECs was identified by CCK-8 and angiogenesis assay. Exosomes purified from tsRNA-15797 overexpressed BMSCs were cocultured with HUVECs to examine their role in angiogenesis. The molecule mechanism of tsRNA-15797-modified exosomes was explored by RNA sequencing, dual-luciferase assay, and immunofluorescence., Results: A tRNA-derived small RNA tsRNA-15797 was down-regulated in plasma exosomes of ONFH patients. We found the effects of BMSCs-derived exosomes on accelerating HUVECs angiogenesis and migration, which were further enhanced after overexpressing tsRNA-15797. Besides, overexpression of tsRNA-15797 would lead to down-regulation of LFNG correlated with angiogenesis. tsRNA-15797 could directly interact with LFNG. We demonstrated that LNFG overexpression weakened the pro angiogenic and migratory effects of tsRNA-15797-modified BMSCs-derived exosomes., Conclusion: We successfully constructed tsRNA-15797-modified BMSC-derived exosomes and demonstrated that it induced the angiogenesis of HUVECs by targeting the down-regulation of LFNG. Thus, tsRNA-15797-loaded BMSCs-derived exosomes may be a potential target therapy drug for ONFH., Competing Interests: Conflict of interest We declare that we have no conflict of interest., (© TÜBİTAK.)

Background: Animal studies have demonstrated the therapeutic effect of mesenchymal stem cells (MSCs) on osteogenesis, but little is known about the functions of exosomes (Exos) released by bone MSCs (BMSCs). Here, we investigated the effect of BMSC Exos on steroid-induced femoral head necrosis (SFHN) and explored the vital genes involved in this process., Materials and Methods: BMSCs were isolated from healthy and SFHN rats. BMSC Exos were isolated using the Exosome Precipitation Kit and characterized by transmission electron microscopy and Western blotting. SFHN BMSCs were incubated with Exos from healthy BMSCs. Osteogenic ability was assessed by oil red O staining and alizarine red staining. Differentially expressed genes (DEGs) induced by Exos were screened using the Osteogenesis RT2 Profiler PCR Array. The effect of upregulated Sox9 was examined using lentivirus-mediated siRNA., Results: The results revealed that BMSC Exos were 100-150 nm in size and expressed CD63. Moreover, BMSC Exo-treated SFHN cells exhibited suppressed adipogenesis compared to model cells. PCR array showed that eleven and nine genes were upregulated and downregulated, respectively, in the BMSC Exo-treated SFHN cells compared to the model group. Among the DEGs, osteogenesis-related genes, including Bmp2 , Bmp6 , Bmpr1b , Mmp9 , and Sox9 , may play important roles in SFHN. Furthermore, the DEGs were mainly involved in immune response, osteoblast differentiation, and in the transforming growth factor-β/bone morphogenetic protein signaling pathway. The level of the SOX9 protein was upregulated by Exos, and Sox9 silencing significantly decreased the osteogenic effect of BMSC Exos., Conclusion: Our data suggest that Exos derived from BMSCs mainly affect SFHN osteogenesis, and this finding can be further investigated to develop a novel therapeutic agent for SFHN., Competing Interests: Disclosure The authors report no conflicts of interest in this work.