BACKGROUND:Degenerative scoliosis is defined as a condition that occurs in adulthood with a coronal cobb angle of the spine>10° accompanied by sagittal deformity and rotational subluxation,which often produces symptoms of spinal cord and nerve compression,such as lumbar pain,lower limb pain,numbness,weakness,and neurogenic claudication.The finite element method is a mechanical analysis technique for computer modelling,which can be used for spinal mechanics research by building digital models that can realistically restore the human spine model and design modifications. OBJECTIVE:To review the application of finite element method in the etiology and treatment of degenerative scoliosis. METHODS:The literature databases CNKI,PubMed,and Web of Science were searched for articles on the application of finite element method in degenerative scoliosis published before October 2023.Search terms were"finite element analysis,biomechanics,stress analysis,degenerative scoliosis,adult spinal deformity"in Chinese and English.Fifty-four papers were finally included. RESULTS AND CONCLUSION:(1)The biomechanical findings from the degenerative scoliosis model constructed using the finite element method were identical to those from the in vivo experimental studies,which proves that the finite element method has a high practical value in degenerative scoliosis.(2)The study of the etiology and treatment of degenerative scoliosis by the finite element method is conducive to the prevention of the occurrence of the scoliosis,slowing down the progress of the scoliosis,the development of a more appropriate treatment plan,the reduction of complications,and the promotion of the patients'surgical operation.(3)The finite element method has gradually evolved from a single bony structure to the inclusion of soft tissues such as muscle ligaments,and the small sample content is increasingly unable to meet the research needs.(4)The finite element method has much room for exploration in degenerative scoliosis.

Metabolic reprogramming, a newly recognized trait of tumor biology, is an intensively studied prospect for oncology medicines. For numerous tumors and cancer cell subpopulations, oxidative phosphorylation (OXPHOS) is essential for their biosynthetic and bioenergetic functions. Cancer cells with mutations in isocitrate dehydrogenase 1 (IDH1) exhibit differentiation arrest, epigenetic and transcriptional reprogramming, and sensitivity to mitochondrial OXPHOS inhibitors. In this study, we report that berberine, which is widely used in China to treat intestinal infections, acted solely at the mitochondrial electron transport chain (ETC) complex I, and that its association with IDH1 mutant inhibitor (IDH1^mi) AG-120 decreased mitochondrial activity and enhanced antileukemic effect in vitro andin vivo. Our study gives a scientific rationale for the therapy of IDH1 mutant acute myeloid leukemia (AML) patients using combinatory mitochondrial targeted medicines, particularly those who are resistant to or relapsing from IDH1^mi.
Humans ; Oxidative Phosphorylation ; Berberine ; Electron Transport ; Mitochondria ; Leukemia, Myeloid, Acute ; Isocitrate Dehydrogenase

Objective:To explore the coverage of influenza and pneumonia vaccination and factors influencing the vaccination in children.Methods:A cross-sectional questionnaire survey was conducted in children's parents in Beijing and Gansu by using two-stage cluster-sampling to investigate the influenza and pneumonia vaccination rates and influencing factors in children.Results:A total of 2 377 parents were included in the study, and the results indicated that the influenza vaccination coverage was 35.93% and the pneumonia vaccination coverage was 16.58% in children in survey areas, the vaccination rate of both vaccines was 11.65%. The top three reasons for vaccination for both vaccines were being aware of severity of the diseases (influenza vaccine: 36.02%; pneumonia vaccine: 49.61%), being required by school or organization (influenza vaccine: 28.76%; pneumonia vaccine: 25.45%) and being aware of the susceptibility of the diseases (influenza vaccine: 26.41%; pneumonia vaccine: 13.88%). The top three reasons for having no vaccinations were personal unwillingness, concern about vaccine and vaccine accessibility. Families with multi children, living in rural areas and lower family income were the negative factors for both types of vaccinations.Conclusions:The influenza and pneumonia vaccination coverage in children need further improvement, and rural families and families with multi children are the key concern groups for expanding vaccination coverage. Health education about influenza and pneumonia vaccinations, coordinating vaccine supply and decreasing vaccine prices play an important role in improving influenza and pneumonia vaccination coverage.

Dermatomyositis (DM) is a kind of idiopathic inflammatory myopathy characterized by chronic proximal skeletal muscle weakness and unique skin lesions. However, DM with exfoliation of esophageal mucosa is rare. A 36-year-old male patient complained of muscular soreness of extremities, dysphagia, and pharyngalgia was diagnosed with DM with exfoliation of esophageal mucosa. After treatment with glucocorticoid, immunosuppressant, acupuncture, and endoscopic submucosal dissection (ESD), the above symptoms were disappeared. During the 3-year follow-up period, the results of routine physical examination, laboratory examination, gastroscopy, and imaging examination were normal. High-dose of corticosteroid is needed in the initial treatment, but it must be reduced regularly to avoid adverse reactions. Acupuncture and ESD are also effective as adjuvant therapy.
Adult ; Dermatomyositis/complications* ; Endoscopic Mucosal Resection ; Esophageal Mucosa ; Esophageal Neoplasms ; Gastroscopy ; Humans ; Male ; Treatment Outcome

Objective:To master the changes of Kashin-Beck disease and the examination and acceptance in Zhalantun City, and to provide scientific basis for formulating prevention and control strategies of Kashin-Beck disease.Methods:From 2016 to 2017, in each county under the jurisdiction of Zhalantun City, 5 townships affected by the disease were selected, 3 villages were selected from each township, and the prevalence of Kashin-Beck disease of all residential children aged 7 to 12 years who lived in the villages for more than 6 months were investigated. The clinical and X-ray diagnosis were performed according to the "Diagnosis of Kashin-Beck Disease" (WS/T 207-2010) standard, and the prevalence of Kashin-Beck disease in children aged 7 to 12 years in Zhalantun City in 2016 and 2017 were compared. In accordance with the "Key Endemic Disease Control and Elimination Evaluation Measures" ([2014]79), the condition of Kashin-Beck disease and the implementation of its prevention and control measures was assessed.Results:From 2016 to 2017, 1 697 children aged 7 to 12 years were examined, there were no clinical cases of Kashin-Beck disease and 11 cases of X-ray positive changes. Among them, 844 children were examined in 2016, the positive rate of X-ray was 0.24% (2/844), the positive rate of metaphyseal was 0.24% (2/844), and no positive changes of extremities and triad were detected. A total of 853 children were examined in 2017, the positive rate of X-ray was 1.06% (9/853), the positive rate of metaphyseal was 1.06% (9/853), and no positive changes of extremities and triad were detected. The positive rate of X-ray and metaphyseal of Kashin-Beck disease in children aged 7 - 12 years in 2017 were higher than those in 2016 (χ 2 = 4.409, 4.409, P < 0.05). All surveyed villages had reached the national elimination standard (no clinical cases for children aged 7 - 12 years, X-ray positive rate ≤3% and no cases of hand bone end changes); the organization management scores of Kashin-Beck disease prevention and treatment in Zhalantun City in 2016 and 2017 were 88 points, reaching the qualified standard ( > 85 points). Conclusion:The condition of Kashin-Beck disease in Zhalantun City has reached the standard of elimination, which lays a foundation for further comprehensive elimination of Kaschin-Beck disease in Hulunbuir City.

OBJECTIVES: Lung cancer is one of the most common malignant tumors in the world, and its lethality ranks the first among many malignant tumors. For non-small cell lung cancer (NSCLC) patients, due to the high mortality rate, the overall 5-year survival rate is less than 15%. When NSCLC undergoes local invasion, the 5-year survival rate is only 20%, and it is even lower when distant metastasis occurs up to 4%. Almonertinib is an innovative drug independently researched and developed by China with independent intellectual property rights. As an epidermal growth factor receptor tyrosine kinase inhibitor, almonertinib is mainly used for locally advanced or metastatic NSCLC patients with epidermal growth factor receptor (EGFR) T790M mutation. This study aims to investigate the effects of almonertinib on the proliferation, invasion and migration of NSCLC cells in vitro. METHODS: NSCLC cells H1975 and PC-9 were cultured in vitro. The effects of almonertinib on the proliferation, apoptosis, invasion, and migration of H1975 and PC-9 cells were detected by CCK-8 assay, apoptotic assay and Transwell assay. The expression of invasion and migration related proteins was detected by Western blotting. RESULTS: The CCK-8 experiment showed that almonertinib inhibited the proliferation of H1975 and PC-9 cells in a time- and dose-dependent manner. The IC CONCLUSIONS Almonertinib can inhibit the proliferation, invasion, and migration of NSCLCH1975 and PC-9 cells in vitro and vivo, and promote the apoptosis of H1975 and PC-9 cells. The underlying mechanism may be related to the inhibition of tumor cell epithelial mesenchymal transformation and metalloproteinase expression.
Acrylamides ; Animals ; Apoptosis ; Carcinoma, Non-Small-Cell Lung/drug therapy* ; Cell Line, Tumor ; Cell Proliferation ; Drug Resistance, Neoplasm ; ErbB Receptors/genetics* ; Humans ; Indoles ; Lung Neoplasms ; Mice ; Mice, Nude ; Mutation ; Protein Kinase Inhibitors/pharmacology* ; Pyrimidines

Objective:To investigate the application value of electroencephalogram (EEG) combined with regional cerebral oxygen saturation (rSO 2) in monitoring cerebral perfusion during carotid endarterectomy (CEA). Methods:A retrospective analysis of clinical data of 42 patients with atherosclerotic carotid artery stenosis admitted to and accepted CEA in our hospital from January 2018 to December 2019 was performed. CEA was performed under EEG combined with rSO 2 monitoring. The efficacy and safety of EEG combined with rSO 2 in monitoring cerebral perfusion abnormalities during CEA were analyzed. Results:After carotid artery occlusion, 24 patients (57.1%) had normal EEG and rSO 2; 15 (35.7%) had abnormal changes of EEG, among whom 13 (31.0%) were accompanied by rSO 2 anomaly; 16 (38.1%) had abnormal rSO 2, among whom 13 (31.0%) were accompanied by EEG anomaly. Of these 18 patients with abnormal EEG and/or rSO 2 monitoring, 17 patients recovered after increasing their blood pressure and 1 patient recovered after diverter tube usage. Intraoperative EEG and rSO 2 monitoring results were consistent (Kappa=0.745, P=0.000). The positive rates of combined monitoring, EEG alone or rSO 2 alone were 42.9%, 35.7% and 38.1%, respectively. All patients were evaluated clinically and radiologically before discharge, and no new ischemic lesions or clinical symptoms were found. Conclusions:EEG and rSO 2 monitoring are well consistent in CEA; the combined monitoring can make up for the deficiency of single monitoring to increase surgical safety.

Objective:To explore the relationship between sleep duration and depressive symptoms in middle-aged and elderly people.Methods:A total of 11 931 middle-aged and elderly people aged ≥55 years who participated in the baseline survey of the "Community Cohort Study of Specialized Nervous System Diseases" in China from 2018 to 2019 were selected to obtain basic information about their lifestyle, food intake frequency, disease history, sleep duration. The body height and weight were measured, and body mass index (BMI) were calculated. The subjects with depressive symptoms were screened with the Geriatric Depression Scale (GDS-30). Restricted cubic spline model and multivariate logistic regression model were used to analyze the relationship between sleep duration and depressive symptoms.Results:Among the middle-aged and elderly people aged ≥55 years, 17.79% reported sleep duration less than 7 hours, 16.84% reported that their sleep duration ≥9 hours, and the detection rate of depression symptoms was 7.95%. After adjusting for factors such as region, age, gender, the restricted cubic spline results showed the U-shaped relationship between sleep duration and the risk for depressive symptoms, the results of multivariate logistic regression analysis showed that the risk for depressive symptom in middle-aged and elderly people aged ≥55 years with sleep duration ≤5 hours, 6 hours, and ≥9 hours were 1.749(95% CI:1.279-2.392), 1.284(95% CI:1.021-1.615) and 1.260(95% CI:1.033-1.538) times higher compared with the counterparts with sleep duration 7-8 hours, the risk for depressive symptom in women with sleep duration ≤5 hours, 6 hours and ≥9 hours were 2.115 (95% CI:1.473-3.038), 1.605(95% CI:1.213-2.123) and 1.313(95% CI:1.011-1.705) times higher, respectively, compared with counterparts with sleep duration 7-8 hours, the risk for depressive symptoms in 55-64-year-old middle-aged and elderly people with sleep duration ≤5 hours and ≥9 hours were 1.806 (95% CI:1.014-3.217) and 1.478 (95% CI:1.060-2.061) times higher compared with counterparts with sleep duration 7-8 hours, and the risk for depressive symptoms in elderly people aged 65-74 years with sleep duration ≤5 hours was 2.112 (95% CI:1.327-3.361)times higher compared with counterparts with sleep duration 7-8 hours, the differences were all significant ( P<0.05). There was no statistically significant association between sleep duration and depressive symptoms in men and in elderly people aged ≥75 years ( P>0.05). Conclusion:Insufficient or prolonged sleep was independently associated with depressive symptoms in middle-aged and elderly people, showing a U-shaped relationship, especially in women and in middle-aged and elderly people aged 55-64 years.

OBJECTIVE: To investigate the inhibitory effect of epidermal growth factor receptor tyrosine kinase inhibitor (EGFRTKI) HS-10296 on the proliferation of triple-negative breast cancer (TNBC) MDA-MB-231 cells and explore the possible molecular mechanism. METHODS: MDA-MB-231 cells were treated with HS-10296 for 24, 48, or 72 h, and CCK-8 assay was used to assess the changes in the cell viability. The inhibitory effect of HS-10296 on cell proliferation was determined by clonogenic assay. JC-1 and flow cytometry were employed for analyzing the cell apoptosis, and the ultrastructure of the cells was observed under electron microscope. After pretreatment with autophagy inhibitor chloroquine (CQ), MDA-MB-231 cells were divided into control group, CQ treatment group, HS-10296 (4 and 6 μmol/L) treatment groups and combined treatment groups, and the sensitivity of the treated cells to HS-10296 was determined using CCK-8 assay. The effects of HS-10296 on EGFR pathway and apoptosis- and autophagy-related proteins in MDA-MB-231 cells were investigated using Western blotting. RESULTS: HS-10296 significantly inhibited the proliferation of MDA-MB-231 cells with IC values at 24, 48 and 72 h of 8.393, 2.777 and 2.016 μmol/L, respectively. JC-1 and flow cytometry showed that HS-10296 induced obvious apoptosis of MDA-MB-231 cells, which showed an apoptosis rate of (21.63 ± 2.97)% following treatment with 8 μmol/L HS-10296. Autophagy vesicles were observed in the cells treated with HS-10296 under electron microscope. In MDA-MB-231 cells pretreated with CQ, inhibition of autophagy significantly enhanced HS-10296-induced cell death. Western blotting showed that the apoptosis-related protein caspase-3 was activated after HS-10296 treatment to cut its substrate PARP. The expression of autophagy-related protein light chain 3B (LC3B) was significantly enhanced after HS-10296 treatment ( < 0.01), which also resulted in inhibited phosphorylation of EGFR and AKT proteins in the cells. CONCLUSIONS HS-10296 can inhibit the proliferation and induce autophagy and apoptosis of MDA-MB-231 cells by inhibiting the EGFR/PI3K/AKT signaling pathway.
Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Autophagy ; drug effects ; Breast Neoplasms ; drug therapy ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; ErbB Receptors ; metabolism ; Humans ; Protein Kinase Inhibitors ; pharmacology ; Signal Transduction ; drug effects

OBJECTIVE: To investigate the inhibitory effect of epidermal growth factor receptor tyrosine kinase inhibitor (EGFRTKI) HS-10296 on the proliferation of triple-negative breast cancer (TNBC) MDA-MB-231 cells and explore the possible molecular mechanism. METHODS: MDA-MB-231 cells were treated with HS-10296 for 24, 48, or 72 h, and CCK-8 assay was used to assess the changes in the cell viability. The inhibitory effect of HS-10296 on cell proliferation was determined by clonogenic assay. JC-1 and flow cytometry were employed for analyzing the cell apoptosis, and the ultrastructure of the cells was observed under electron microscope. After pretreatment with autophagy inhibitor chloroquine (CQ), MDA-MB-231 cells were divided into control group, CQ treatment group, HS-10296 (4 and 6 μmol/L) treatment groups and combined treatment groups, and the sensitivity of the treated cells to HS-10296 was determined using CCK-8 assay. The effects of HS-10296 on EGFR pathway and apoptosis- and autophagy-related proteins in MDA-MB-231 cells were investigated using Western blotting. RESULTS: HS-10296 significantly inhibited the proliferation of MDA-MB-231 cells with IC values at 24, 48 and 72 h of 8.393, 2.777 and 2.016 μmol/L, respectively. JC-1 and flow cytometry showed that HS-10296 induced obvious apoptosis of MDA-MB-231 cells, which showed an apoptosis rate of (21.63 ± 2.97)% following treatment with 8 μmol/L HS-10296. Autophagy vesicles were observed in the cells treated with HS-10296 under electron microscope. In MDA-MB-231 cells pretreated with CQ, inhibition of autophagy significantly enhanced HS-10296-induced cell death. Western blotting showed that the apoptosis-related protein caspase-3 was activated after HS-10296 treatment to cut its substrate PARP. The expression of autophagy-related protein light chain 3B (LC3B) was significantly enhanced after HS-10296 treatment ( < 0.01), which also resulted in inhibited phosphorylation of EGFR and AKT proteins in the cells. CONCLUSIONS HS-10296 can inhibit the proliferation and induce autophagy and apoptosis of MDA-MB-231 cells by inhibiting the EGFR/PI3K/AKT signaling pathway.
Apoptosis ; Autophagy ; Breast Neoplasms ; Cell Line, Tumor ; Cell Proliferation ; ErbB Receptors ; Humans ; Phosphatidylinositol 3-Kinases ; Protein Kinase Inhibitors