Osteoporotic proximal humeral fracture (OPHF) is one of the common osteoporotic fractures in the aged, with an incidence only lower than vertebral compression fracture, hip fracture, and distal radius fracture. OPHF, secondary to osteoporosis and characterized by poor bone quality, comminuted fracture pattern, slow healing, and severely impaired shoulder joint function, poses a big challenge to the current clinical diagnosis and treatment. In the field of diagnosis, treatment, and rehabilitation of OPHF, traditional Chinese and Western medicine have accumulated rich experience and evidence from evidence-based medicine and achieved favorable outcomes. However, there is still a lack of guidance from a relevant consensus as to how to integrate the advantages of the two medical systems and achieve the integrated diagnosis and treatment. To promote the diagnosis and treatment of OPHF with integrated traditional Chinese and Western medicine, relevant experts from Orthopedic Expert Committee of Geriatric Branch of Chinese Association of Gerontology and Geriatrics, Youth Osteoporosis Group of Orthopedic Branch of Chinese Medical Association, Osteoporosis Group of Orthopedic Surgeon Branch of Chinese Medical Doctor Association, and Osteoporosis Committee of Shanghai Association of Integrated Traditional Chinese and Western Medicine have been organized to formulate Expert consensus on the diagnosis and treatment of osteoporotic proximal humeral fracture with integrated traditional Chinese and Western medicine ( version 2024) by searching related literatures and based on the evidences from evidence-based medicine. This consensus consists of 13 recommendations about the diagnosis, treatment and rehabilitation of OPHF with integrated traditional Chinese medicine and Western medicine, aimed at standardizing, systematizing, and personalizing the diagnosis and treatment of OPHF with integrated traditional Chinse and Western medicine to improve the patients ′ function.

Objective:According to the international cooperation project of Peking University Cancer Hospital on human genetic resource management practices, combined with the development direction of human genetic resource management laws and regulations, and propose reference suggestions for medical institutions to strengthen human genetic resource management.Methods:Sort out the projects that Peking University Cancer Hospital obtained international cooperation approval on the government platform of the Ministry of Science and Technology from July 2019 to June 2023, analyze the current situation of human genetic resource management in the hospital, summarize the challenges brought by the implementation of new regulations on human genetic resource management in medical institutions, and propose corresponding suggestions.Results:A total of 1276 international cooperation projects on human genetic resources have been approved, including 345 initial declarations and 931 change declarations. Involving 453 studies, including 286 clinical trials of drugs or devices on the market, accounting for 63.13%, and 100 clinical trials of Phase I drugs, accounting for 34.97% of the market studies. On average, there are 3.14 changes per project for listed research, and 1.56 changes per project for non listed research.Conclusions:Regulations on the Management of Human Genetic Resources ( short for Rules) limit the management scope of international cooperation projects involving human genetic resources and delegate management authority to medical institutions. Adjusting the scope of application for international cooperative clinical trial filing may result in some administrative approval projects being transferred to filing. The approval process for international cooperative scientific research projects on human genetic resources has been adjusted. Suggest medical institutions to strengthen the management of samples and intellectual property outside the scope of application of Rules.Strengthen the entire process management of international cooperation in scientific research. Pay attention to and timely communicate the dynamics of human genetic resource management.

Objective:To explore the clinical value of a trinity strategy for the treatment of multiple orthopedic trauma.Methods:A retrospective case series study was conducted to analyze the clinical data of 1 267 patients with multiple orthopedic trauma admitted to Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine and the First Affiliated Hospital of Navy Medical University from June 2013 to May 2023, including 862 males and 405 females, aged 18-93 years [(55.2±19.8)years]. Associated injuries included hemorrhagic shock in 632 patients, traumatic wet lung in 274, cranial injuries in 135, abdominal and pelvic bleeding in 116, pneumothorax in 89, urinary injury in 13, and vesical rupture in 8. All the patients were treated with the trinity strategy and the treatment process was divided into the phases of first aid, remodeling, and rehabilitation. The first aid phase focused on stabilizing symptoms and saving lives; the remodeling phase centered on restoring the anatomical structure and alignment; the rehabilitation phase aimed for functional recovery through the integration of both Western and traditional Chinese medicine. The all-cause mortality within 30 days after surgery and fracture healing time were calculated; the excellent and good rates of Constant-Murley shoulder score, Mayo elbow score, Gartland-Werley wrist score, Harris hip score, Hospital for Special Surgery (HSS) knee score and the American Orthopedic Foot & Ankle Society (AOFAS) ankle-hindfoot score at the last follow-up and the overall excellent and good rate of all joint function scores were measured. The short form health survey (SF-36) scores were collected preoperatively and at 6 months postoperatively, including 8 aspects such as physical functioning, physical role, bodily pain, general health, vitality, social functioning, emotional role, and mental health. The incidence of postoperative complications was recorded.Results:All the patients were followed up for 6-18 months [(10.2±4.2)months]. The mortality rate during the acute phase (within 30 days after surgery) was 2.37% with 12 deaths due to hemorrhagic shock, 10 due to traumatic brain injury, 6 due to multiple organ dysfunction syndrome (MODS), and 2 due to pulmonary infection. The average fracture healing time averaged 3.8-18 months [(11.5±4.2)months], with 89.49% of the patients having bone union within 12 months after surgery, 8.93% having bone union within 18 months after surgery, and 1.58% undergoing reoperation. For the patients with internal fixation failure and nonunion, the average healing time was extended to (10.2±2.2)months and (13.7±3.3)months respectively. At the last follow-up, the excellent and good rates of Constant-Murley shoulder score, Mayo elbow score, Gartland-Werley wrist score, Harris hip score, HSS knee score, and AOFAS ankle-hindfoot score were 83.93%, 90.24%, 94.12%, 85.57%, 88.46%, and 92.31% respectively, with an overall excellent and good rate of 89.11%. At 6 months after surgery, the SF-36 scores of all the patients in the eight dimensions,including the physical functioning, physical role, bodily pain, general health, vitality, social functioning, emotional role, and mental health were (74.4±8.6)points, (44.7±14.4)points, (77.4±10.9)points, (68.4±18.2)points, (72.5±16.0)points, (76.8±8.7)points, (49.9±17.6)points, and (72.8±17.9)points, significantly improved compared with those before operation [(63.4±12.7)points, (30.9±17.4)points, (56.4±18.0)points, (55.4±24.7)points, (53.5±21.0)points, (55.8±24.3)points, (36.9±24.0)points, (58.8±21.6)points] ( P<0.01). Complications of different degrees occurred in 214 patients (16.89%), including lung infections in 118 patients (9.31%), lower extremity deep vein thrombosis in 50(3.95%), pressure injuries in 26(2.05%), internal fixation failure in 12(0.95%), and nonunion in 8(0.63%). Conclusions:The trinity strategy provides whole-process management, personalized treatment, and overall rehabilitation for multiple orthopedic trauma. It can decrease mortality, shorten fracture healing time, improve joint function and quality of life, and reduce the incidence of complications.

Bone organoids can simulate the complex structure and function of the bone tissues, which makes them a frontier technology in organoid researches. Bone organoids show a tremendous potential of applications in bone disease modeling, bone injury repair, and medicine screening. Although advancements have been made so far in constructing bone organoids with functional structures like mineralization, bone marrow, trabecular bone, callus, woven bone, etc, the researches in this field are confronted with numerous challenges such as lack of standardized construction strategies and unified evaluation criteria, which limits their further promotion and application. To standardize researches in bone organoids, the Orthopedic Expert Committee of Geriatric Branch of Chinese Association of Gerontology and Geriatrics, the Youth Osteoporosis Group of Orthopedic Branch of Chinese Medical Association, the Osteoporosis Group of Orthopedic Surgeon Branch of Chinese Medical Doctor Association, and the Osteoporosis Committee of Shanghai Association of Integrated Traditional Chinese and Western Medicine organized related experts to formulate Expert consensus on the construction, evaluation, and application of bone organoids ( version 2024) based on an evidence-based approach. A total of 17 recommendations were put forth, aiming to standardize researches and clinical applications of bone organoids and enhance their value in scientific research and clinical practice.

Objective:To explore the effect of long non-coding RNA (lncRNA) C10orf25 on the proliferation and invasion ability of prostate cancer cells and the possible role of miRNA-671-5p (miR-671-5p).Methods:Data from the Gene expression omnibus (GEO) database (data updated in January 2023) were used to analyze the differences in the expression levels of C10orf25 in 137 cases of prostate cancer tissues and paracancerous tissues. Prostate cancer C4-2B, DU-145, 22Rv1, PC-3, LNCaP cell lines and immortalized prostate epithelial RWPE-1 cell lines were selected, and then real-time quantitative fluorescence polymerase chain reaction (qRT-PCR) was used to detect the relative expression levels of C10orf25 in cell lines. The 22Rv1 cells with the lowest relative expression level of C10orf25 were selected and divided into the control group (transfected with negative plasmid) and the C10orf25 group (transfected with C10orf25 plasmid); the CCK-8 method was used to detect the proliferation activity of 22Rv1 cells in both groups at day 1, 2, 3, 4, 5 (expressed as absorbance value); the Transwell method was used to detect the invasion ability of 22Rv1 cells. Linc2GO software was used to predict miR-671-5p with binding sites for C10orf25. Dual luciferase reporter gene assay was used to verify the targeting relationship between C10orf25 and miR-671-5p. qRT-PCR was used to detect the relative expression levels of C10orf25 and miR-671-5p. Western blot was used to detect the expression of proteins related to the NF-κB signaling pathway of 22Rv1 cells in the both groups.Results:In the GEO database, the relative expression level of C10orf25 in prostate cancer tissues was lower than that in paracancerous tissues ( P < 0.01). The relative expression levels of C10orf25 in immortalized prostate epithelial cell line RWPE-1 and prostate cancer cell lines C4-2B, DU-145, 22Rv1, PC-3, and LNCaP were 1.00±0.05, 0.63±0.04, 0.42±0.03, 0.18±0.04, 0.81±0.02, 0.50±0.07, and the difference was statistically significant ( F = 43.29, P < 0.05). The proliferation ability of 22Rv1 cells in C10orf25 group was lower than that in the control group from the second day, and the differences were statistically significant (all P < 0.05). The number of invasive cells in the control group and C10orf25 group were (97±11) and (36±9), respectively, and the difference was statistically significant ( t = 4.15, P < 0.01). Linc2GO software prediction results showed that C10orf25 had a binding site for miR-671-5p. The dual luciferase reporter gene assay showed that the relative luciferase activity of miR-671-5p and C10orf25 wild plasmid co-transfecting 22Rv1 cells was lower than that of miR-NC and C10orf25 wild plasmid co-transfecting 22Rv1 cells, and the difference was statistically significant ( P < 0.01); when miR-671-5p or miR-NC was co-transfected with C10orf25 mutant plasmid, the difference in the luciferase activity of 22Rv1 cells was not statistically significant ( P > 0.05). The relative expression levels of miR-671-5p in 22Rv1 cells were 7.33±0.99 and 0.98±0.16, respectively in the control group and C10orf25 group, and the difference was statistically significant ( t = 6.32, P < 0.01). The results of Western blot showed that the expression levels of NF-κB signaling pathway protein p50, matrix metalloproteinase 9, c-myc, and vascular endothelial growth factor protein in 22Rv1 cells in C10orf25 group were lower than those in the control group. Conclusions:The overexpression of C10orf25 may inhibit the proliferation and invasion of prostate cancer cells through the miR-671-5p-NF-κB axis.

Objective:To explore the expression of microRNA (miRNA)-6516-5p in renal cancer cell lines and the molecular mechanisms regulating the proliferation and migration of renal cancer cells.Methods:quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of miR-6516-5p in renal cancer cell lines and normal proximal renal tubular epithelial cell lines. The liposome method was used to transiently transfect miR-6516-5p mimic and nonsense sequence (NC) into renal cancer cells with the lowest expression of miR-6516-5p, namely miR-6516-5p group and NC group. qRT-PCR was used to detect the expression of miR-6516-5p in transfected cells. CCK-8 and Transwell migration experiment were used to detect the proliferation and migration of transfected cells. Bioinformatics software and dual luciferase gene report experiment were used to predict and verify the regulation of miR-6516-5p on target gene, respectively. qRT-PCR and Western blotting were used to detect the expression of target gene in transfected cells. Measurement data were expressed as mean±standard deviation ( ± s), t-test was used for comparison between two groups, and one-way analysis of variance was used for comparison between multiple groups. Results:The expression of miR-6516-5p in renal cancer cell lines was significantly lower than that of normal proximal tubular epithelial cells ( P<0.01), and the expression of miR-6516-5p in 786-O cells was the lowest ( F=27.69, P<0.01). The expression of miR-6516-5p in 786-O cells in NC group and miR-6516-5p group was 1.01±0.08 and 9.91±1.16, respectively. Compared with the NC group, the expression of miR-6516-5p in 786-O cells in the miR-6516-5p group was significantly increased ( t=7.63, P<0.01). Up-regulation of miR-6516-5p can significantly inhibit the proliferation of 786-O cells ( P<0.05). The migration numbers of NC group and miR-6516-5p group were 85.65±8.77 and 28.05±6.20, respectively. Overexpression of miR-6516-5p could inhibit the migration of 786-O cells ( t=5.36, P< 0.01). The target gene of miR-6516-5p may be ornithine decarboxylase 1 ( ODC1), miR-6516-5p can significantly inhibit the luciferase activity of wild-type ODC1-3′UTR ( t=9.83, P<0.01). Up-regulation of miR-6516-5p can reduce the expression of ODC1 mRNA and protein in 786-O cells ( P<0.01). Conclusion:The expression of miR-6516-5p is reduced in renal cancer cell lines, miR-6516-5p inhibits the proliferation and migration of renal cancer 786-O cells by targeting ODC1, miR-6516-5p may become a potential molecular target of renal cancer.

Objective:To investigate the mechanism of physcion affecting the cell cycle and proliferation of prostate cancer DU145 cell line by regulating the expression of miR-380-3p.Methods:Prostate cancer DU145 cells were treated with 50 μg/mL physcion as physcion group, and normal cultured DU145 cells without any treatment were used as control group. Flow cytometry was used to detect DU145 cell cycle changes. MTT proliferation test was used to detect the proliferation of DU145 cells. quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of miR-380-3p in DU145 cells. The bioinformatics software RNAhybrid was used to predict the target genes of miR-380-3p. qRT-PCR and Western blotting methods were used to detect the expression of miR-380-3p target gene. Measurement data were expressed as mean ± standard deviation ( ± s), t-test was used for comparison between two groups. Results:Compared with the control group, DU145 cells in the physcion group were blocked in the G 0/G 1 phase ( P<0.01), and the proliferation ability of DU145 cells was significantly inhibited ( P<0.05). The expression of miR-380-3p in DU145 cells in the control group and physcion group was 8.36 ± 1.42 and 1.08 ± 0.39, respectively. Physcion could promote the expression of miR-380-3p ( t=4.96, P<0.01). The functional target gene of miR-380-3p may be UHRF1. The relative expression levels of UHRF1 mRNA in DU145 cells in the physcion group and control group were 0.23±0.06 and 1.04±0.15, respectively. Compared with the control group, the expression of UHRF1 gene in DU145 cells in the physcion group was decreased ( t=4.55, P<0.01). Conclusion:Physcion can inhibit the proliferation of prostate cancer DU145 cells and induce G 0/G 1 block in DU145 cells, which may be closely related to the regulation of miR-380-3p.

Objective:To explore the expression of long non-coding RNA LINC00630 in bladder cancer cell lines, and to explore the effect of interference with its expression in vitro on the proliferation and migration of bladder cancer cells.Methods:Real-time fluorescent quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression of LINC00630 in bladder cancer cell lines 5637, BIU-87, T24, J82 and normal bladder epithelial cell line SV-HUC-1. The bladder cancer cell line with the highest LINC00630 expression was selected for follow-up experiments, then the cell line infected with the control lentivirus was used as the control group, and the cell line infected with the lentivirus that could interfere with the expression of LINC00630 was used as the experimental group. qRT-PCR was used to detect the expression of LINC00630 in the two groups of cells. MTS method and cell scratch test were used to detect the proliferation and migration abilities of cells in the two groups. qRT-PCR was used to detect the expression of neuregulin 1 (NRG1) mRNA in the two groups of cells, and Western blot was used to detect the expressions of NRG1 protein, cell proliferation-related proteins (cyclin D3 and CDK2) and cell migration-related proteins (Vimentin and N-cadherin) in the two groups of cells.Results:Compared with SV-HUC-1 cells (1.05±0.17), the expression of LINC00630 was significantly increased in all bladder cancer cell lines (all P < 0.01), and the expression was highest in J82 cells (relative expression 5.83±0.42). Compared with J82 cells of the control group, the expression of LINC00630 in J82 cells of the experimental group decreased (0.18±0.02 vs. 1.00±0.05, t=14.36, P < 0.01); from day 2 of transfection, the cell proliferation activity of the experimental group was lower than that of the control group (all P < 0.05). The cell scratch closure rate of the experimental group was lower than that of the control group [(27.4±7.1)% vs. (66.0±5.4)%, t = 4.31, P < 0.01]. Therelative expression of NRG1 mRNA in the experimental group was lower than that in the control group (0.34±0.03 vs. 1.07±0.24, t = 2.99, P < 0.05). Compared with the control group, the expressions of NRG1 protein, cell proliferation-related proteins and cell migration-related proteins in the experimental group were reduced. Conclusions:LINC00630 is up-regulated in bladder cancer cell lines, and interference with LINC00630 may inhibit the proliferation and migration of J82 cells by down-regulating the expression of NRG1 gene. LINC00630 may be a new molecular target for the treatment of bladder cancer.

Objective:To explore the effect of long non-coding RNA (lncRNA) AC068768.1 on the cycle and proliferation of renal cancer cells and its molecular mechanism.Methods:Real-time quantitative polymerase chain reaction (qPCR) was used to detect the expression of AC068768.1 in renal cancer cell lines. The OS-RC-2 cells with the lowest expression of AC068768.1 were used as the transfection objects, OS-RC-2 transfected with the negative control plasmid was set as the control group, and the cells transfected with the AC068768.1 plasmid were set as the AC068768.1 group. qPCR was used to detect the expression of AC068768.1 in transfected OS-RC-2 cells. The effects of AC068768.1 on the cell cycle and proliferation of OS-RC-2 were detected by flow cytometry and tetramethylazazole blue colorimetric (MTT) proliferation experiments. Using bioinformatics methods to predict the microRNA (miRNA) that AC068768.1 may bind. qPCR was used to detect the expression of miRNA and downstream gene mRNA, and Western blot was used to detect the expression of downstream gene protein.The measurement data were expressed as mean±standard deviation ( Mean± SD), the comparison between the two groups adopts the t-test, and the comparison among multiple groups adopts the One-way analysis of variance. Results:Compared with normal renal tubular epithelial cells, the expression of AC068768.1 in renal cancer cell lines was significantly reduced, the difference was statistically significant ( P<0.01). The expression of AC068768.1 in OS-RC-2 cells in the AC068768.1 group was significantly higher than that in the control group, the difference was statistically significant ( P<0.01). Up-regulating the expression of AC068768.1 can inhibit the cycle ( P<0.05) and proliferating ability ( P<0.05) of renal cancer cells. miR-21-5p may be the functional target gene of AC068768.1. Up-regulation of AC068768.1 can significantly inhibit the expression of miR-21-5p ( P<0.01) and promote the expression of tissue inhibitor of metalloproteinase 3 (TIMP3) ( P<0.01). Conclusion:AC068768.1 promotes the expression of TIMP3 gene by regulating the expression of miR-21-5p, thereby inhibiting the cell cycle and proliferation of renal cancer OS-RC-2 cells.

Objective:To evaluate the effect of propofol on right ventricular hypertrophy induced by pulmonary arterial hypertension (PAH) in rats.Methods:Twenty-two clean-grade healthy adult male Wistar rats, weighing 250-280 g, were divided into 3 groups using a random number table method: control group (group C, n=8), PAH group (group PH, n=6) and propofol group (group P, n=8). In PH and P groups, monocrotaline 60 mg/kg was injected intraperitoneally to establish the model of PAH, while the equal volume of normal saline was administered in group C. Propofol 100 mg/kg was injected intraperitoneally twice a week for 6 consecutive weeks starting from 2 weeks after establishment of the model in group P. The weight of rats was measured before establishment of model and after administration, and the weight difference (△BW=weight after administration-weight before administration) was calculated.At the end of administration, the right ventricular end-diastolic dimension (RVEDD), right ventricular wall thickness in diastole (RVWTd), intraventricular septum in diastole (IVSd), left ventricular posterior wall in diastole (LVPWd) and maximal velocity of pulmonic valve (PV) were measured using cardiac ultrasound.The animals were then sacrificed, and the lungs and hearts were removed for examination of the pathological changes (after haematoxylin and eosin staining) and for determination of the degree of myocardial fibrosis in right ventricular (by Masson staining), expression of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) in lung tissues and myocardial tissues of the right ventricle (by immunohistochemistry). Results:Compared with group C, △BW and PV were significantly decreased, RVWTd, IVTd and RVEDD were increased, the thickness of the wall of pulmonary arterioles and myocardial cell penetration area in right ventricular were increased, the expression of IL-6 and TNF-α in lung tissues and myocardial tissues of right ventricle was up-regulated ( P<0.05 or 0.01), inflammatory cell infiltration and structural disorders were found in lung tissues, and intercellular spaces were widened, and the myocardial tissue was extensively fibrotic in group PH.Compared with group PH, △BW and PV were significantly increased, RVWTd, IVTd and RVEDD were decreased, the thickness of the wall of pulmonary arterioles and myocardial cell penetration area (the area of cardiomyocytes in which the nucleus located in the middle) were decreased, the expression of IL-6 and TNF-α in lung tissues and myocardial tissues of right ventricle was down-regulated ( P<0.05 or 0.01), inflammatory cell infiltration, structural disorders, intercellular spaces and degree of fibrosis were improved in group P. Conclusion:Propofol can alleviate right ventricular hypertrophy induced by PAH, and the mechanism is probably related to reduction of inflammatory responses in rats.