BACKGROUND:Coronary drug-eluting stent implantation is the best treatment for acute ST-segment elevation myocardial infarction, but because of many combined risk factors in elderly patients, the mortality rate is increased with aging. OBJECTIVE:To analyze whether age differences is a significant independent predictor of in-hospital clinical outcomes in patients with acute ST-elevation myocardial infarction treated with domestic rapamycin drug-eluting stent implantation. METHODS:A retrospective analysis was done in 307 patients with first acute ST-elevation myocardial infarction treated with emergent rapamycin drug-eluting stent implantation for primary percutaneous coronary intervention. According to the age, there were three groups: non-elderly group (< 65 years old,n=175), low-elderly group (65-74 years old,n=83), and high-elderly group (≥ 75 years old,n=49). Clinical features, mortality, cardiac events during in-hospital stay were compared among three groups. RESULTS AND CONCLUSION: Compared with the non-elderly group, the proportion of female patients and the history of hypertension were higher in the low-elderly or high-elderly group (P < 0.05). The history of smoking was higher in the non-elderly group than the other groups (P < 0.05). The incidences of Kilip classification≥II, three-lesion or left main coronary artery disease were higher in the high-elderly group than the other groups (P < 0.05). Hemoglobin, total cholesterol, triglycerides, low-density lipoprotein, and cholesterol levels were higher in the non-elderly group than the other groups (P < 0.05). Serum creatinine level, incidence of malignant arrhythmia and incidence of in-hospital cardiac death were increased with aging. Successful reperfusion was higher in the high-elderly group than in the low-elderly or non-elderly group. Rate of acute heart failure and combined cardiovascular events were higher in the high-elderly group than in the low-elderly or non-elderly group (P < 0.05). Multivariate logistic regression analysis show that age is an independent risk factor for in-hospital mortality in patients with acute ST-elevation myocardial infarction treated with rapamycin drug-eluting stent implantation.

Objective:To determine the effects of enforced expression of Foxp3 in lung cancer cell with regards to proliferation and tumorgeneity. Methods: A stable subline NCIH-hFoxp3 was established by liopfectamin-mediated pcDNA plasmid transfection carrying exogenous hFoxp3. The growth curve and secrection of IL-8 and IL-10 of NCIH-hFoxp3 were evaluated using MTT and ELISA, respectively. The in vivo tumorigeneity was assessed as well by inoculation of NCIH-hFoxp3 subcutaneously in nude mice. Results:Lung cancer cell NCIH-hFoxp3 with enforced expression of Foxp3 proliferated slowly but exihited increased in vivo tumorgeneity compared with corresponding control subline. In addition,increased expression of hFoxp3 in NCIH-hFoxp3 augmented secretion and at-tenuated secretion of IL-8 and IL-10,respectively. Conclusion:Increased expression of Foxp3 may promote progression of lung cancer cell by change of cellular microenvironment and evasion of immune surveillance.

Objective To evaluate the potential differences in serum proteomic profiles between patients with esophageal squamous cell carcinoma(ESCC)and precancerous lesions in order to establish proteomic pattern model for diagnosis of ESCC and precancerous lesions in high risk area,and to investigate its value in screening ESCC.Methods The serum and endoscopic biopsy samples were obtained from 38 normal controls,63 patients with atypical hyperplasia(class Ⅰ 26 cases,class Ⅱ 26 cases,class Ⅲ 11 cases)and 36 patients with advanced esophageal carcinoma.The serum proteomic patterns were examined using surface enhanced laser desorption/ionization time of flight mass spectrometry(SELDI-TOF-MS)and CM10 protein chip.The data was analyzed and disease diagnostic models were established using support vector machine(SVM).The diagnostic model was evaluated and validated by leave one cross validation.Results ①The diagnostic model could differentiate advanced esophageal carcinoma from normal controls with a specificity of 89.47%and a sensitivity of 83.33%.②The results delivered 92.31%,80.77% and 90.91%specificity,and 80.56%,83.33%and 94.44%sensitivity for discrimination of atypical hyperplasia Ⅰ,Ⅱand Ⅲ,respectively,using diagnostic models.③Four(4291,5644,5664,8775)m/z peaks observed repeatedly using diagnostic models.Conclusions The SELDI-TOF-MS and SVM provide a new approach for discrimination of ESCC and precancerous lesions in high risk area.Four(4291,5644,5664,8775)m/z peaks may considered as potential biomarkers which related to the ESCC and esophageal precancerous lesions.

Inner ear diseases are common in the field of otolaryngology,including hearing loss,tinnitus and peripheral vestibular dysfunction.Their pathogenesis is relatively complex,which is one of the hot spots in current research.A large number of studies have demonstrated that sleep disorder is an important inducement of inner ear diseases.This paper reviews the impact of sleep deprivation on inner ear diseases in order to pro-vide a theoretical basis for the mechanisms of sleep deprivation on inner ear diseases.

Objective To investigate the role of TLR4/NF-κB signaling pathway in mediating sleep depriva-tion induced endolymphatic hydrops.Methods A total of 30 healthy sprague-dawley(SD)rats were randomly di-vided into the control group、big platform control group,and 2 w,3 w,4 w sleep deprivation group,with 6 rats in each group.Modified multiple platform method was adopted to establish the rat sleep deprivation model.Before and after the experiment,the open field and acoustic brain-stem response(ABR)was conducted to evaluate the behavior and hearing level.After ABR test,blood samples were collected from abdominal aorta,and serum levels of TNF-αand MCP-1 were detected by ELISA.The cochlea was dissected,the severity of endolymphatic hydrops was as-sessed by calculating the ratio of the cross sectional area of the membranous cochlear duct(SM)to that of the mem-branous cochlear duct+scale vestibuli(SM+SV).Positive expression of IL-1β,TNF-α,MCP-1,TLR4,NF-κB P65 in rat cochlear tissues was detected via immunohistochemical staining.After the experiment,the changes of hearing level,the severity of endolymphatic hydrops and TLR4/NF-κB signaling pathway related proteins and down-stream inflammatory factors expression level were observed.The correlation between TLR4/NF-κB signaling path-way and hearing level and endolymphatic hydropsin rats was analyzed.Results ABR results showed an increased threshold of wave Ⅱ in the sleep deprivation group compared to those of the control group and big platform control group(P＜0.05).The rate of hydrops was 0％in control and big platform control groups,16.67％in 2w sleep deprivation group and 25％in 3 w and 4 w sleep deprivation group.The concentrations of TNF-αand MCP-1 in ser-um of rats in sleep deprivation groups were higher than those in control and big platform control groups,and the 4w sleep deprivation group were statistically significant compared with control and big platform control groups.The ex-pressions of IL-1β,TNF-α,MCP-1,TLR4 and NF-κB P65 in the cochlear spiral ganglion,spiral canal,stria vascu-laris and spiral ligament of rats in sleep deprivation groups were higher than those in control and big platform control groups.Conclusion Sleep deprivation may induce endolymphatic hydrops by the TLR4/NF-κB signaling pathway.

Objective: To explore the hot issues and developing trend of the research of campus bulling,and to provide a reference for the research on campus bullying. Methods: The power of research, high-impact authors, highly cited journals, high-frequency keywords, and burst terms related to school bullying from the Web of Science database were analyzed using CiteSpace software. The data collection time was May 9, 2018. Results: A total of 3 561 literature data were obtained. The results showed that the country with the highest number of publications was the United States; England had the highest centrality and was in a critical position in the research. The University of Turku in Finland was the core research institution. Salmivalli C was the author of the highest publication, Olweus D was the most frequent cited author. The high-impact journal was Aggressive Behavior. In terms of high-frequency keywords, the core vocabulary such as bully, adolescence, and victim were listed. Middle school students were the most frequently studied; in the form of bullying, the frequency of violence, aggression, and cyberbully was more common; depression, mental health and health appeared more frequently in terms of bullying outcomes. Mutant words including school children, bullying, victimization, relational aggression were more common. Conclusion The research hotspots on campus bullying during the past decade include violence, gender, social support, and mental health. Bullying among college students will be a hot research topic in the future. Continued efforts should be carried out in the field of campus bullying in China.

Background/Aims: Dexamethasone (DEX) is a widely used exogenous therapeutic glucocorticoid in clinical settings. Its long-term use leads to many side effects. However, its effect on metabolic disorders in individuals on a high-fat diet (HFD) remains poorly understood. Methods: In this study, HFD-fed mice were intraperitoneally injected with DEX 2.5 mg/kg/day for 30 days. Lipid metabolism, adipocyte proliferation, and inflammation were assayed using typical approaches. Results: DEX increased the epididymal fat index and epididymal adipocyte size in HFD-fed mice. The number of epididymal adipocytes with diameters > 70 μm accounted for 0.5% of the cells in the control group, 30% of the cells in the DEX group, 19% of the cells in the HFD group, and 38% of all the cells in the D+H group. Adipocyte proliferation in the D+H group was inhibited by DEX treatment. Adipocyte enlargement in the D+H group was associated with increased the lipid accumulation but not the adipocyte proliferation. In contrast, the liver triglyceride and total cholesterol levels and their metabolism were downregulated by the same treatment, indicating the therapeutic potential of DEX for nonalcoholic fatty liver disease. Conclusions DEX synergizes with HFD to promote lipid deposition in adipose tissues. A high risk of obesity development in patients receiving HFD and DEX treatment is suggested.

Background/Aims: Dexamethasone (DEX) is a widely used exogenous therapeutic glucocorticoid in clinical settings. Its long-term use leads to many side effects. However, its effect on metabolic disorders in individuals on a high-fat diet (HFD) remains poorly understood. Methods: In this study, HFD-fed mice were intraperitoneally injected with DEX 2.5 mg/kg/day for 30 days. Lipid metabolism, adipocyte proliferation, and inflammation were assayed using typical approaches. Results: DEX increased the epididymal fat index and epididymal adipocyte size in HFD-fed mice. The number of epididymal adipocytes with diameters > 70 μm accounted for 0.5% of the cells in the control group, 30% of the cells in the DEX group, 19% of the cells in the HFD group, and 38% of all the cells in the D+H group. Adipocyte proliferation in the D+H group was inhibited by DEX treatment. Adipocyte enlargement in the D+H group was associated with increased the lipid accumulation but not the adipocyte proliferation. In contrast, the liver triglyceride and total cholesterol levels and their metabolism were downregulated by the same treatment, indicating the therapeutic potential of DEX for nonalcoholic fatty liver disease. Conclusions DEX synergizes with HFD to promote lipid deposition in adipose tissues. A high risk of obesity development in patients receiving HFD and DEX treatment is suggested.

Background/Aims: Dexamethasone (DEX) is a widely used exogenous therapeutic glucocorticoid in clinical settings. Its long-term use leads to many side effects. However, its effect on metabolic disorders in individuals on a high-fat diet (HFD) remains poorly understood. Methods: In this study, HFD-fed mice were intraperitoneally injected with DEX 2.5 mg/kg/day for 30 days. Lipid metabolism, adipocyte proliferation, and inflammation were assayed using typical approaches. Results: DEX increased the epididymal fat index and epididymal adipocyte size in HFD-fed mice. The number of epididymal adipocytes with diameters > 70 μm accounted for 0.5% of the cells in the control group, 30% of the cells in the DEX group, 19% of the cells in the HFD group, and 38% of all the cells in the D+H group. Adipocyte proliferation in the D+H group was inhibited by DEX treatment. Adipocyte enlargement in the D+H group was associated with increased the lipid accumulation but not the adipocyte proliferation. In contrast, the liver triglyceride and total cholesterol levels and their metabolism were downregulated by the same treatment, indicating the therapeutic potential of DEX for nonalcoholic fatty liver disease. Conclusions DEX synergizes with HFD to promote lipid deposition in adipose tissues. A high risk of obesity development in patients receiving HFD and DEX treatment is suggested.

Background/Aims: Dexamethasone (DEX) is a widely used exogenous therapeutic glucocorticoid in clinical settings. Its long-term use leads to many side effects. However, its effect on metabolic disorders in individuals on a high-fat diet (HFD) remains poorly understood. Methods: In this study, HFD-fed mice were intraperitoneally injected with DEX 2.5 mg/kg/day for 30 days. Lipid metabolism, adipocyte proliferation, and inflammation were assayed using typical approaches. Results: DEX increased the epididymal fat index and epididymal adipocyte size in HFD-fed mice. The number of epididymal adipocytes with diameters > 70 μm accounted for 0.5% of the cells in the control group, 30% of the cells in the DEX group, 19% of the cells in the HFD group, and 38% of all the cells in the D+H group. Adipocyte proliferation in the D+H group was inhibited by DEX treatment. Adipocyte enlargement in the D+H group was associated with increased the lipid accumulation but not the adipocyte proliferation. In contrast, the liver triglyceride and total cholesterol levels and their metabolism were downregulated by the same treatment, indicating the therapeutic potential of DEX for nonalcoholic fatty liver disease. Conclusions DEX synergizes with HFD to promote lipid deposition in adipose tissues. A high risk of obesity development in patients receiving HFD and DEX treatment is suggested.