Clinical analysis of severe/critical 2019 novel coronavirus Omicron variant infection combined with atrial fibrillation / 中华危重病急救医学

Objective:To investigate the clinical characteristics and prognosis of coronavirus disease 2019 (COVID-19) patients with Omicron variant combined with atrial fibrillation (AF).Methods:From March 23, 2022 to May 15, 2022, 2 675 aged ≥ 50 years old COVID-19 patients with AF were admitted to Zhoupu Hospital, the designated hospital for COVID-19 in Shanghai. Patients were divided into mild symptoms group, normal group, and serious/critical group according to the symptoms. The clinical data, imaging examination and laboratory results and prognosis of the three group patients were compared.Results:The median age of 2 675 COVID-19 patients was 69.0 (60.0, 81.0) years old, the incidence of AF was 5.05% (135/2 675), the age range of AF patients were from 55 to 101 years old, with a median age of 84.0 (74.0, 89.0), and the number of mild symptoms, normal, serious/critical patients were 68, 30, 37, respectively, including 9 of serious and 28 of critical patients. In the serious/critical patients, aged 55-75 years old accounted for 43.2%, the rate of 2019 novel coronavirus vaccination was 32.4%. The identified new-onset AF was the highest among the three groups, but the rate of persistent AF was the highest in the mild symptoms group (58.8%). The severe/critical group complicated with fever (29.7%), hepatic insufficiency (13.5%), renal insufficiency (46.0%), type 2 diabetes (46.0%), and heart failure were higher in NYHA classification [compared with the mild symptoms and normal group (score): 1.8±1.1 vs. 1.1±0.8, 1.2±0.7, respectively, all P < 0.05]. In term of laboratory examinations, C-reactive protein (CRP), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) levels were significantly higher in serious/critical patients compared to the mild symptoms and normal groups [CRP (mg/L): 27.2 (6.0, 60.8) vs. 7.6 (3.1, 19.3), 12.8 (4.9, 26.3), ALT (U/L): 31.3±15.4 vs. 15.4±9.3, 19.3±11.7, AST (U/L): 78.0±21.7 vs. 34.7±15.6, 38.1±24.4, all P < 0.05]. The hemoglobin (Hb) and albumin (ALB) levels were significantly lower than those in the mild symptoms and normal groups [Hb (g/L): 105.3±22.5 vs. 125.8±25.4, 123.0±20.4, ALB (g/L): 33.7±6.0 vs. 39.0±5.5 and 39.6±13.1, all P < 0.05]. In addition, MB isoenzyme of creatine kinase (CK-MB) was significantly higher in the serious/critical group than that in the mild symptoms group [μg/L: 2.5 (1.5, 3.4) vs. 2.2 (1.2, 2.8), P < 0.05]. In terms of the treatment, the percentage of antiplatelet agents and low-molecular heparin ratio compared among the three groups were statistically significant, with the serious/critical group using the lowest percentage of antiplatelet agents (27.0%) and a higher percentage of low-molecular heparin usage than that in mild symptoms group [81.1% (30/37) vs. 51.5% (35/68), P < 0.05]. In terms of prognosis, the mortality of patients with AF was 18.5% (25/135), all of whom were critical ill, including 32.0% (8/25) with cerebral embolism, pulmonary embolism and cerebral hemorrhage. Among them, 40.0% (10/25) died of multiple organ failure (40.0% combined with gastrointestinal hemorrhage), 20.0% (5/25) died of heart failure, and 12.0% (3/25) died of respiratory failure; while there were no death cases recorded in the mild symptoms, normal group and 9 serious patients. Conclusions:The serious/critical patients infected with COVID-19 Omicron variant with AF, have a worse prognosis and high mortality. Multiple organ failure, heart failure, sudden cardiac death, respiratory failure and embolic disease are the major causes of death.

Regulation of drug release performance using mixed doxorubicin-doxorubicin dimer nanoparticles as a pH-triggered drug self-delivery system / 药物分析学报

A mixed drug self-delivery system(DSDS)with high drug content(＞50％)was developed to regulate pH-triggered drug release,based on two doxorubicin(DOX)-DOX dimmers:D-DOXADH and D-DOXcar con-jugated with acid-labile dynamic covalent bonds(hydrazone and carbamate,respectively)and stabilized with PEGylated D-DOXADH(D-DOXADH-PEG).Owing to the different stability of the dynamic covalent bonds in the two dimers and the noncovalent interaction between them,pH-triggered drug release could be easily regulated by adjusting the feeding ratios of the two DOX-DOX dimers in the mixed DSDS.Similar in vitro cellular toxicity was achieved with the mixed DSDS nanoparticles prepared with different feeding ratios.The mixed DSDS nanoparticles had a similar DOX content and diameter but different drug releasing rates.The MTT assays revealed that a high anti-tumor efficacy could be achieved with the slow-release mixed DSDS nanoparticles.

Upregulation of miR-20b Protects Against Cerebral Ischemic Stroke by Targeting Thioredoxin Interacting Protein (TXNIP)

Dysregulation of microRNAs (miRNAs) is involved in abnormal development and pathophysiology in the brain. Although miR-20b plays essential roles in various human diseases, its function in cerebral ischemic stroke remains unclear. A cell model of oxygen glucose deprivation/reoxygenation (OGD/R) and A rat model of middle cerebral artery occlusion/reperfusion (MCAO/R) were constructed. qRT-PCR and western blot were used to evaluate the expression of miR-20b and TXNIP. Cell viability was detected by MTT assay, and cell apoptosis was evaluated by flow cytometry. Targetscan and Starbase were used to predict the potential targets of miR-20b. Luciferase reporter assay was applied to determine the interaction between miR-20b and TXNIP. Rescue experiments were conducted to confirm the functions of miR-20b/TXNIP axis in cerebral ischemic stroke. MiR-20b was significantly downregulated after I/R both in vitro and in vivo. Upregulation of miR-20b inhibited OGD/R-induced neurons apoptosis and attenuated ischemic brain injury in rat model. Bioinformatic prediction suggested that TXNIP might be a target of miR-20b, and luciferase reporter assay revealed that miR-20b negatively regulated TXNIP expression by directly binding to the 3’-UTR of TXNIP. Downregulation of TXNIP inhibited OGD/R-induced neurons apoptosis in vitro and ischemic brain injury in vivo. Rescue experiments indicated that downregulation of TXNIP effectively reversed the effect of miR-20b inhibitor in neurons apoptosis after OGD/R-treatment and ischemic brain injury in a mouse model after MCAO/R-treatment. Our study demonstrated that upregulation of miR-20b protected the brain from ischemic brain injury by targeting TXNIP, extending our understanding of miRNAs in cerebral ischemic stroke.

Effect of miR-5590-3p on the invasion and proliferation of gastric cancer cell line HS-746T by regulating TGFBR2 expression / 中国医师杂志

Objective:To explore the inhibition of microRNA (miRNA, miR)-5590-3p on the expression of transforming growth factor beta typeⅡreceptor (TGFBR2) gene and its effect on the invasion and proliferation of gastric cancer cell line HS-746T.Methods:The gastric cancer cell line was cultured in vitro. Real-time quantitative polymerase chain reaction (qRT-PCR) was used to analyze the expression of miR-5590-3p in gastric cancer tissues and cell lines. The miR-NC and miR-5590-3p mimic were transfected into gastric cancer cell line HS-746T by lipofection, and named as miR-NC group and miR-5590-3p group, respectively. qRT-PCR was used to measure transfection effects. Transwell assay and cell counting kit-8 (CCK-8) assay were used to detect cell invasion and proliferation after transfection. The bioinformatics software predicts and the dual luciferase reporter gene system validates the target gene of miR-5590-3p. qRT-PCR and western blot were used to measure the expression of TGFBR2 and its downstream proteins in the transfected cells. Results:The expression of miR-5590-3p in gastric cancer tissues was significantly lower than that in adjacent tissues ( P<0.01). The expression of miR-5590-3p in gastric cancer cell lines was significantly lower than that in normal gastric mucosal epithelial cells ( P<0.05), and lowest in HS-746T cells ( P<0.01). After transfection, the expression of miR-5590-3p in miR-5590-3p group (11.76±0.21) was significantly higher than that in miR-NC group (1.06±0.21), with statistically significant difference ( P<0.01). The number of invasive cells in miR-NC group and miR-5590-3p group were (101.20±15.47) and (26.53±6.53), respectively, and the invasion ability of miR-5590-3p group was significantly decreased ( P<0.01). Compared with the miR-NC group, the cell proliferation ability of the miR-5590-3p group was significantly decreased ( P<0.05). Bioinformatics software showed that the target gene for miR-5590-3p is TGFBR2. The dual luciferase reporter gene system confirmed that miR-5590-3p can target the TGFBR2 gene ( P<0.01). Western blot results showed that compared with miR-NC group, the expression of TGFBR2 in HS-746T cells in miR-5590-3p group was significantly decreased ( P<0.01), the expression of ZEB-1 and ZEB-2, and the expression of CDK1 and cyclin B proteins were decreased as well. Conclusions:miR-5590-3p can inhibit the invasion and proliferation of gastric cancer cell HS-746T by targeting and regulating the expression of TGFBR2 gene.

Effect of lncRNA PP7080 on the migration and proliferation of gastric cancer cell MGC803 by regulating TMSG-1 expression / 国际外科学杂志

Objective:To observe the expression of long non-coding RNA (lncRNA) PP7080 in gastric cancer tissues and cell lines, and clarify its effect on the migration and proliferation of gastric cancer cell MGC803 and its molecular mechanism.Methods:Real-time PCR was used to detect the expression of lncRNA PP7080 in gastric cancer tissues and adjacent tissues, gastric cancer cell lines and immortalized normal gastric mucosal epithelial cell lines. The gastric cancer cell line with the least expression was selected, and the expression plasmid of lncRNA PP7080 and the negative control plasmid were transfected into gastric cancer cells, respectively, and named as lncRNA PP7080 group and NC group. Real-time PCR to verify the effect of transfection. Cell scratch test and CCK-8 test were used to detect the regulation of lncRNA PP7080 on the migration and proliferation of gastric cancer cells.The statistical saftware SPSS 20.0 was used for statistical analysis, the measurement data of normal distribution were expressed as ( Mean± SD). Real-time PCR and Western blot were used to detect the expression of tumor metastasis suppressor gene 1 ( TMSG-1) in the transfected cells. The t test was used for comparison between groups. Results:The expression of lncRNA PP7080 in gastric cancer tissue was less than that in adjacent tissues [(0.85±0.34) vs (5.33 ± 0.76), P<0.01]. The expression of lncRNA PP7080 in gastric cancer cell lines is less than that of immortalized normal gastric mucosal epithelial cells ( P<0.05), and the least expression in MGC803 cells ( P<0.01). The expression of lncRNA PP7080 in the lncRNA PP7080 group was significantly higher than that in the NC group, and the difference was statistically significant ( P<0.01). The cell migration rates of NC group and lncRNA PP7080 group were (72.67±6.39)% and (26.45±6.63)%, respectively, and the cell migration ability of lncRNA PP7080 group was significantly reduced ( P<0.01). Compared with the NC group, the cell proliferation ability of the lncRNA PP7080 group was significantly reduced ( P<0.05). Compared with the NC group, the expression of TMSG-1 in MGC803 cells of the lncRNA PP7080 group was significantly reduced ( P<0.01). Conclusion:lncRNA PP7080 is lowly expressed in gastric cancer tissues and cell lines. lncRNA PP7080 can inhibit the migration and proliferation of gastric cancer cell MGC803 by promoting the expression of TMSG-1 gene.

Molecular mechanism of lncRNA HAGLR regulating the proliferation and migration of gastric cancer cells by targeting miR-93-5p / 国际外科学杂志

Objective:To investigate the effect of long non-coding RNA (lncRNA) HAGLR on the proliferation and migration of gastric cancer cells by inhibiting the expression of microRNA (miRNA, miR)-93-5p.Methods:Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression of HAGLR in gastric cancer cell lines (HS-746T, BGC823, SGC7901, MGC803) and normal gastric mucosal epithelial cells (GES-1). Selected the cell line with the lowest HAGLR expression and transfected with the negative control plasmid (negative control group) or HAGLR-high-expression plasmid (HAGLR group) respectively. The MTS method and the scratch healing test were used to detect the proliferation and migration ability of the cells after transfection. The bioinformatics software miRcode database was used to predict the target gene of HAGLR, and the dual luciferase reporter gene experiment was used to verify the binding of HAGLR to the target gene. qRT-PCR was used to detect the expression of the target gene. Western blot was used to detect the expression of Hippo signaling pathway. The software SPSS 21.0 was used to conduct statistical analysis. The t test was used for comparison between two groups, and the one-way analysis of variance was used for comparison between multiple groups. Results:Compared with GES-1 cells, the expression level of HAGLR in gastric cancer cell lines was lower (all P<0.05), and the cell line with the lowest HAGLR expression was SGC7901 cells ( P<0.01). The HAGLR expression in SGC7901 cells in the HAGLR group and the negative control group were 1.03±0.13 and 9.75±1.10, respectively. The expression level of HAGLR in the negative control group was significantly lower than that in the HAGLR group ( t=7.87, P<0.01). Compared with the negative control group, the absorbance of SGC7901 cells in the HAGLR group was significantly reduced ( P<0.05), and the scratch healing rate was significantly reduced ( P<0.01). The miRcode database showd that HAGLR and miR-93-5p have complementary binding sites. The dual luciferase reporter gene experiment showed that HAGLR can complement miR-93-5p ( P<0.01). Compared with the negative control group, the expression of miR-93-5p in SGC7901 cells in the HAGLR group was significantly reduced ( P<0.01), and the expression of Hippo signaling pathway protein was significantly reduced (all P<0.01). Conclusions:HAGLR is low expressed in gastric cancer cell lines. HAGLR inhibits the proliferation and migration of gastric cancer SGC7901 cells by negatively regulating miR-93-5p.

Mechanism of miR-3126-5p targeting LASP1 to inhibit the proliferation and migration of colorectal cancer cells / 国际外科学杂志

Objective:To explore the effect of microRNA (miRNA)-3126-5p on the proliferation and migration of colorectal cancer cells by inhibiting the expression of LIM and SH3 protein 1 ( LASP1). Methods:Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression levels of miR-3126-5p in colorectal cancer cell lines (HT-29, HCT116, LoVo, SW480) and normal intestinal mucosal epithelial cells (HIEC). The cell line with the lowest expression level was selected as the experimental object. The experiment was divided into 2 groups: the negative control group (transfected with miR-NC) and the miR-3126-5p group (transfected with miR-3126-5p). Cells of each group were collected 48h after transfection. qRT-PCR method was used to detect the expression level of miR-3126-5p in each group. The MTS method and the scratch healing experiment were used to detect the proliferation level and migration ability of the cells in each group. The bioinformatics software microRNA.org and the dual-luciferase reporter gene experiment were used to predict and verify the target genes of miR-3126-5p, respectively. qRT-PCR and Western blot were used to detect the expression levels of target genes in each group of cells. Measurement data were expressed as mean±standard deviation ( Mean± SD), t test was used for comparison between two groups, and one-way analysis of variance was used for comparison between multiple groups. Results:Compared with normal intestinal mucosal epithelial cells (HIEC), the expression level of colorectal cancer cell line miR-3126-5p was significantly reduced ( P<0.05), and the cell line with the lowest expression level was HCT116 cells ( P<0.01). The expression of miR-3126-5p in HCT116 cells in the negative control group and miR-3126-5p group were (1.05±0.16) and (7.91±1.26) respectively, and the difference was statistically significant ( t=5.40, P<0.01). Compared with the negative control group, the proliferation ability of HCT116 cells in the miR-3126-5p group was significantly reduced ( t=4.52, P<0.05), and the migration ability was significantly reduced ( P<0.01). microRNA.org shows that miR-3126-5p has complementary binding sites with LIM and SH3 protein 1 ( LASP1) gene mRNA. miR-3126-5p can target LASP1 mRNA ( P<0.01). Compared with the negative control group, the expression of LASP1 gene in HCT116 cells of the miR-3126-5p group was significantly reduced ( t=4.56, P<0.01). Conclusion:The expression of miR-3126-5p in colorectal cancer cell lines is low, and miR-3126-5p can reduce the proliferation and migration ability of colorectal cancer HCT116 cells by inhibiting the expression of the target gene LASP1.

Upregulation of miR-20b Protects Against Cerebral Ischemic Stroke by Targeting Thioredoxin Interacting Protein (TXNIP)

Dysregulation of microRNAs (miRNAs) is involved in abnormal development and pathophysiology in the brain. Although miR-20b plays essential roles in various human diseases, its function in cerebral ischemic stroke remains unclear. A cell model of oxygen glucose deprivation/reoxygenation (OGD/R) and A rat model of middle cerebral artery occlusion/reperfusion (MCAO/R) were constructed. qRT-PCR and western blot were used to evaluate the expression of miR-20b and TXNIP. Cell viability was detected by MTT assay, and cell apoptosis was evaluated by flow cytometry. Targetscan and Starbase were used to predict the potential targets of miR-20b. Luciferase reporter assay was applied to determine the interaction between miR-20b and TXNIP. Rescue experiments were conducted to confirm the functions of miR-20b/TXNIP axis in cerebral ischemic stroke. MiR-20b was significantly downregulated after I/R both in vitro and in vivo. Upregulation of miR-20b inhibited OGD/R-induced neurons apoptosis and attenuated ischemic brain injury in rat model. Bioinformatic prediction suggested that TXNIP might be a target of miR-20b, and luciferase reporter assay revealed that miR-20b negatively regulated TXNIP expression by directly binding to the 3’-UTR of TXNIP. Downregulation of TXNIP inhibited OGD/R-induced neurons apoptosis in vitro and ischemic brain injury in vivo. Rescue experiments indicated that downregulation of TXNIP effectively reversed the effect of miR-20b inhibitor in neurons apoptosis after OGD/R-treatment and ischemic brain injury in a mouse model after MCAO/R-treatment. Our study demonstrated that upregulation of miR-20b protected the brain from ischemic brain injury by targeting TXNIP, extending our understanding of miRNAs in cerebral ischemic stroke.

Effect of miR-7856-5p on migration and proliferation of colorectal cancer cell line SW480 by targeting EPHA3 / 国际外科学杂志

Objective:To explore the regulation of microRNA (miRNA, miR)-7856-5p on the expression of EPH receptor A3 (EPHA3) gene and its effect on the migration and proliferation of colorectal cancer cell line SW480.Methods:Real-time quantitative polymerase chain reaction (Real-time PCR) was used to detect the expression of miR-7856-5p in colorectal cancer tissues and cell lines. The miR-7856-5p mimic and miR-NC were transfected into colorectal cancer cell line SW480 by lipofection, respectively, and defined as miR-7856-5p group and miR-NC group, respectively. Real-time PCR was used to detect transfection effects. Transwell assay and CCK-8 assay were used to detect cell migration and proliferation after transfection. The bioinformatics software predicts and the dual luciferase reporter gene system validates the target gene of miR-7856-5p. Real-time PCR and Western blot were used to detect the expression of EPHA3 in the transfected cells. The measurement data in accordamce with normal distribution were expressed as mean±standard deviation, t test was used for inter grap comparison, and single factor analysis of variance was used for multi group comparison. Results:The expression of miR-7856-5p in colorectal cancer tissues was significantly lower than that in adjacent tissues ( P<0.01). The expression of miR-7856-5p in colorectal cancer cell lines was significantly lower than that in normal intestinal mucosal epithelial cells ( P<0.05), and lowest in SW480 cells ( P<0.01). The expression of miR-7856-5p in miR-7856-5p group was significantly higher than that in miR-NC group, the difference was statistically significant [(9.49 ± 1.09) vs (1.06 ±0.18), P<0.01]. The number of migrated cells in miR-NC group and miR-7856-5p group were (125.70±14.05) and (42.01±8.98), respectively, and the migration ability of miR-7856-5p group was significantly decreased ( P<0.01). Compared with the miR-NC group, the cell proliferation ability of the miR-7856-5p group was significantly decreased ( P<0.05). Bioinformatics software showed that the target gene for miR-7856-5p was EPHA3. The dual luciferase reporter gene system confirmed that miR-7856-5p can target the EPHA3 gene ( P<0.05). Compared with the miR-NC group, the expression of EPHA3 in the SW480 cells of the miR-7856-5p group was significantly decreased ( P<0.05). Conclusion:miR-7856-5p can inhibit the migration and proliferation of colorectal cancer cell SW480 by regulating the expression of EPHA3.

Evaluation of the life quality of the patients with oral cancer / 实用口腔医学杂志

Objective: To evaluate the life quality of the patients with oral cancer. Methods: A questionnaire survey was conducted on 200 patients with oral cancer who met the inclusion criteria by the Chinese version of the University of Washington Quality of Life Questionnaire (UW-QOL, V4. 0) . The data were statistically analyzed by SPSS 20. 0. Results: A total of 200 questionnaires were issued and 145 valid questionnaires (72. 50％) were returned. The scores of somatic function domain and social emotional health domain were 60. 29 ± 15. 62 and 46. 65 ± 23. 21 respectively (P ＜ 0. 05) . Physical health scores and social emotional health scores were positively correlated (r = 0. 584) . Conclusion: Oral cancer patients have poor social and psychological status. Necessary psychological intervention and clinical intervention are of great significance to improve the life quality of the patients. Strengthening of social support can improve their physical health of the patients.

Effect of human trophoblast cell-surface antigen 2 gene expression by RNA interference on proliferation and apoptosis of tongue squamous cell carcinoma and its mechanism / 中华口腔医学杂志

Objective@#To investigate the effect and its mechanism of human trophoblast cell-surface antigen 2 (Trop2) gene expression was inhibited in squamous cell carcinoma of tongue on the proliferation and apoptosis of cancer cells.@*Methods@#A total of 46 patients from February 2014 to May 2016 received radical treatment of tongue cancer from oral and maxillofacial surgery of the First Affiliated Hospital of Zhengzhou University were enrolled in this study. Real time PCR and Western blotting were used to detect mRNA and protein expression of Trop2 in tongue squamous cell carcinoma and corresponding adjacent tissues; NC-siRNA and Trop2-siRNA were transfected into human tongue squamous cell carcinoma CAL-27 cells, a blank control group (control) was set, the expression of Trop2, Ki-67, cyclin D1, cleaved caspase3, Notch1, Hes1 protein after transfected for 48 h were detected by Western bloting; cell proliferation was detected by cell counting kit-8; cell cycle and apoptosis rate were detected by flow cytometry.@*Results@#The mRNA (5.72±1.13) and protein expression (0.77±0.06) of Trop2 gene in tongue squamous cell carcinoma were significantly higher than those in adjacent tissues (0.92±0.15, 0.11±0.01, P<0.05); Trop2 protein expression after transfeced Trop2-siRNA (0.08±0.01) in CAL-27 cells decreased significantly (0.46±0.05); the survival rate (64.28±4.12)%, S cells (14.54±1.02)% and Ki-67 (0.12±0.01), cyclin D1 (0.04±0.01) protein expression in Trop2-siRNA group were significantly lower than those in control group [(100.00±1.02)%, (27.33±1.11)%, (0.24±0.02), (0.20±0.02)] and NC-siRNA group [(96.55±2.43)%, (26.67±1.23)%, (0.26±0.03), (0.21±0.024)], the apoptosis rate (23.55±1.45)%, G0/G1 cells (72.32±0.94)% and the expression of cleaved caspase 3 (0.16±0.02), Notch1 (0.62±0.06) and Hes1 (0.50±0.05) protein were significantly higher than control group and NC-siRNA group (P<0.05).@*Conclusions@#The expression of Trop2 gene was inhibited in tongue squamous carcinoma cells can reduce the proliferation of cancer cells, block the cells in phase G1, and promote the apoptosis of cells. The mechanism is related to the up regulation of Notch1 signaling pathway.

Effects of EZH2 siRNA on apoptosis induction and radiosensitivity of tongue cancer Tca-8113 cells / 中华放射医学与防护杂志

Objective To investigate the effect of EZH2 on apoptosis and radiosensitivity of squamous cell carcinoma of tongue.Methods Tongue squamous carcinoma cells Tca-8113 were transfected with small interfering RNA of EZH2 (EZH2 siRNA1,EZH2 siRNA2) and its negative controls (siRNA-NC),the expression levels of EZH2 were detected by RT-PCR and Western blot and EZH2 siRNA2 was used for further studied since its better interference efficiency.The cells with siRNA transfection were irradiated with 8 Gy doses,and cell proliferation was detected by MTT,apoptosis was detected by flow cytometry,the expression of p-STAT3,STAT3 and Cleaved Caspase-3 was detected by Western blot.In addition,the cells were irradiated with 0,2,4,6,and 8 Gy to detect radiosensitivity by cell colony formation assay.Results EZH2 siRNA1 and EZH2 siRNA2 decreased the expression of EZH2 in Tca-8113 cells and EZH2 siRNA2 had a better interference efficiency (tmRNA =8.660,PmRNA ＜ 0.01;tprotein =2.883,Pprotein ＜0.05).The apoptotic rate in the EZH2 siRNA group was (29.90 ± 1.64)％,and was increased by 8 Gy irradiation to (38.17 ± 1.59) ％ (t =4.742,P ＜ 0.05).At the same time,EZH2 siRNA reduced the level of p-STAT3,but promoted the expression of Cleaved Caspase-3 protein,and enhanced the sensitivity of Tca-8113 cells to 1.668-times of control.Conclusions Interfering EZH2 could promote apoptosis,inhibit proliferation and increase radiosensitivity of squamous cell carcinoma of tongue.

Optimization of Fermentation Conditions for Enterococcus faecalis and Saccharomyces cerevisiae Mixed Probiotic Formulation / 中国医科大学学报

Objective To optimize the fermentation conditions for Enterococcus faecalis (E.faecalis) and Saccharomyces cerevisiae (S.cerevisiae) mixed culture.Methods The optimum fermentation conditions for E.faecalis and S.cerevisiae mixed culture were identified by investigating the influence of initial pH,inoculum size,and ventilation rate of the culture broth on mixed microbial growth.Results The optimal initial pH of mixed microbial culture was 7.0 and the inoculation amounts of E.faecalis and S.cerevisiae were 4％ and 10％ respectively,when fermented in 600-mL pilot fermentor (liquid volume 40％) at 30 ℃,with ventilation rate of 0.2 L/min,for 20 h.At the end of the fermentation,the E.faecalis and S.cerevisiae counts were approximately 3.8 × 108 CFU/mL and 2.4 × 108 CFU/mL,respectively.Ventilation for the amount difference of E.faecalis was no significant (P ＞ 0.05),and for the amount difference of S.cerevisiae was statistically significant (P ＜ 0.05).Conclusion The E.faecalis and S.cerevisiae counts increased by 32.2％ and 31.5％ respectively,when the optimized conditions of fermentation culture were used.In this study,high mixed microbial counts were obtained,thus providing a reference for the preparation of large-scale production of mixed microbes.

Characteristics of Coronary CT Angiography in Patients With Myocardial Bridge Combining Arrhythmia / 中国循环杂志

Objective: To study the characteristics of coronary CT angiography (CTA) in patients with myocardial bridge (MB) with arrhythmia. Methods: Our study included 2 groups: MB+arrhythmia group,n=31, clinical information as medical record, electrocardiogram (ECG), myocardial enzyme, echocardiography and coronary CTA findings were collected; MB group, n=30, the MB patients were without arrhythmia. Results: In MB+arrhythmia group, all patients were with mere MB, coronary artery disease, valve-structural heart diseases and other systemic diseases were excluded. There were 2/31 patients with ventricular fibrillation, 1 with atrial fibrillation, 5 with supraventricular tachycardia and 23 with ventricular tachycardia; 17/31 patients having deep type MB and 14 having superficial type MB. The myocardial systolic end diameter, diastolic end diameter by retrospective ECG gating and the stenosis at cross section of mural coronary MB by CTA were similar between 2 groups,P>0.05. Conclusion: MB+arrhythmia patients had no specific characteristics in coronary CTA; anatomical CTA feature may partly explain the myocardial ischemic symptom while couldn't clarify arrhythmia occurrence in relevant patients.

Construction of Recombinant Pichia pastoris Expressing Human SOD / 中国医科大学学报

Objective To optimize the expression of active human Cu,Zn-superoxide dismutase (SOD) in recombinant Pichia pastoris (P.pastoris).Methods A recombinant human SOD expression construct was generated and expressed in P.pastoris.The culture time,concentration of copper ions in the medium,and conditions for methanol induction were optimized,and SOD was preliminarily purified.Results Five P.pastoris recombinants that stably expressed human SOD were obtained.SOD could be purified from the culture supernarants of the recombinant strains by chromatography.The amount of SOD secreted into the supernatant was high with optimal activity,when the incubation time was 48 h,copper ion concentration in the medium was 0.5％,and methanol concentration was 1％.Conclusion An effective method for the expression of soluble human Cu,Zn-SOD in P.pastoris was established,and the enzyme produced using this method exhibited high activity.This method provides a foundation for further research on the production of human SOD by fermentation.

Effects of mild hypothermia in secondary brain injury in patients with severe brain injury / 中华急诊医学杂志

Objective To evaluate the effect of mild hypothermia combined with hypbaric oxygen (HBO) treatment on secondary brain injury in patients with severe craniocerebral injury.Methods A prospective study was conducted in this study.Forty-two patients with severe craniocerebral injury admitted to hospital within 8 hours were randomly divided into sub-hypothermia combined with HBO treatment group and conventional HBO control group,21 cases in either group.Cerebral hemorrhage and brain edema were calculated by reviewed head CT on the 1st day,15th day and 30th day after injury.GCS (Glasgow Coma Scale) score was calculated at the same time.The number of cases of cerebral infarction was counted in the two groups.GOS (Glasgow Outcome Score) prognosis was scored for both groups of patients six months after injury.Two groups of sample rates were compared using a chi-square test with continuous correction,The intergroup comparisons were analyzed by independent sample t test by using SPSS version 13.0 software.Differences were considered statistically significant if P ＜ 0.05.Results (1) The amount of cerebral hemorrhage and edema in the treatment group were significantly lower than those in the control group on the 15th day and 30th day after injury [(21.71 ±4.3) vs.(26.33 ±5.23);(14.33 ± 1.93) vs.(16.86 ±2.86),P ＜0.05].(2) The GCS score of the treatment group was higher than that of the control group on the 15th day and 30th day after injury [(4.62 ±0.49) vs.(2.49 ±0.56);(9.76 ± 1.37) vs.(8.57 ± 0.92),P ＜ 0.05];(3) There were 2 cases of traumatic cerebral infarction in the treatment group and 9 cases in the control group (x2 =4.434,P =0.035).The GOS score in the treatment group was higher than that in the control group six months after injury [(4.29 ± 0.84) vs.(3.38 ± 0.74),P =0.001].Conclusions Mild hypothermia combined with hyperbaric oxygen treatment can reduce the secondary brain injury and improve the prognosis of patients with severe craniocerebral injury.It is worth further study,the mechanism of hypothermia remains to be further studied.

CTA features of pure myocardial bridge on the patients without symptom / 实用放射学杂志

Objective To analyze the CTA features of asymptomatic myocardial bridge.Methods The CTA images of 69 cases with asymptomatic solitary myocardial bridge were studied retrospectively, and CTA images of 60 cases with symptoms as the contrast group.The type, age, thickness of myocardial bridge, mural coronary artery length and diameter changes of each cases of two groups were analyzed.Results In the study group, 51 cases of 69 (74%) were superficial style, while 18 cases were deep type (26%).In the contrast group, the superficial and deep style were 13 (22%) and 47 (78%) respectively.The mean age,thickness of myocardial bridge,mural coronary artery length and the diameter of mural coronary artery were (53.01±11.17) years old,(1.25±1.16) mm,(21.33±7.32) mm,(2.86±0.45) mm and (51.36±9.31) years old,(1.45±1.87) mm,(20.07±6.60) mm and (1.37±0.41) mm.The rate of type and diameter of mural coronary artery had significant differences between two groups (P0.05).Conclusion The CTA features of asymptomatic myocardial bridge are mostly superficial type.The diameter of mural coronary artery on the end systolic is a factor to judge the rate on the occurrence of clinical symptom.

Mechanism of Sodium arsenite by Wnt signaling pathway inhibits the proliferation of oral squamous cell carcinoma and promote apoptosis / 中国生化药物杂志

Objective To investigate the effect of sodium arsenite by Wnt signaling pathway on proliferation and apoptosis of oral squamous cell carcinoma.Methods Cell proliferation was detected after 1.25,2.5,5,10,20μmol/L sodium arsenite treatment human oral squamous cell carcinoma cell line Tca8113 for 24,48,72 hours by CCK8 experiment.0 and 14μmol/L sodium arsenite was used to treatment Tca8113 cells with 48h,cell apoptosis were detected by flow cytometry,Cleaved Caspase3,β-catenin,Cyclin D1 protein expression were detected by Western blot.Tca8113 cells were divided into control group,sodium arsenite group,activating agent+sodium arsenite group,all treated for 48hour,cell proliferation,apoptosis and Cleaved Caspase3,β-catenin,Cyclin D1 protein expression were detected by CCK8 assay,flow cytometry and Western blot.Results Tca8113 cell proliferation was inhibited significantly with the increase of treatment time and sodium arsenite concentration,and has a time and concentration dependent manner(P<0.05 or P<0.01).10μmol/L sodium arsenite as a follow-up study according to the IC50.Cell inhibition rate,apoptosis rate and Cleaved Caspase3 protein expression in 10μmol/L group were significantly higher than that of 0 mol/L group,the expression of β-catenin,Cyclin D1 protein was significantly lower than that of 0 mol/L group(P<0.01).Apoptosis rate,cell inhibition rate and Cleaved Caspase 3 protein expression in sodium arsenite group and activating agent+sodium arsenite group were significantly higher than control group,the expression of β-catenin and Cyclin D1 protein were significantly lower than control group(P<0.01).Apoptosis rate,cell inhibition rate and Cleaved Caspase 3 protein expression in activating agent + sodium arsenite group were significantly lower than that of sodium arsenite group,the expression of β-catenin and Cyclin D1 protein were significantly higher than that of sodium arsenite group(P<0.01).Conclusion Sodium arsenite can inhibit the proliferation of oral squamous cell carcinoma and promote apoptosis,and the mechanism was related to regulation of Wnt signaling pathway.

Effects of Dexmedetomidine Hydrochloride on Glutamate-induced Neurotoxicity in Rats / 中国医科大学学报

Objective To investigate the effects and mechanism of dexmedetomidine hydrochloride preconditioning against glutamate-induced neurotoxicity.Methods The model of glutamate-induced neurotoxicity was established by the injection of glutamate into lateral cerebral ventricle.Thirty-six SD rats were randomly divided into control group (C group),glutamate-induced neurotoxicity group (G group),Dex1 group and Dex2 group.Dex1 group and Dex2 group received intraperitoneal injection of dexmedetomidine respectively at a dose of 50 μg/kg or 100 μg/kg before glutamate application.Two hours later,the rats were sacrificed and hippocampus was separated to measure the level of SOD and MDA.The rest of each brain was used to measure the degree of brain edema.Pathological changes were observed under microscope with Nissl's staining.Results In contrast to G group,brain edema and MDA concentration in Dex1 group and Dex2 group were significant lower,while SOD concentrations were significantly increased and the pathological change in Dex1 group and Dex2 group were relieved obviously compared to glutamate-induced neurotoxicity group.Conclusion Dexmedetomidine preconditioning can significantly attenuate glutamate-induced neurotoxicity,which is properly related to the inhibition of oxidative-stress reaction.

Risk factors related to postoperative death in patients with rectosigmoid junction tumor perforation / 中华普通外科杂志

Objective To investigate risk factors related to postoperative death of patients with rectosigmoid junction tumor perforation.Methods The clinical data of 76 cases with rectosigmoid junction tumor perforation confirmed by laparotomy from January 2000 to October 2015 were collected.Results Of the 76 cases,17 patients died postoperatively,the mortality rate was 22％,the single factor analysis showed that age(x2 =4.649,P =0.031),duration of abdominal pain(x2 =8.218,P =0.016),severe heart and lung diseases(x2 =11.996,P =0.007),circulatory and renal function(x2 =10.360,P =0.016),serum albumin(x2 =7.252,P =0.027),white blood cell count(x2 =7.633,P =0.022),Perforation diameter (x2 =9.770,P =0.008),Geroge grade of intraperitoneal contamination (x2 =10.086,P =0.006) were related to postoperative death (P ＜ 0.05).Multivariate analysis showed that complicating severe heart and lung diseases,preexisted circulatory and renal dysfunction,white blood cell count ＜ 4 × 109/L,size ＞ 3 cm,intraperitoneal contamination larger than one quadrant were independent risk factors for postoperative death.Conclusion Risk factors related to postoperative death of rectosigmoid junction tumor perforation were preoperative important organ dysfunction and intraperitoneal infection.