Objective:To investigate the risk factors and cumulative risk of myopia in children and adolescents, providing a basis for identifying cumulative risk factors in preventing and controlling myopia.Methods:Baseline data from the mental and physical health cohort of children and adolescents established in Inner Mongolia Autonomous Region were used. A stratified random cluster sampling method was adopted to select 138 974 students from fourth to twelfth grade as participants. Distance visual exams, refractive assessments, and questionnaires were conducted on the included students. Logistic regression analysis was used to evaluate each risk factor's impact on myopia's prevalence. The number of risk factors was summed to form a cumulative risk score, and logistic regression analysis was conducted to examine the association between the cumulative risk score and the prevalence of myopia. Additionally, the association between the cumulative risk score of myopic students and their degree of refractivity was analyzed using a generalized estimating equation.Results:The study found a high prevalence of myopia among children and adolescents at baseline (70.2%). Girls exhibited a higher prevalence (74.8%) than boys (65.6%), urban areas (74.3%) surpassed suburban ones (68.6%), and the incidence was greater in high schools (80.3%) compared to middle schools (75.3%), which, in turn, was higher than in elementary schools (57.7%) (all P<0.05). Analysis of risk factors revealed that children and adolescents experiencing improper reading and writing distances ( OR=1.10, 95% CI: 1.07-1.13), excessive homework ( OR=1.09, 95% CI: 1.06-1.12), insufficient sleep ( OR=1.10, 95% CI: 1.07-1.13), having myopic father ( OR=1.98, 95% CI: 1.91-2.05), having myopic mother ( OR=2.04, 95% CI: 1.97-2.10), or using classroom chairs not matched to their height faced ( OR=1.04, 95% CI: 1.01-1.07) increased myopia risks. Additionally, the prevalence and significant odds ratio of myopia increased with the increase in cumulative risk score, with every additional unit of cumulative risk score increasing the right eye's refractive error by -0.10 D. Conclusion:The presence of multiple factors and their comprehensive score increases the prevalence of myopia in children and adolescents.

Objective To investigate the role of high-mobility group AT-hook 2(HMGA2)in osteogenic differentiation of adipose-derived mesenchymal stem cells(ADSCs)and the effect of Hmga2 knockdown for promoting bone defect repair.Methods Bioinformatics studies using the GEO database and Rstudio software identified HMGA2 as a key factor in adipogenic-osteogenic differentiation balance of ADSCs.The protein-protein interaction network of HMGA2 in osteogenic differentiation was mapped using String and visualized with Cytoscape to predict the downstream targets of HMGA2.Primary mouse ADSCs(mADSCs)were transfected with Hmga2 siRNA,and the changes in osteogenic differentiation of the cells were evaluated using alkaline phosphatase staining and Alizarin red S staining.The expressions of osteogenic markers Runt-related transcription factor 2(RUNX2),osteopontin(OPN),and osteocalcein(OCN)in the transfected cells were detected using RT-qPCR and Western blotting.In a mouse model of critical-sized calvarial defects,mADSCs with Hmga2-knockdown were transplanted into the defect,and bone repair was evaluated 6 weeks later using micro-CT scanning and histological staining.Results GEO database analysis showed that HMGA2 expression was upregulated during adipogenic differentiation of ADSCs.Protein-protein interaction network analysis suggested that the potential HMGA2 targets in osteogenic differentiation of ADSCs included SMAD7,CDH1,CDH2,SNAI1,SMAD9,IGF2BP3,and ALDH1A1.In mADSCs,Hmga2 knockdown significantly upregulated the expressions of RUNX2,OPN,and OCN and increased cellular alkaline phosphatase activity and calcium deposition.In a critical-sized calvarial defect model,transplantation of mADSCs with Hmga2 knockdown significantly promoted new bone formation.Conclusion HMGA2 is a crucial regulator of osteogenic differentiation in ADSCs,and Hmga2 knockdown significantly promotes osteogenic differentiation of ADSCs and accelerates ADSCs-mediated bone defect repair in mice.

Objective To investigate the role of high-mobility group AT-hook 2(HMGA2)in osteogenic differentiation of adipose-derived mesenchymal stem cells(ADSCs)and the effect of Hmga2 knockdown for promoting bone defect repair.Methods Bioinformatics studies using the GEO database and Rstudio software identified HMGA2 as a key factor in adipogenic-osteogenic differentiation balance of ADSCs.The protein-protein interaction network of HMGA2 in osteogenic differentiation was mapped using String and visualized with Cytoscape to predict the downstream targets of HMGA2.Primary mouse ADSCs(mADSCs)were transfected with Hmga2 siRNA,and the changes in osteogenic differentiation of the cells were evaluated using alkaline phosphatase staining and Alizarin red S staining.The expressions of osteogenic markers Runt-related transcription factor 2(RUNX2),osteopontin(OPN),and osteocalcein(OCN)in the transfected cells were detected using RT-qPCR and Western blotting.In a mouse model of critical-sized calvarial defects,mADSCs with Hmga2-knockdown were transplanted into the defect,and bone repair was evaluated 6 weeks later using micro-CT scanning and histological staining.Results GEO database analysis showed that HMGA2 expression was upregulated during adipogenic differentiation of ADSCs.Protein-protein interaction network analysis suggested that the potential HMGA2 targets in osteogenic differentiation of ADSCs included SMAD7,CDH1,CDH2,SNAI1,SMAD9,IGF2BP3,and ALDH1A1.In mADSCs,Hmga2 knockdown significantly upregulated the expressions of RUNX2,OPN,and OCN and increased cellular alkaline phosphatase activity and calcium deposition.In a critical-sized calvarial defect model,transplantation of mADSCs with Hmga2 knockdown significantly promoted new bone formation.Conclusion HMGA2 is a crucial regulator of osteogenic differentiation in ADSCs,and Hmga2 knockdown significantly promotes osteogenic differentiation of ADSCs and accelerates ADSCs-mediated bone defect repair in mice.

Helicobacter pylori infection is an important causative factor in a variety of gastrointestinal diseases,such as atrophic gastritis,peptic ulcer disease,and gastric cancer.Timely eradication treatment is con-ducive to maintaining the health of patients.With the increase of drug resistance in Helicobacter pylori,dual therapy with proton pump inhibitors combined with high-dose amoxicillin has gradually gained attention.Potassium-competitive acid blockers are new types of antacids that have a faster onset of action and a longer lasting acid sup-pression effect than traditional proton pump inhibitors,making it more suitable for dual therapy.In recent years,scholars have carried out a lot of exploration,improvement and verification of potassium-competitive acid blockers dual therapy,and this article reviews its research progress.

Spinal cord injury (SCI) is a serious nervous system disease that usually leads to the impairment of the motor, sensory, and autonomic nervous functions of the spinal cord, and it places a heavy burden on families and healthcare systems every year. Due to the complex pathophysiological mechanism of SCI and the poor ability of neurons to regenerate, the current treatment scheme has very limited effects on the recovery of spinal cord function. In addition, due to their unique advantages, exosomes can be used as carriers for cargo transport. In recent years, some studies have confirmed that treatment with mesenchymal stem cells (MSCs) can promote the recovery of SCI nerve function. The therapeutic effect of MSCs is mainly related to exosomes secreted by MSCs, and exosomes may have great potential in SCI therapy. In this review, we summarized the repair mechanism of mesenchymal stem cells-derived exosomes (MSCs-Exos) in SCI treatment and discussed the microRNAs related to SCI treatment based on MSCs-Exos and their mechanism of action, which is helpful to further understand the role of exosomes in SCI.

Objective:To explore the effects of hospital-family multidisciplinary 5E rehabilitation model on clinical status, athletic ability, respiratory muscle strength, quality of life and psychological states of patients with myasthenia gravis (MG).Methods:This was a quasi-experimental study. According to the convenient sampling method, patients with type 2 MG treated in the First Affiliated Hospital of Harbin Medical University from January 2020 to September 2021 were divided into intervention group and control group. The control group was treated with routine nursing methods, and the intervention group was treated with hospital-family multidisciplinary 5E rehabilitation model for 12 weeks. The effects of intervention were compared by using Myasthenia Gravis Composite (MGC), 6-minute walking test (6MWT), maximum inspiratory pressure (MIP), Fatigue Scale-14 (FS-14), Myasthenia Gravis Quality of Life-15(MGQOL-15), Herth Hope Level Scale(HHI) and Self-Efficacy for Managing Chronic Disease 6-Item Scale (SES6C).Results:Repeated measurement analysis of variance showed that there were significant differences between 6MWT score and MGQOL-15 score twelve weeks after intervention, the intervention group scores were (477.95 ± 29.23), (6.25 ± 3.40) points, the control group scores were(435.85 ± 19.82), (9.95 ± 3.22) points, the differences were statistically significant ( t= 4.51, -3.58, both P<0.05). Besides, the differences of MIP, FS-14 score, SES6C score and HHI score were also statistically significant, the intervention group scores were (102.09 ± 19.56), (2.56 ± 1.31), (34.78 ± 8.68), (33.43 ± 6.39) points, the control group scores were (90.85 ± 12.25), (4.65 ± 2.50), (24.15 ± 6.62), (25.90 ± 8.30)points, the differences were statistically significant ( t values were -4.46-3.35, all P<0.05). Repeated measurement analysis of variance showed that there were significant differences in the time effect and interaction effect of MGQOL-15 score between the two groups ( F=28.28, 22.01, both P<0.05), there were also significant differences in the group effect, time effect, and interaction effect of 6MWT between the two groups ( F=13.94, 8.24, 12.85, all P<0.05). Conclusions:The rehabilitation of patients with MG could be promoted by the hospital-family multidisciplinary 5E rehabilitation model. Detailed research should be further strengthened to lay a foundation for the development of rehabilitation guidelines for patients with MG.

Objective To investigate the etiology，clinical manifestations，imaging features，and treatment of superficial siderosis of the central nervous system （SSCNS）. Methods A patient confirmed with SSCNS was reported.Sixty-one patients confirmed with SSCNS were found through a search of China National Knowledge Infrastructure and Wanfang Data and were analyzed in categories for the epidemiology， etiology， clinical manifestations， and laboratory test results. Results Among the 61 patients with SSCNS reported in the literature， ataxia was the most common clinical symptom （49 cases， 80%）， followed by hearing loss （43 cases，70%） and pyramidal signs（30 cases， 49%）.A probable cause was found in 25 （39%） of these cases. Conclusion SSCNS can last for several years or even decades， with hearing loss， ataxia， and pyramidal signs as its main clinical symptoms.Magnetic resonance imaging is the most valuable basis for diagnosis， and susceptibility-weighted imaging is more sensitive in the diagnosis of microhemorrhage.

The gastrointestinal microbiome is the most important and complex microecosystem in the human microecosystem,which participates in a variety of physiological processes of the human body and is related to a variety of disease processes.In recent years,the relationship between gastrointestinal microbiome and gastrointestinal tumors has attracted the attention of scholars,and a series of studies have been carried out on the exploration of gastrointestinal microbiota as a new non-invasive biomarker.This article reviewed the relationship between gastrointestinal microbiome and the diagnosis,occurrence and treatment of gastrointestinal tumors through esophageal cancer,gastric cancer,colorectal cancer,gastrointestinal microbiome and tumor treatment,so as to provide new ideas for finding potential molecular targets for prevention,treatment and intervention of tumors.

Objective:To investigate the therapeutic effect of humanized TRAB domain-containing protein 2A (TRABD2A) monoclonal blocking antibody to HIV-1 reservoir cells, and to explore novel methods for measuring the sizes/capacities of HIV-1 infected reservoirs in HIV-1 infected individuals on receiving combined antiretroviral therapy (cART).Methods:A total number of 51 subjects were collected from the First Affiliated Hospital of China Medical University from May 2021 to December 2021. Among them, there were 2 healthy persons, 41 HIV-1 infected persons receiving cART (cART group) and 8 HIV-1 infected persons not receiving cART (no cART group). Humanized TRABD2A monoclonal antibody was constructed based on the phage display technology, the PBMCs and CD4+T cells separated from the peripheral blood mononuclear cells (PBMCs) and CD4+T cells of HIV-1 infected patients treated with receiving cART, or the HIV-1 infected patients without cART treatment and healthy controls were treated with TRABD2A monoclonal antibodies. The luciferase reporter system, single molecule immune array detection technology and other methods were used to detect the virus content in the supernatant of cell culture. At the same time, flow cytometry and fluorescence real-time quantitative polymerase chain reaction were used to detect the activation of the treated cells and the expression of virus genes. The statistical differences between different treatment the amount of virus release and the level of surface activation markers CD25, CD69, human leukocyte antigen DR (HLA-DR) of different groups in the amount of virus release and the expression of surface activation markers CD25, CD69, HLA-DR were compared.Results:The PBMCs of HIV-1 infected persons receiving cART were tested for HIV-1 production after being treated with humanized TRABD2A monoclonal antibody. The amount of virus released by the untreated group was 0 (0, 440), and the amount of virus released by the use of negative antibody was 0 (0, 390). There was no significant difference between the two ( P>0.05). The amount of virus released by the use of positive antibody was 1 259 (0, 4 269), 3 142 (1 292, 5 060), compared with the amount of virus released by the use of negative antibody, The difference was statistically significant ( P<0.05). The healthy control PBMC was used to conduct multiple dilutions to the infected PBMC. After positive antibody treatment, the amount of virus release decreased in equal proportions [the HIV-1 production corresponding to 5, 25, 125, 625 times of undiluted, diluted PBMC was 4 670 (3 339, 7 697), 1 860 (1 509, 4 615), 1 550 (1 150, 2 680), 602 (255, 1 441), 2 (0, 37), respectively].In addition, there was no significant difference in the resting state of cells treated with TRABD2A antibodies compared with the untreated group (The percentage of CD25 positive cells in the untreated group and positive antibody 1 treated group were 3.89±1.31 and 4.60±1.74, the percentage of CD69 positive cells were 2.50±1.27 and 2.18±0.51, and the percentage of HLA-DR positive cells were 7.66±3.78 and 8.79±3.42, respectively, P>0.05). The viral gag expression levels of untreated and positive antibody 1 were 1 and 0.82±0.55, respectively, with no significant difference. Conclusions:The humanized TRABD2A monoclonal antibody can effectively block the protein activity of TRABD2A, and can significantly promote the release of progeny viruses from viral reservoir in the peripheral blood of HIV-1 infected persons without changing the cell resting state and the whole genome transcription level. The amount of virus released in this way is positively related to the number of reservoir cells.

Objective To summarize clinical experience of transabdominal pericardial anastomosis of suprahepatic vena cava of the donor and right atrium of the recipient in liver transplantation for Budd-Chiari syndrome (BCS) complicated with liver cancer. Methods Clinical data of a BCS patient complicated with liver cancer undergoing transabdominal pericardial anastomosis of suprahepatic vena cava and right atrium in liver transplantation were retrospectively analyzed. Results The hepatic vein and suprahepatic vena cava were partially occluded in the patient. Liver transplantation was completed by transabdominal pericardial anastomosis of suprahepatic vena cava and right atrium with beating-heart. In addition, due to pathological changes of the recipient's hepatic artery, splenic artery of the recipient was cut off, distal ligation was performed, and the proximal end was reversed and anastomosed with the common hepatic artery of the donor liver, and the reconstruction of hepatic artery was completed. The surgery was successfully performed. At approximately postoperative 1 week, the function of the liver allograft was gradually restored to normal, and no major complications occurred. The patient was discharged at postoperative 25 d. No signs of BCS recurrence was reported after 8-month follow-up. Conclusions It is safe and feasible to treat BCS by liver transplantation with transabdominal pericardial anastomosis of suprahepatic vena cava and right atrium. BCS patients complicated with liver cancer obtain favorable prognosis.