Sepsis is characterized by a severe and life-threatening host immune response to polymicrobial infection accompanied by organ dysfunction.Studies on the therapeutic effect and mechanism of immunomod-ulatory drugs on the sepsis-induced hyperinflammatory or immunosuppression states of various im-mune cells remain limited.This study aimed to investigate the protective effects and underlying mechanism of artesunate(ART)on the splenic microenvironment of cecal ligation and puncture-induced sepsis model mice using single-cell RNA sequencing(scRNA-seq)and experimental validations.The scRNA-seq analysis revealed that ART inhibited the activation of pro-inflammatory macrophages recruited during sepsis.ART could restore neutrophils'chemotaxis and immune function in the septic spleen.It inhibited the activation of T regulatory cells but promoted the cytotoxic function of natural killer cells during sepsis.ART also promoted the differentiation and activity of splenic B cells in mice with sepsis.These results indicated that ART could alleviate the inflammatory and/or immunosuppressive states of various immune cells involved in sepsis to balance the immune homeostasis within the host.Overall,this study provided a comprehensive investigation of the regulatory effect of ART on the splenic microenvironment in sepsis,thus contributing to the application of ART as adjunctive therapy for the clinical treatment of sepsis.

Objective:To explore the application and practice of "flipped classroom" in the teaching of general surgery interns.Methods:A total of 20 internship groups (3 to 5 people in each group) were randomly selected from the general surgery practice group in the Department of General Surgery of the Second Clinical Medical College of North Sichuan Medical College. They were randomly divided into the flipped group (45 people) and the traditional group (40 people), with 10 subgroups in each group. The flipped group adopted the flipped classroom teaching mode (students' self-study by handing out materials before class, students and teachers' discussion in class, and students and teachers' evaluation after class), while the control group adopted the current conventional teaching mode (students' preview before class, teachers' explanation in class, and teachers' question answering after class). At the end of the teaching, a questionnaire was used to evaluate the participation and completion of each student. The teaching effect was evaluated by medical history collection and case analysis. The participation, completion, and teaching effect between the two groups were compared and analyzed. SPSS 23.0 software was used for t-test and Chi-square test. Results:The participation of the flipped group was better than that of the traditional group [(17.45±1.83) vs. (15.57±1.52)], and the difference was statistically significant ( P < 0.05). There was no statistically significant difference between the flipped group and the traditional group. There was no significant difference in medical history collection scores between the two groups. The case analysis of the flipped group was better than that of the traditional group [(87.30±6.06) vs. (81.50±5.88), P < 0.05]. The questionnaire shows that about 90% of the students think that flipped classroom can improve their interest in learning [96% (43/45)], improve their autonomous learning ability [89% (40/45)], and have better learning effect. At the same time, 78% (35/45) of students think that learning time is too long. Conclusion:The flipped classroom teaching model can improve the teaching participation of general surgery students, improve students' interest in learning, improve their self-learning ability, and improve students' thinking ability of medical record analysis.

Hepatic stellate cells(HSCs)are essential drivers of fibrogenesis.Inducing activated-HSC apoptosis is a promising strategy for treating hepatic fibrosis.18beta-glycyrrhetinic acid(18β-GA)is a natural com-pound that exists widely in herbal medicines,such as Glycyrrhiza uralensis Fisch,which is used for treating multiple liver diseases,especially in Asia.In the present study,we demonstrated that 18β-GA decreased hepatic fibrosis by inducing the apoptosis in activated HSCs.18β-GA inhibited the expression of α-smooth muscle actin and collagen type Ⅰ alpha-1.Using a chemoproteomic approach derived from activity-based protein profiling,together with cellular thermal shift assay and surface plasmon reso-nance,we found that 18β-GA covalently targeted peroxiredoxin 1(PRDX1)and peroxiredoxin 2(PRDX2)proteins via binding to active cysteine residues and thereby inhibited their enzymatic activities.18β-GA induced the elevation of reactive oxygen species(ROS),resulting in the apoptosis of activated HSCs.PRDX1 knockdown also led to ROS-mediated apoptosis in activated HSCs.Collectively,our findings revealed the target proteins and molecular mechanisms of 18β-GA in ameliorating hepatic fibrosis,highlighting the future development of 18β-GA as a novel therapeutic drug for hepatic fibrosis.

Objective: To investigate the role of microRNA-96-5p in the proliferation and invasion of gastric cancer cells and its molecular mechanism. Methods: From June 2015 to January 2017, 53 resected specimens were collected. The transcriptional levels of microRNA-96-5p and forkhead box Q1 (FoxQ1) in gastric cancer tissues and the matched para-cancerous tissues were quantified by quantitative real-time PCR (qRT-PCR). The expression of FoxQ1 protein was also detected by immunohistochemistry (IHC). The relationship between microRNA-96-5p expression and the clinicopathological features of gastric cancer and its correlation with FoxQ1 expression were analyzed. The expressions of miRNA-96-5p in gastric cancer tissue and adjacent normal tissue were detected by qRT-PCR. miRNA-96-5p mimics was transfected to BGC-823 gastric cancer cells. The effects of miRNA-96-5p on cell proliferation and invasion were detected by cell counting kit-8 (CCK-8) assay and Transwell assay, respectively. The protein expressions of FoxQ1, E-cadherin and vimentin were determined by western blot. The relationship between FoxQ1 and miRNA-96-5p expressed in BGC-823 cells was detected by dual-luciferase reporter assay. Results: The median expression of miRNA-96-5p in gastric cancer tissue was 1.05, significantly lower than 3.23 of para-cancerous tissues (P<0.05). The positive rate of FoxQ1 expression in gastric cancer tissue was 71.7%, significantly higher than 28.3% of para-cancerous tissues (P<0.05). The expression of FoxQ1 was negatively corelated with the level of miRNA-96-5p (r=-0.613, P=0.006). The expression of miRNA-96-5p in gastric cancer cell BGC-823 was significantly decreased compared with normal gastric epithelial cell (0.96±0.08 vs 2.84±0.15, P<0.05). The results of CCK-8 assay and Transwell assay showed that overexpression of miRNA-96-5p significantly reduced the proliferation and invasion abilities of gastric cancer cells (P<0.05). Overexpression of miRNA-96-5p decreased the protein level of FoxQ1. Moreover, it upregulated the expression of E-cadherin and downregulated the expression of vimentin. The result of dual-luciferase-3′-UTR reporter assay confirmed that miRNA-96-5p binds to the 3′UTR of FoxQ1. Conclusion miRNA-96-5p may suppress the proliferation, migration and epithelial-mesenchymal transition (EMT) of gastric cancer cell by down-regulation of FoxQ1.

Objective: To check Forkhead box M1 (FoxM1) expression in nasal mucosal of chronic rhinosinusitis (CRS) patients and the effect of inflammatory factors on FoxM1 expression, in order to research the significance of FoxM1 in CRS. Methods: From January to October of 2018, 50 patients hospitalized in the Department of Otorhinolaryngology, Head and Neck Surgery, First Affiliated Hospital of Nanchang University were enrolled in this study. Twenty CRS patients with polyps (CRSwNP), 20 CRS patients without nasal polyps (CRSsNP) and 10 patients with simple deviation of nasal septum (the control groups) were selected. The expression of FoxM1 in nasal mucosa of these patients was detected by immunohistochemistry (IHC) and real-time fluorescent quantitative PCR (qRT-PCR). Meanwhile, HE stain was used to observe the pathologic changes in each sample. By establishing human nasal epithelium cells cultivating model in vitro and identifying via immumofluorescence method, experimental group and control group were set up, then activation factors including interleukin (IL)-1β, IL-4, IL-5, IL-17, interferon-γ (IFN-γ) and staphylococcal entemtoxin B (SEB) were added in the models after stabilizing passage, and qRT-PRC and Western blot method were applied to check the expressing change of FoxM1. Software SPSS 18.0 was used for statistical analysis. Results: HE stain showed that the mainly pathologic change in nasal mucosa of CRS patients with or without nasal polyp was mucosal epithelial cells, goblet cell and submucosal gland hyperplasia, accompanied by a large number of inflammatory cells infiltration. The result of IHC demonstrated that both of the expression of FoxM1 in nasal mucosal tissue of CRS patients in the CRSwNP and CRSsNP groups exceed that of the control group (80% vs 75% vs 20%, χ² value was 10.000, 8.213, respectively, all P<0.05); there was no difference of expression between the two groups of CRS patients (χ²=0.143, P>0.05). The result of qRT-PCR demonstrated that the expression of FoxM1 mRNA in nasal mucosa of CRSwNP and CRSsNP was increased compared with that of the control group (3.309±1.511 vs 3.261±1.336 vs 1.000±0.774, t value was 4.519, 4.928, respectively, all P<0.05), but the difference between the two groups of CRS patients had no statistic significance (t=0.107, P=0.909). Nasal mucosa epithelial cells cultivating models was established successfully. Q-RT PCR and Western blot were conducted after stimulation of 100 ng/ml IL-1β, IL-4, IL-5, IL-17, IFN-γ and SEB for 36 h, and the proteins expression levels of FoxM1 exceeded the groups without stimulation with statistic significance. Conclusions The expression of FoxM1 in CRS increases and many types of cytokine can induce the increase of FoxM1 in human nasal epithelial cells. FoxM1 may participate in the process of pathogenesis in CRS.

Objective To investigate the role of microRNA?96?5p in the proliferation and invasion of gastric cancer cells and its molecular mechanism. Methods From June 2015 to January 2017, 53 resected specimens were collected. The transcriptional levels of microRNA?96?5p and forkhead box Q1 (FoxQ1) in gastric cancer tissues and the matched para?cancerous tissues were quantified by quantitative real?time PCR (qRT?PCR). The expression of FoxQ1 protein was also detected by immunohistochemistry (IHC). The relationship between microRNA?96?5p expression and the clinicopathological features of gastric cancer and its correlation with FoxQ1 expression were analyzed. The expressions of miRNA?96?5p in gastric cancer tissue and adjacent normal tissue were detected by qRT?PCR. miRNA?96?5p mimics was transfected to BGC?823 gastric cancer cells. The effects of miRNA?96?5p on cell proliferation and invasion were detected by cell counting kit?8 (CCK?8) assay and Transwell assay, respectively. The protein expressions of FoxQ1, E?cadherin and vimentin were determined by western blot. The relationship between FoxQ1 and miRNA?96?5p expressed in BGC?823 cells was detected by dual?luciferase reporter assay. Results The median expression of miRNA?96?5p in gastric cancer tissue was 1.05, significantly lower than 3.23 of para?cancerous tissues (P＜0.05).The positive rate of FoxQ1 expression in gastric cancer tissue was 71.7%, significantly higher than 28.3% of para?cancerous tissues ( P＜0.05). The expression of FoxQ1 was negatively corelated with the level of miRNA?96?5p (r＝－0.613, P＝0.006). The expression of miRNA?96?5p in gastric cancer cell BGC?823 was significantly decreased compared with normal gastric epithelial cell (0.96±0.08 vs 2.84± 0.15, P＜0.05). The results of CCK?8 assay and Transwell assay showed that overexpression of miRNA?96?5p significantly reduced the proliferation and invasion abilities of gastric cancer cells ( P＜ 0.05 ). Overexpression of miRNA?96?5p decreased the protein level of FoxQ1. Moreover, it upregulated the expression of E?cadherin and downregulated the expression of vimentin. The result of dual?luciferase?3′?UTR reporter assay confirmed that miRNA?96?5p binds to the 3′UTR of FoxQ1. Conclusion miRNA?96?5p may suppress the proliferation, migration and epithelial?mesenchymal transition (EMT) of gastric cancer cell by down?regulation of FoxQ1.

The construction of teaching faculty is not only a core element to carry out medical education in municipal general hospitals, but also a weak link. Constructing a performance evaluation system of teaching faculty has important significance in promoting teaching reform and innovation, and improving teachers' enthusiasm for teaching as well as their teaching quality in municipal general hospitals. Taking the Affiliated Dongguan People's Hospital of Southern Medical University as an example, this paper focused on the construction of teaching faculty and aimed to provide references for municipal general hospitals to build a performance evaluation system through the promotion of a series of measures such as teaching ability assessment, quantitative assessment of teaching work, teaching quality evaluation, and teaching contribution assessment.

Objective To investigate the role of microRNA?96?5p in the proliferation and invasion of gastric cancer cells and its molecular mechanism. Methods From June 2015 to January 2017, 53 resected specimens were collected. The transcriptional levels of microRNA?96?5p and forkhead box Q1 (FoxQ1) in gastric cancer tissues and the matched para?cancerous tissues were quantified by quantitative real?time PCR (qRT?PCR). The expression of FoxQ1 protein was also detected by immunohistochemistry (IHC). The relationship between microRNA?96?5p expression and the clinicopathological features of gastric cancer and its correlation with FoxQ1 expression were analyzed. The expressions of miRNA?96?5p in gastric cancer tissue and adjacent normal tissue were detected by qRT?PCR. miRNA?96?5p mimics was transfected to BGC?823 gastric cancer cells. The effects of miRNA?96?5p on cell proliferation and invasion were detected by cell counting kit?8 (CCK?8) assay and Transwell assay, respectively. The protein expressions of FoxQ1, E?cadherin and vimentin were determined by western blot. The relationship between FoxQ1 and miRNA?96?5p expressed in BGC?823 cells was detected by dual?luciferase reporter assay. Results The median expression of miRNA?96?5p in gastric cancer tissue was 1.05, significantly lower than 3.23 of para?cancerous tissues (P＜0.05).The positive rate of FoxQ1 expression in gastric cancer tissue was 71.7%, significantly higher than 28.3% of para?cancerous tissues ( P＜0.05). The expression of FoxQ1 was negatively corelated with the level of miRNA?96?5p (r＝－0.613, P＝0.006). The expression of miRNA?96?5p in gastric cancer cell BGC?823 was significantly decreased compared with normal gastric epithelial cell (0.96±0.08 vs 2.84± 0.15, P＜0.05). The results of CCK?8 assay and Transwell assay showed that overexpression of miRNA?96?5p significantly reduced the proliferation and invasion abilities of gastric cancer cells ( P＜ 0.05 ). Overexpression of miRNA?96?5p decreased the protein level of FoxQ1. Moreover, it upregulated the expression of E?cadherin and downregulated the expression of vimentin. The result of dual?luciferase?3′?UTR reporter assay confirmed that miRNA?96?5p binds to the 3′UTR of FoxQ1. Conclusion miRNA?96?5p may suppress the proliferation, migration and epithelial?mesenchymal transition (EMT) of gastric cancer cell by down?regulation of FoxQ1.

Objective To investigate the survival status of people with disabilities in urban areas of Lanzhou, China and discuss the correlation of their quality of life to disability attitude and quality of care and support of disabled people. Methods From August to November, 2016, 606 persons with disability registered in Chengguan District of Lanzhou were selected by multistage stratified cluster sampling. They were investigated in home-based visit with World Health Organization Quality of Life-Disability Scale for physical disability, World Health Organization-Disability Attitude Scale and World Health Organization Quality of Care and Support Scale-Disability Scale. Results The quality of life scored in average of (40.76±14.79), and different with the demographic characteristics (P<0.05). Pearson's correlation analysis showed that the score in all fields of quality of life and the total score positively correlated with most dimensions of disability attitude score (r>0.080, P<0.05) and most dimensions score of quality of care and support (r>0.083, P<0.05).Conclusion It is important to strengthen the precise security system for people with disabilities, and strive to establish a full-cycle, all-round social support system for them.

Objective To investigate the expression of hypoxia inducible factor-1α (HIF-1α) in chronic rhinosinusitis (CRS) and relationship with mucin MUC5AC,MUC5B secretion.Methods The expression of HIF-1 α,MUC5 AC and MUC5 B were measured by immunohistochemistry (IHC),Western Blot and reverse transcription polymerase chain reaction (RT-PCR) in CRS with or without nasal polyps (CRSwNP:twenty-three or CRSsNP:twenty)and fifteen normal sinus mucosa without CRS.The relationship between HIF-1α and MUC5AC,MUC5B were analyzed by SPSS 16.0 software.Results PAS and IHC showed that HIF-1α,MUC5AC,MUC5B,total mucins were expressed in nuclear of epithelium and gland cells,which were higher than normal control (t values in epithelium cells were 8.650,9.305,9.382,8.524,7.533,5.417,5.507,5.556,all P ＜ 0.05 ; t values in gland cells were 8.285,7.098,6.798,7.308,8.574,7.933,6.798,7.308,all P ＜ 0.05),but there was no significant difference between CRSwNP and CRSsNP (t values in epithelium cells were 0.734,0.415,0.572,0.248,all P ＞ 0.05 ; t values in gland cells were 0.331,0.662,0.249,0.644,P ＞ 0.05).Western Blot revealed that HIF-lα protein in CRSwNP and CRSsNP were higher than in normal contral (t values were 3.522,3.314,respectively,P ＜ 0.05).The relative expression levels of HIF-1α,MUC5AC,MUC5B mRNA in CRSwNP and CRSsNP were 1.35 ± 0.84,1.36 ± 0.94,0.81 ± 0.54,0.78 ± 0.46,1.13 ± 1.00,1.22 ± 1.02.But the relative expression levels of HIF-1 α,MUC5AC,MUC5 B mRNA in control subjects were 0.43 ± 0.34,0.42 ± 0.36,0.48 ± 0.42.There were significant differences between the groups of CRSwNP and control subiects(t values were 4.087,4.089,2.519,2.550,2.738,2.955,respectively,all P ＜ 0.05).There was a positive correlation among the expression of HIF-1 α and MUC5AC,5 B mRNA in CRSwNP (r values were 0.474,0.464,respectively,all P ＜0.05).There was a positive correlation among the expression of HIF-1α and MUC5AC,5B mRNA in CRSsNP (r values were 0.477,0.514,respectively,all P ＜ 0.05).Conclusions HIF-1 α,MUC5AC and MUC5B expression were upregulated in CRS with or without nasal polyps,indicating CRS is a disease of mucus hypersecretion and there is a close association between HIF-1α with hypersecretion of MUC5AC and MUC5B in mucus.