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ObjectiveTo investigate the effect of cSN50.1 on the proliferation， migration， invasion， and colony formation of HepG2 cells and its mechanism. MethodsHepG2 cells were divided into cSN50.1 0 μmol/L， cSN50.1 10 μmol/L， cSN50.1 30 μmol/L， cSN50.1 50 μmol/L， cSN50.1 70 μmol/L， and cSN50.1 90 μmol/L groups， and CCK－8 assay was used to investigate the effect of different concentrations of cSN50.1 on the proliferation of HepG2 cells and calculate half－maximal inhibitory concentration （IC50）. HepG2 cells were divided into cSN50.1 0 μmol/L， cSN50.1 10 μmol/L， cSN50.1 30 μmol/L， and cSN50.1 50 μmol/L groups， and wound healing assay， Transwell assay， and colony－forming assay were used to investigate the effect of different concentrations of cSN50.1 on the migration， invasion， and colony formation of HepG2 cells. HepG2 cells were divided into Control group， SP600125 group （an inhibitor of the AP－1 signaling pathway）， and cSN50.1 group to investigate the influence of the AP－1 signaling pathway on the effect of cSN50.1 on hepatocellular carcinoma cells， and RT－PCR and Western Blot were used to measure the expression of CXCL5， TNF－α， and c－Jun protein in cytoplasm and nucleus. HepG2 cells were divided into Control group， PDTC group （an inhibitor of the NF－κB signaling pathway）， and cSN50.1 group to investigate the influence of the NF－κB signaling pathway on the effect of cSN50.1 on hepatocellular carcinoma cells， and RT－PCR and Western Blot were used to measure the expression of CXCL5， TNF－α， and NF－κB protein in cytoplasm and nucleus. A one－way analysis of variance was used for comparison between multiple groups， and the SNK－q test was used for further comparison between two groups. ResultsCompared with the 0 μmol/L group， the 10 μmol/L group had no significant changes in proliferation， migration， invasion， and colony formation abilities （P >0.05）； the 30 μmol/L group had no significant change in proliferation ability （P>0.05）， but with significant reductions in migration， invasion， and colony formation abilities （P<0.05）； the 50 μmol/L group had significant reductions in proliferation， migration， invasion， and colony formation abilities （all P<0.01）； the 70 μmol/L and 90 μmol/L groups had a significant reduction in cell proliferation ability （P<0.01）， but with a cell survival rate of below 50%. Compared with the Control group， the SP600125， PDTC， and cSN50.1 groups had significant reductions in the mRNA and protein expression levels of CXCL5 and TNF－α （all P<0.05）. Compared with the Control group， the SP600125 group， the PDTC group， and the cSN50.1 group had a significant reduction in nuclear protein of c－Jun and NF－κB expression （P<0.05）； the SP600125 group and the PDTC group had a significant reduction in cytoplasmic protein of c－Jun and NF－κB expression （P<0.05）； the cSN50.1 group had a significant increase in cytoplasmic protein of c－Jun and NF－κB expression （P<0.05）. ConclusionThis study shows that cSN50.1 can inhibit the malignant behavior of hepatocellular carcinoma cells and reduce the expression of CXCL5 and TNF－α by inhibiting the nuclear import of c－Jun and NF－κB in hepatocellular carcinoma cells.
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Objective@#To provide a largescale assessment the prevalence of poor vision in 2020 among children and adolescents in Wuhan City, Hubei province and to provide basis for healthy vision promotion.@*Methods@#This crosssectional epidemiological study was conducted among 156 783 students, who lived in Wuhan during the COVID-19 period participated the vision screening through the online applet designed by Wuhan Center for Adolescent Poor Vision Prevetion and Control under the guidance of their guardians between June 19 and July 6, 2020. The demographic information and daily hours spent on various activities in the past week were investigated. The corresponding visual acuity data of students in 2019 before the COVID-19 outbreak was extracted from school vision monitoring records for each semester, which was measured by the experienced eye care professionals.@*Results@#The detection rate of poor vision (51.04%) in 2020 was significantly higher than that in 2019(43.04%)( χ 2=68 944.95, P <0.01). After adjustment for covariates, the odds ratio and 95% confidence interval for poor vision were 1.17(1.13-1.20), 1.07(1.04-1.10), 0.67 (0.65-0.69) and 0.62(0.60-0.64) in students with online class time, recreational screen time, indoor and outdoor activity time in the highest tertile, compared with the lowest tertile groups.@*Conclusion@#Increased rate of poor vision among primary and secondary schoool students deserves further concern. It is necessary to strengthen intervention of eyesight protection. Policies and programs aimed at improving opportunities for physical activities and decreasing multiple screen behaviors should be given priority.
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Objective:To investigate the association of body weight and body mass index (BMI) with bone mineral density (BMD) and osteoporotic risk in elderly men with type 2 diabetes mellitus (T2DM).Methods:210 elderly male patients with T2DM admitted to the Department of Endocrinology of the First Hospital of Changsha from June 2017 to May 2018 were selected as the research objects. The height, weight and bone mass index (BMI) were measured. BMDs of the left hip [including femoral neck (FN), greater trochanter (G.T.), intertrochanter (InTro), and total hip (TH)] and lumbar spine (LS) were measured in 210 elderly male patients with T2DM by dual-energy X-ray absorption method. Patients were divided into three groups according to BMI: the overweight group (24.0 kg/m 2≤BMI<28.0 kg/m 2), the obesity (BMI≥28.0 kg/m 2) group, and the normal group (18.5 kg/m 2≤BMI<24.0 kg/m 2). The influence of body weight and BMI on BMD and osteoporotic risk in these elderly men with T2DM was analyzed. Results:The BMDs in various sites of the hip of the overweight group and obesity group were higher compared with those in the normal weight group ( P<0.05). There was a positive correlation between weight and BMI with BMDs in various sites of the hip femoral neck (including FN, G. T., InTro, and TH) ( r=0.239-0.427, P<0.05). All patients were divided into different tertiles (T1-T3) stratified by weight and BMI respectively. The BMDs in various sites of the hip increased with tertiles stratified by weight ( P<0.05). The TH-BMD also increased with tertiles stratified by BMI ( P<0.05). The odd ratios ( OR) were calculated using T3 as the control group and T1 as the case group, using T2 as the control group and T1 as the case group, respectively. The osteoporotic risks of T1/T3, T1/T2 at FN stratified by weight were significantly increased by 4.50 times ( OR=4.50, 95% CI: 1.41-14.35) and 9.27 times ( OR=9.27, 95% CI: 2.03-42.30); The osteoporotic risks of T1/T3, T1/T2 at TH were significantly increased by 3.25 times ( OR=3.25, 95% CI: 1.10-9.59) and 8.50 times ( OR=8.50, 95% CI: 1.85-38.99). The osteoporotic risks of T1/T3, T1/T2 at FN stratified by BMI respectively were significantly increased by 4.13 times ( OR=4.13, 95% CI: 1.28-13.25) and 5.58 times ( OR=5.58, 95% CI: 1.53-20.42); while the osteoporotic risks of T1/T3, T1/T2 at TH stratified by BMI were not significantly increased ( P>0.05). There was no statistically significant difference in BMDs and the osteoporotic risks of the LS among T1, T2, and T3, regardless of stratified by weight or BMI ( P>0.05). Conclusions:For elderly males with T2DM, weight and BMI are important factors affecting BMDs in the hip, and also affecting the osteoporotic risks of the hip, especially that of FN. Osteoporotic risks of the FN decrease with the increase of weight and BMI within a certain range.
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Objective:To investigate the risk factors of Crohn′s disease (CD)-related gastrointestinal stenosis, and to summarize and analyze the corresponding treatments.Methods:From January 2010 to December 2018, 122 patients diagnosed with CD and hospitalized in the Seventh Medical Center, PLA General Hospital were selected including 72 patients in gastrointestinal stenosis group and 50 patients in non-gastrointestinal stenosis group. The gender, age of onset, course of disease, location of lesions involved (Montreal classification), disease activity, extraintestinal manifestations, application of therapeutic drugs, and complications were compared between the two groups. The treatment of CD patients with gastrointestinal stenosis was analyzed. Multivariate logistic regression was used to analyze the risk factors of CD patients with gastrointestinal stenosis. The independent sample t test, Mann-Whitney U test and chi-square test were used for statistical analysis. Results:The age of onset of patients in gastrointestinal stenosis group was older than that in non-gastrointestinal stenosis group ((37.6±15.1) years old vs. (30.8±14.7) years old), and course of disease was longer than that of non-gastrointestinal stenosis group (72 months, 11 to 492 months vs. 45 months, 3 to 240 months); and the differences were statistically significant ( t=-2.044, Z=-2.770; P=0.018, 0.006). The proportion of patients with ileum involvement of the gastrointestinal stenosis group was lower than that of the non-gastrointestinal stenosis group (69.4%, 50/72 vs. 86.0%, 43/50), and the proportion of severe patients was higher than that of the non-gastrointestinal stenosis group (15.3%, 11/72 vs. 4.0%, 2/50); and the differences were statistically significant ( χ2=4.463 and 3.942, P=0.035 and 0.047). There were no significant differences in gender, use of therapeutic drugs, extraintestinal manifestations, application of therapeutic drugs or the incidence of complications between the patients of two groups (all P>0.05). The results of multivariate logistic regression showed that the age of onset and course of disease were risk factors of CD-related gastrointestinal stenosis ( β=0.028, odds ratio ( OR)=1.028, 95% confidence interval ( CI) 1.000 to 1.056, P=0.046; β=0.008, OR=1.008, 95% CI 1.002 to 1.015, P=0.013). Further stratified analysis revealed that the incidence rates of CD-related gastrointestinal stenosis in patients with age of onset over 40 years old and course of disease more than five years were higher than those of patients with age of onset less than 40 years old and course of disease less than five years (76.3%, 29/38 vs. 51.2%, 43/84; 68.4%, 39/57 vs. 50.8%, 33/65), and the differences were statistically significant ( OR=3.072, 95% CI 1.298 to 7.272, P=0.009; OR=2.101, 95% CI 1.002 to 4.406, P=0.048). Among the 72 CD patients with gastrointestinal stenosis, 15 cases (20.8%) were treated with medicine and nutrition, without endoscopic or surgical treatment. Fifty-two patients (72.2%) underwent surgical treatment, among them six patients (11.5%) received twice surgery, the interval between the two operations was 46 months (1 to 204 months), and eight patients (15.4%) had postoperative complications. Twenty-one patients (29.2%) were treated with endoscopic dilatation, and no complications occurred after surgery. Five patients (23.8%) underwent surgical treatment during the follow-up period. Conclusions:The age of onset over 40 years old and the course of disease more than five years are the risk factors of CD-related gastrointestinal stenosis. Individualized medical treatment is the basis for the treatment of CD-related gastrointestinal stenosis. Surgery is still the main treatment. The endoscopic treatment is safety and can delay or avoid surgery to a certain extent.
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Objective To analyze the miss rates of colorectal adenomas during colonoscopy as well as risk factors influencing the adenoma miss rates and to take corresponding measures. Methods A total of 432 patients who underwent index and follow-up colonoscopy in 18 months were randomized and investigated. The results of two colonoscopies were compared and the missed adenomas were defined as the adenomas de-tected only during the second colonoscopy. Miss rates were calculated according to patient-based methods. Chi-square test was used to analyze the relative factors influencing the adenoma miss rate of per-patient. Then the meaningful factors were chosen into the logistic regression model for multiple factors analysis. Results Of 432 patients,116(26. 9%)had missed adenomas on first colonoscopy. Single factor analysis found that the size of adenoma( χ2 = 89. 686,P = 0. 000),the shape of adenoma( χ2 = 68. 488,P = 0. 000),the location of adenoma(χ2 = 77. 055,P = 0. 000)and adenoma tissue types(χ2 = 417. 000,P = 0. 000)were the risk factors for miss rates of colorectal adenomas. Number of polyps(χ2 = 8. 450,P= 0. 038),the organi-zation type of polyp(χ2 = 10. 718,P= 0. 013)and proficiency of colonoscopists(χ2 = 56. 069,P= 0. 000), the quality of bowel preparation(χ2 = 39. 195,P = 0. 000),insertion time(χ2 = 13. 133,P = 0. 001)were also the risk factors for miss rates of colorectal adenomas. Logistic regression analysis showed that the bigger the adenoma size,the less missed adenomas(OR= 0. 341,95%CI:0. 173-0. 671). Also,the longer insertion time took,the lower the adenoma miss rate(OR = 0. 987,95% CI:0. 981-0. 994). Per-patient miss rates were lower for high-risk adenomas compared with low-risk adenomas(OR = 0. 324,95%CI:0. 154-0. 680). Adenomas happening in multiple parts of bowel easily leads to missing(OR= 3. 791,95%CI:1. 505-9. 546). Conclusion The missed diagnosis of adenomas is not only significantly associated with features of missed adenomas,but also with skills of colonoscopists,insertion time,and bowel preparation. The key is high-quality index colonoscopy to avoid adenomas missing.
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Objective To investigate the changes of bone mineral density (BMD) in human immunodeficiency virus (HIV)-infected patients in Changsha,and take intervention measures to prevent the occurrence of osteoporosis and fracture.Methods A total of 278 HIV-infected patients and 154 cases of healthy adults from March 2011 to May 2015 were selected.Dual energy X-ray absorptiometry (DXA) was used to detect BMD,T-score and Z-score of all the research objects,including the whole body,lumbar spine (L2～4),and left hip joint.The height and weight were measured at the same time.Results The HIV infection group had an average age of (31.53 ± 8.56) years old,and the healthy control group was (34.45 ± 8.22) years old.Height between two groups had no significant difference.The average weight of HIV infection group was 6.93 kg [95％ CI,-9.01,-4.97;P ＜0.001] lighter than that in the normal control group.BMD,T-score and Z-score of HIV infection group were significantly lower than those in norrmal control group (P ＜ 0.001).The occurrence rate of osteopenia (Z ≤-1.0)and osteoporosis (Z ≤-2.0)in HIV infection group were correspondingly 43.53％ ～ 54.68％ and 9.71％ ～23.74％,which is about 4 times of that in the healthy control group (14.28％ ～ 20.13％,0.65％ ～ 5.84％).Conclusions The average body weight of HIV-infected patients was significantly lower than that of normal control group,and the incidence of osteopenia and osteoporosis in HIV-infected group was significantly higher than that in normal control group.
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Objective To observe the effects of MSH2 gene re expression on estrogen-induced apoptosis of colon cancer cells LOVO,and to explore its mechanisms.Methods According to different plasmid and whether with estradiol intervention,colon cancer LOVO cells were divided into empty plasmid with ethanol group,empty plasmid with estradiol group,MSH2 with ethanol group,MSH2 with estradiol group,estrogen receptor (ER) β with ethanol group,ERβ with estradiol group,ERβ with MSH2 and ethanol group and ERβ with MSH2 and estradiol group,and received corresponding treatment.The expression of MSH2,ERβ protein and apoptosis related caspase 3 protein were detected by Western blotting.Cell viability was measured by cell counting kit-8.Cell DNA fragments of each group were isolated with apoptosis DNA fragments isolation kit.And the DNA ladder was observed.The rate of apoptosis was detected by flow cytometer.Single factor variance analysis was performed for comparison among multiple groups,and t test was used for comparison between the two groups.Results After transfection,the expression of the MSH2 and ERβ at protein level in LOVO cells significantly increased and neither of their expression was effected by estradiol.The expression levels of caspase 3 cleavaged active fragments of ERβ with estradiol group and ERβ with MSH2 and ethanol group were higher than other groups,and there was no significant difference between these two groups.The LOVO cell viability of empty plasmid with ethanol group,empty plasmid with estradiol group,MSH2 with ethanol group,MSH2 with estradiol group,ERβ with ethanol group,ERβ with estradiol group,ERβ with MSH2 and ethanol group and ERβ with MSH2 and estradiol group was 1.72 ±0.25,1.74 ± 0.31,1.77 ± 0.35,1.74±0.33,1.70±0.34,1.02±0.48,1.71±0.31 and 1.07±0.18,respectively,and the differences between the groups were statistically significant (F=3.791,P＜0.05).Among them,the LOVO cell viability of ERβ with estradiol group was lower than that of ERβ with ethanol group,accordingly,that of ERβ with MSH2 and estradiol group was lower than that of ERβ with MSH2 and ethanol group,that of ERβ with estradiol group was lower than that of empty plasmid with estradiol group,that of ERβ with MSH2 and estradiol group was lower than that of MSH2 with estradiol group,and the differences were statistically significant (t=3.158,3.075,3.648,3.253,all P＜0.05).DNA ladder formed from DNA fragments of apoptosis cells was seen in ERβ with estradiol group and ERβ with MSH2 and estradiol group.The apoptosis rate of empty plasmid with ethanol group,empty plasmid with estradiol group,MSH2 with ethanol group,MSH2 with estradiol group,ERβ with ethanol group,ERβ with estradiol group,ERβ with MSH2 and ethanol group and ERβ with MSH2 and estradiol group was 7.86±0.19,7.87±0.39,8.39±1.02,9.05±1.54,7.54±0.99,19.77±2.35,7.76±1.32 and 19.30±1.75,respectively,and the differences between groups were statistically significant (F=45.436,P＜0.05).Among them,the apoptosis rate of ERβ with ethanol group was lower than that of ERβ with estradiol group,that of ERβ with MSH2 and ethanol group was lower than that of ERβ with MSH2 and estradiol group,that of empty plasmid with estradiol group was lower than that of ERβ with estradiol group,that of ERβ with MSH2 and estradiol group was lower than that of MSH2 with estradiol group,and the differences were statistically significant (t =8.260,9.133,8.596,7.617,all P＜ 0.05).Conclusions Estrogen may promote colon cancer cell apoptosis through ERβ pathway.The process of apoptosis maybe related with caspase protein,MSH2 may not be involved in the regulation of this signal pathway.
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Background:Clinical and epidemiological studies revealed that estrogen replacement therapy was associated with a significant reduction in risk of colorectal cancer in postmenopausal women.In our previous studies,estrogen increased the expression of mismatch repair (MMR)gene MLH1 in colonic cancer cells,and re-expression of MLH1 in MLH-deficient colonic cancer cells significantly increased the estrogen-induced apoptosis.Aims:To investigate the signaling pathway implicated in the MLH1-mediated apoptosis in colonic cancer cells induced by estrogen and the roles of p53 and its related genes in this apoptotic pathway.Methods:Plasmid containing wild type human MLH1 (hMLH1)full length cDNA was transfected into MLH1-deficient human colonic cancer cell line HCT116.By using HCT116 cells transfected with empty plasmid as controls,the apoptotic DNA ladder was determined by electrophoresis and the expressions of p53 and other apoptosis-related proteins were assessed by Western blotting under the condition with or without estrogen stimulation. Results:17β-estradiol (E2 )at the concentration of 10 -8 mol/L induced significant apoptosis in HCT116 cells transfected with hMLH1.In HCT116 cells transfected with hMLH1 and stimulated with E2 (group D),the protein expressions of caspase-3,caspase-9,p53,Bax and cytoplasmic cytochrome C increased significantly when compared with HCT116 cells stimulated with E2 only (group B);expressions of the abovementioned proteins were also higher in group D than in group C (transfected with hMLH1 only).Conclusions:MMR gene MLH1 is involved in estrogen-induced apoptosis of human colonic cancer cell line HCT116 by activating p53 signaling and mitochondrial apoptotic pathway.
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Objective: To investigate the role of the recombinant S protein of SARS-CoV in the induction of chemokine IP-10 and other cytokines in airway epithelial cells and immunocytes. Methods: Using insect-baculovirus expression system and Nickel affinity Magnet Beads, S protein of SARS-CoV was produced and then used to stimulate cultured human bronchial epithelial cells (16HBE), human peripheral blood mononuclear cells(PBMC), human peripheral blood monocytes and alveolar macrophages. The levels of IP-10 and the cytokines involved in immunoreaction in response to virus infection were detected in the supernatants of those cells cultured with the S protein by liquid chip system. Results: Under normal condition, no detectable IP-10 was found in 16HBE. A high level of IP-10(79.97? 13.81) pg/ml was detected in the 16HBE 12 hrs after being treated with the S protein, and the induction of IP-10 by S protein displayed at a significant quantity-effect reaction, but not in PBMC, monocytes and alveolar macrophages. In contrast, IFN-? was able to induce the production of IP-10 in either 16HBE or the immunocytes. Conclusion: 1.S protein of SARS-CoV can induce a high level of IP-10 in lung epithelial cells at early stage after the virus infection, which may initiate the process of the immune damage in the lung. 2. S protein of SARS-CoV induces the production of IP-10 by a way of IFN-? independent.
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AIM: To investigate the molecular mechanism by which the SARS-CoV S protein induces chemokine IP-10 in airway epithelial cells.METHODS: cDNA microarrays were used to screen the gene expression profiles of human bronchial epithelial cells(16HBEs) stimulated by SARS-CoV S protein.In addition,RT-PCR,EMSA,and Western blotting were performed to analyze the phosphorylation of JAK/STAT signal pathway.The changes of IRF-1 and IP10 gene expression and the influence by the corresponding inhibitors were analyzed.RESULTS: IRF-1,a key transcription factor of the JAK/STAT signal pathway,was activated in human bronchial epithelial cells after stimulation by the S protein of SARS-CoV.The IP-10 gene expression was detected 2 h following the phosphorylation of STAT1 after 15 min,which was blocked by STAT1or JAK2 inhibitors.Electrophoretic mobility shift assay(EMSA) demonstrated that the nuclear proteins bound to ISRE and GAS but not NF-?B DNA motif.CONCLUSION: The SARS-CoV S protein induces IP-10 gene expression in human bronchial epithelial cells through activation of the JAK/STAT signal pathway,suggesting that the JAK/STAT signal pathway activated by virus plays key roles in virus infection related acute lung injury.