GPX8 regulates pan-apoptosis in gliomas to promote microglial migration and mediate immunotherapy responses.

Introduction: Gliomas have emerged as the predominant brain tumor type in recent decades, yet the exploration of non-apoptotic cell death regulated by the pan-optosome complex, known as pan-apoptosis, remains largely unexplored in this context. This study aims to illuminate the molecular properties of pan-apoptosis-related genes in glioma patients, classifying them and developing a signature using machine learning techniques. Methods: The prognostic significance, mutation features, immunological characteristics, and pharmaceutical prediction performance of this signature were comprehensively investigated. Furthermore, GPX8, a gene of interest, was extensively examined for its prognostic value, immunological characteristics, medication prediction performance, and immunotherapy prediction potential. Results: Experimental techniques such as CCK-8, Transwell, and EdU investigations revealed that GPX8 acts as a tumor accelerator in gliomas. At the single-cell RNA sequencing level, GPX8 appeared to facilitate cell contact between tumor cells and macrophages, potentially enhancing microglial migration. Conclusions: The incorporation of pan-apoptosis-related features shows promising potential for clinical applications in predicting tumor progression and advancing immunotherapeutic strategies. However, further in vitro and in vivo investigations are necessary to validate the tumorigenic and immunogenic processes associated with GPX8 in gliomas.

Effect of "Internet + tertiary hospital-primary hospital-family linkage home care" model on self-care ability and quality of life of discharged stroke patients.

OBJECTIVE: To investigate the intervention effect of an "Internet + tertiary hospital-primary hospital-family linkage home care" model on the quality of life and self-care abilities of discharged stroke patients. METHODS: The clinical data of 90 patients with stroke who were hospitalized and discharged from the Department of Neurology of the Affiliated Hospital of Youjiang Medical College for Nationalities from October 2020 to September 2021 were retrospectively analyzed. They were split into a control group (41 cases) and an intervention group (40 cases) based on different care modes. The intervention group was given the "Internet + tertiary hospital-primary hospital-family connection home care" paradigm, while the control group received normal nursing interventions. The degree of nerve defect, quality of life, anxiety and depression, self-care ability and exercise ability of the patients were evaluated by National Institutes of Health Stroke Scale (NIHSS), Stroke Specific Quality of Life Scale (SS-QOL), General Hospital Anxiety and Depression Scale (HADS), Self-care Ability Scale (ESCA), and Fugl-Meyer Motor Function Assessment (FMA) before discharge and at 3rd, 6th and 12th month after discharge, respectively. The re-hospitalization rate, treatment compliance and exercise ability of the two groups were compared within a year after discharge. RESULTS: The scores of SS-QOL, ESCA and FMA in the intervention group increased with time, and the scores of SS-QOL, ESCA and FMA at 3rd, 6th and 12th month after discharge were higher than those in the control group (all P<0.05). The NIHSS and HADS scores decreased over time, and the NIHSS and HADS scores were lower than the control group at 12th month after discharge (P<0.05). Within a year of discharge, the intervention group had a lower rehospitalization rate than the control group (P<0.05), and the treatment compliance score was higher in the intervention group than that in the control group (P<0.05). CONCLUSION: The "Internet + tertiary hospital-primary hospital-family nursing" model can improve self-care ability and treatment compliance of patients, improve their nerve defects and psychological status as well as quality of life, and reduce rehospitalization rate.

Long noncoding RNA MSC-AS1 promotes hepatocellular carcinoma oncogenesis via inducing the expression of phosphoglycerate kinase 1.

BACKGROUND AND OBJECTIVES: Increasing studies report that lncRNAs are dysregulated in hepatocellular carcinoma (HCC), which might function as significant diagnostic biomarkers of HCC. LncRNA MSC-AS1 has been newly discovered in several cancers. However, its biological effect in HCC remains to be clearly elucidated. The aim of our work was to test MSC-AS1 expression level and assess its function in HCC progression. METHODS: Expression levels of MSC-AS1 and PGK1 in HCC were tested by qRT-PCR in HCC cells including HUH-7, BEL-7404, SNU449, HepG2, QGY-7701, and human normal liver cells (HL-7702 cells). Association of MSC-AS1 expression with various clinicopathological features and patients' survival were analyzed by chi-squared test and Kaplan-Meier, respectively. The functions of MSC-AS1 in HCC cells were investigated using EdU assay, colony formation, flow cytometry, would healing assay, and Transwell matrigel invasion assays. The correlation between MSC-AS1 and PGK1 was confirmed using a RIP assay. Protein expression of PGK1 was evaluated using a western blot assay. RESULTS: MSC-AS1 was obviously upregulated in HCC tissues and HCC cells. Knockdown of MSC-AS1 repressed HepG2 and BEL-7404 cell proliferation, colony formation capacity, and triggered cell apoptosis. HepG2 and BEL-7404 cell cycle was blocked in G1 phase and cell migration/invasion was remarkably depressed. Downregulation of MSC-AS1 in HCC cells reduced PGK1 expression. In vivo data demonstrated that silence of MSC-AS1 suppressed HCC development via activating PGK1. CONCLUSIONS: Taken these together, we indicated that MSC-AS1 promoted HCC oncogenesis via inducing the expression of PGK1.

Correction to: Re­fracture and correlated risk factors in patients with osteoporotic vertebral fractures.

In the Original publication of the article, the funding ID has been incorrectly published as (815602390) in the Acknowledgements.

Re-fracture and correlated risk factors in patients with osteoporotic vertebral fractures.

Re-fracture risk is higher following osteoporotic fracture. However, there is no accurately reported rate of re-fracture incidence in southwest China. The purpose of this study was to describe the osteoporotic vertebral fracture (OVF) survival for re-fracture state and analyze the risk of re-fracture. This historical cohort study was conducted in four hospitals in southwest China. Patients aged ≥ 50 years (n = 586) with OVF who were supposed to receive anti-osteoporosis drugs after the fracture were included (2012-2017). Telephone follow-up and referring case files were used to estimate the survival for re-fracture and identify the determinants of re-fracture. A total of 555 patients completed the follow-up investigation. Overall, 285 patients experienced a re-fracture, and the longest follow-up investigation time was 72 months. The survival rates for re-fracture at 12 months, 24 months, 36 months, and 48 months were 82.0%, 71.5%, 61.7%, and 34.0%, respectively. The factors correlated with re-fracture hazard were advanced age [hazard ratio (HR) = 1.996], being female (HR = 1.342), smoking (HR = 1.435), history of hypertension (HR = 1.219) and diabetes (HR = 3.271), and persistence of taking anti-osteoporosis drugs after fracture [0-3 months, 4-6 months, 7-12 months, and more than 12 months (HR = 0.703)]. OVF patients with advanced age, who were female, smoked, had fracture with hypertension or diabetes, and who complied poorly with anti-osteoporosis drug treatment presented higher prevalence of re-fracture and low anti-osteoporosis adherence in southwest China. The management of anti-osteoporosis after fracture is necessary in this area.