Objective:To analyze the prevalence, trends in disease burden, and risk factors of esophageal cancer in various provinces of China from 1990 to 2019.Methods:Utilizing data from the 2019 global burden of disease study, the disease burden of esophageal cancer of 31 provinces, municipalities, and autonomous regions, as well as Hong Kong Special Administrative Region and Macao Special Administrative Region of China from 1990 to 2019 were analyzed. The disease burden of esophageal cancer in China was described with the number (and incidence) of cases, the number (and mortality) of death, and disability-adjusted life year (DALY) and their age-standardized rates. Joinpoint regression analysis and t-test were used to evaluate the annual percent change and the average annual percent change (AAPC). Scatter plots and Spearman correlation coefficients were performed to analyze the correlation between the disease burden of esophageal cancer and the socio-demographic index (SDI), as well as DALY in each province. Results:In 2019, there were 278 121 new cases of esophageal cancer and 257 316 deaths in China, increased by 60.13% and 45.70% respectively compared with 1990. The top 3 provinces with the highest age-standardized incidence of esophageal cancer were Sichuan Province (25.96/100 000), Jiangsu Province (23.80/100 000), and Fujian Province (21.98/100 000). From 1990 to 2019, except for Jiangsu Province and Sichuan Province, the age-standardized incidence in other provinces showed a declining trend. The age-standardized mortality and DALYs of esophageal cancer decreased in all provinces as well as in Hong Kong and Macao Special Administrative Regions of China. The attributable risk factors of esophageal cancer caused deaths in China mainly included smoking, alcohol consumption, high body mass index, and low fruit intake, accounting for 91.38% of all the cases. With the increase of the SDI, the age-standardized rates of DALY in high incidence areas of esophageal cancer (Sichuan Province, Jiangsu Province, Fujian Province, Henan Province, Chongqing City, Xinjiang Uygur Autonomous Region, Shanxi Province, and Anhui Province) demonstrated a trend of initially decline and then an upward. In contrast, the age-standardized rates of DALY of esophageal cancer in other provinces, as well as in Hong Kong and Macao Special Administrative Regions of China, showed a trend of initially upward and then decline. The age-standardized rate of DALY of esophageal cancer showed a negative correlation with SDI ( r=-0.315, P<0.001). From 1990 to 2019, the age-standardized incidence and mortality of esophageal cancer generally demonstrated a downward trend. The AAPC was -1.43% ( t=-19.16, P<0.001) for incidence and -1.83% ( t=-29.63, P<0.001) for mortality, respectively. It is projected that by 2044, the actual number of new esophageal cancer cases in China will increase from 278 121 in 2019 to 291 206 in 2044, and the actual number of deaths will increase from 257 316 to 275 856. Conclusions:In recent years, the disease burden of esophageal cancer in China remains a serious status, with significant differences in geography and gender. It is projected that by 2044, the number of new esophageal cancer cases and deaths in China will continue to increase. Effective strategies and policies are urgently needed to reduce the disease burden.

Objective:To analyze the prevalence, trends in disease burden, and risk factors of esophageal cancer in various provinces of China from 1990 to 2019.Methods:Utilizing data from the 2019 global burden of disease study, the disease burden of esophageal cancer of 31 provinces, municipalities, and autonomous regions, as well as Hong Kong Special Administrative Region and Macao Special Administrative Region of China from 1990 to 2019 were analyzed. The disease burden of esophageal cancer in China was described with the number (and incidence) of cases, the number (and mortality) of death, and disability-adjusted life year (DALY) and their age-standardized rates. Joinpoint regression analysis and t-test were used to evaluate the annual percent change and the average annual percent change (AAPC). Scatter plots and Spearman correlation coefficients were performed to analyze the correlation between the disease burden of esophageal cancer and the socio-demographic index (SDI), as well as DALY in each province. Results:In 2019, there were 278 121 new cases of esophageal cancer and 257 316 deaths in China, increased by 60.13% and 45.70% respectively compared with 1990. The top 3 provinces with the highest age-standardized incidence of esophageal cancer were Sichuan Province (25.96/100 000), Jiangsu Province (23.80/100 000), and Fujian Province (21.98/100 000). From 1990 to 2019, except for Jiangsu Province and Sichuan Province, the age-standardized incidence in other provinces showed a declining trend. The age-standardized mortality and DALYs of esophageal cancer decreased in all provinces as well as in Hong Kong and Macao Special Administrative Regions of China. The attributable risk factors of esophageal cancer caused deaths in China mainly included smoking, alcohol consumption, high body mass index, and low fruit intake, accounting for 91.38% of all the cases. With the increase of the SDI, the age-standardized rates of DALY in high incidence areas of esophageal cancer (Sichuan Province, Jiangsu Province, Fujian Province, Henan Province, Chongqing City, Xinjiang Uygur Autonomous Region, Shanxi Province, and Anhui Province) demonstrated a trend of initially decline and then an upward. In contrast, the age-standardized rates of DALY of esophageal cancer in other provinces, as well as in Hong Kong and Macao Special Administrative Regions of China, showed a trend of initially upward and then decline. The age-standardized rate of DALY of esophageal cancer showed a negative correlation with SDI ( r=-0.315, P<0.001). From 1990 to 2019, the age-standardized incidence and mortality of esophageal cancer generally demonstrated a downward trend. The AAPC was -1.43% ( t=-19.16, P<0.001) for incidence and -1.83% ( t=-29.63, P<0.001) for mortality, respectively. It is projected that by 2044, the actual number of new esophageal cancer cases in China will increase from 278 121 in 2019 to 291 206 in 2044, and the actual number of deaths will increase from 257 316 to 275 856. Conclusions:In recent years, the disease burden of esophageal cancer in China remains a serious status, with significant differences in geography and gender. It is projected that by 2044, the number of new esophageal cancer cases and deaths in China will continue to increase. Effective strategies and policies are urgently needed to reduce the disease burden.

Background::Evaluating the impact of digestive system diseases is vital for devising effective prevention strategies. However, comprehensive reports on the burden of digestive system diseases in China are lacking. Our study aimed to provide an overview of the burden and trends of digestive system diseases from 1990 to 2019 in China and its provinces.Methods::This cross-sectional study utilized the Global Disease Burden Study 2019 to estimate the incidence, mortality rate, disability-adjusted life years (DALYs), years of life disability, years of life lost, and changes in the burden of digestive diseases across Chinese provinces from 1990 to 2019. The analysis of disease burden primarily examines the characteristics of sub-disease distribution, time trends, age distribution, and sex distribution. Additionally, we compared provincial age-standardized DALYs for digestive diseases with the expected rates based on the socio-demographic index (SDI).Results::In 2019, there were 499.2 million cases of digestive system diseases in China, resulting in 1,557,310 deaths. Stomach cancer, colon and rectal cancer, and esophageal cancer are the top three diseases associated with mortality and DALY related to digestive system diseases. Meanwhile, cirrhosis and other chronic liver diseases, gastroesophageal reflux disease, and gallbladder and biliary diseases are the top three kinds of diseases with the highest prevalence among digestive system diseases. The risk of gastric cancer sharply increases among men after the age of 40 years, leading to a significant disparity in burden between men and women. As the SDI increased, the DALYs associated with digestive system diseases in China and its provinces showed a downward trend.Conclusion::Our study highlights the inverse correlation between DALYs associated with digestive system diseases and the SDI.

Periarticular fracture of the shoulder is a common type of fractures in the elderly. Postoperative adverse events such as internal fixation failure, humeral head ischemic necrosis and upper limb dysfunction occur frequently, which seriously endangers the exercise and health of the elderly. Compared with the fracture with normal bone mass, the osteoporotic periarticular fracture of the shoulder is complicated with slow healing and poor rehabilitation, so the clinical management becomes more difficult. At present, there is no targeted guideline or consensus for this type of fracture in China. In such context, experts from Youth Osteoporosis Group of Chinese Orthopedic Association, Orthopedic Expert Committee of Geriatrics Branch of Chinese Association of Gerontology and Geriatrics, Osteoporosis Group of Youth Committee of Chinese Association of Orthopedic Surgeons and Osteoporosis Committee of Shanghai Association of Chinese Integrative Medicine developed the Chinese expert consensus on the diagnosis and treatment of osteoporotic periarticular fracture of the shoulder in the elderly ( version 2023). Nine recommendations were put forward from the aspects of diagnosis, treatment strategies and rehabilitation of osteoporotic periarticular fracture of the shoulder, hoping to promote the standardized, systematic and personalized diagnosis and treatment concept and improve functional outcomes and quality of life in elderly patients with osteoporotic periarticular fracture of the shoulder.

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 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 investigate the significance and mechanism of ten-eleven translocation (Tet1) against Mycobacterium marinum ( Mm) infection in mice. Methods:SPF wild-type C57BL/6 and Tet1-knockout (Tet1KO) mice were injected intravenously with Mm. All mice were monitored and the abscesses formed in tail were observed and quantified. Pathological changes in mouse tail tissues were observed using hematoxylin and eosin (HE) staining and transmission electron microscopy and the differences between the two groups were analyzed. Immunohistochemistry staining was used to detect the expression and distribution of TNF-α and TGF-β in mouse tail tissues. Moreover, mouse tail tissues were cultured on 7H10 plates for bacterial counting. The expression of NF-κBp65 and TGF-β was detected by Western blot. Results:Obvious lesions including abscesses and ulcers were formed in the Mm-infected C57BL/6, but only scattered small abscesses were observed in Mm-infected Tet1KO mice. During Mm infection, the bacterial load was gradually increased in C57BL/6 mice, but decreased in Tet1KO mice. Histopathological examination showed that obvious inflammatory cell infiltration and typical granulomatous lesions were found in Mm-infected C57BL/6 mice, while no significant inflammatory cell infiltration was detected in Mm-infected Tet1KO mice. Immunohistochemistry staining demonstrated that the expression of TNF-α and TGF-β was lower in Mm-infected Tet1KO mice than in Mm-infected C57BL/6 mice. Moreover, the expression of phosphorylated NF-κBp65 and TGF-β was significantly reduced in Mm-infected Tet1KO mice as compared with that in Mm-infected C57BL/6 mice. Conclusions:Deletion of Tet1 could alleviate the inflammatory damage mediated by Mm and enhance the host immune response to bacteria.

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.