Objective To observe the effect ofYinqiao Powder on the mouse models with upper respiratory trace mucosal immunity dysfunction infected with influenza virus A, and explore mechanism of action.Methods The mouse models of upper respiratory trace mucosal immunity dysfunction induced by cold stimulation with the influenza A/PR/8/34 (H1N1) virus through the nasal cavity were established. The mice were randomly divided into normal group, model group, positive medicine (Ribavirin) group, andYinqiao Powder group. All administration groups received gavage with relevant medicine, and then mortality, the life prolonging rate, average survival time and the lung index of each group were observed.Results Compared with the model group, the mortalities in positive medicine group andYinqiao Powder group decreased significantly (P<0.05,P<0.01), with longer survival time. The lung indexes in positive medicine group andYinqiao Powder group decreased significantly (P<0.05,P<0.01), and the inhibition ratios of lung index were 35.5% and 24.6%, respectively.ConclusionYinqiao Powder can realize the protective effects on upper respiratory infection through upregulating the mucosal immunity of the upper respiratory tract of mouse models.

Objective To determine the pharmacokinetic parameters of P-methoxybenzyl alcohol from Gastrodiae Rhizoma in plasma of rats by HPLC. Methods Gavage and intravenous injection were employed for administration. HPLC was used to determine the concentrations of P-methoxybenzyl alcohol from Gastrodiae Rhizoma in plasma of rats in different time points. The pharmacokinetic parameters were computed by DAS3.0. Results The linear range of P-methoxybenzyl alcohol in plasma was 0.63-321.17 μg/mL, r 2=0.994 5. Intra-day accuracy, inter-day accuracy, absolute recovery and stability were in specified range. Conclusion The method is simple and accurate for the determination of the pharmacokinetic parameters of P-methoxybenzyl alcohol from Gastrodiae Rhizoma in plasma of rats.

Objective To study the characteristics of ? cell function change and to explore the predictive value of glutamic acid decarboxylase (GAD)-Ab and other factors for ? cell function in the patients with latent autoimmune diabetes of adults (LADA). Methods Sixteen LADA patients (positive GAD-Ab) and 24 type 2 diabetic patients (negative GAD-Ab) were followed-up at 0, 6th, 12th, 30th, 36th, 42th and 48th months respectively. Their fasting and postprandial 2h C-peptide and glycemic control were measured. GAD-Ab was determined by radioimmunoprecipitation assay and C-peptide by RIA. Results Decreased fasting C peptide (FCP) levels (Month 30, 36, 42, 48 compared with Month 0, P

Objective:To explore the role of endothelial biomarkers in predicting damp-heat syndrome in diabetic kidney disease (DKD).Methods:A total of 183 patients with DKD were divided into 3 groups:the early DKD group,established DKD group,and advanced DKD group.All patients were classified according to traditional Chinese medicine (TCM) syndrome type,and clinical indexes were collected for statistical analysis.Results:A total of 183 DKD patients were included in this study.Fibroblast growth factor 23 (FGF23),chitinase-3-like protein 1 (CHI3L1),endocan,tumor necrosis factor receptor 1 (TNFR1),secretory leukocyte protease inhibitor (SLPI),and vascular endothelial growth factor A (VEGF-A) were increased in advanced DKD.FGF23,CHI3L1,endocan,SLPI,and TNFR1 showed a negative correlation with estimated glomerular filtration rate (eGFR),while they had a positive correlation with 24 h urine protein.After adjusting for age,gender,diabetes duration,body mass index (BMI),hemoglobin,glucose,uric acid,24 h urine protein,cholesterol,triglyceride,low-density lipoprotein,and hemoglobin A1c (HbA1c),the multiple regression analysis showed that FGF23,endocan,TNFR1,and SLPI significantly correlated with eGFR.Conclusions:FGF23,endocan,TNFR1,and SLPI are elevated in advanced DKD compared with early stage,and they may take part in the pathogenesis and progression of DKD.Our study provides useful bio-markers for predicting the appearance of damp-heat syndrome,including FGF23,endocan,TNFR1,and SLPI.

Objective:To evaluate the recurrence and progression of patients with pT1 high grade urothelial carcinoma of bladder (UCB) and glandular differentiation.Methods:We retrospectively analyzed the clinical and pathological information of 208 patients diagnosed as pT1 high grade urothelial carcinoma in the Fifth Central Hospital of Tianjin from January 2006 to February 2019.Among them, 78 cases were diagnosed as glandular differentiation (UCGD), the other 130 patients without histologic variants were served as control. The UCGD group included 62 male and 16 female, whose median age was 67 years old (range 38-81 years old). The control group contained 105 male and 25 female, whose median age was 66 years old (range 40-82 years old). Kaplan-Meier and Cox proportional hazard regression analyses were used to evaluate the predictors of oncologic outcomes.Results:The disease recurrence rate and progression rate in UCGD group were 65.4% (51/78) and 28.2% (22/78), higher than 38.5%(50/130) and 14.6%(19/130) of control group ( P<0.05). The median recurrence time in UCGD group was 41 months while 55 months in the control group. The median progression time in UCGD group was 39 months while 54 months in the control group. According to the univariate analysis, largest tumor size ( P=0.030), UCGD ( P=0.003) and lymphovascular invasion (LVI) ( P=0.032) were associated with disease recurrence. UCGD ( P=0.036) and LVI ( P=0.011) were associated with progression. Additionally, Cox multivariate analysis revealed that UCGD ( P=0.001), LVI ( P=0.038) were the independent factors of disease recurrence. UCGD ( P=0.007) and LVI ( P=0.037) were also found to be the independent factors of disease progression. Conclusions:Patients with T1 stage UCB and UCGD are at higher risk of disease recurrence and progression. Therefore, these patients should be followed up closely after being diagnosed and undergo individual treatment according to the situation.

Objective:To evaluate the recurrence and progression of patients with pT1 high grade urothelial carcinoma of bladder (UCB) and glandular differentiation.Methods:We retrospectively analyzed the clinical and pathological information of 208 patients diagnosed as pT1 high grade urothelial carcinoma in the Fifth Central Hospital of Tianjin from January 2006 to February 2019.Among them, 78 cases were diagnosed as glandular differentiation (UCGD), the other 130 patients without histologic variants were served as control. The UCGD group included 62 male and 16 female, whose median age was 67 years old (range 38-81 years old). The control group contained 105 male and 25 female, whose median age was 66 years old (range 40-82 years old). Kaplan-Meier and Cox proportional hazard regression analyses were used to evaluate the predictors of oncologic outcomes.Results:The disease recurrence rate and progression rate in UCGD group were 65.4% (51/78) and 28.2% (22/78), higher than 38.5%(50/130) and 14.6%(19/130) of control group ( P<0.05). The median recurrence time in UCGD group was 41 months while 55 months in the control group. The median progression time in UCGD group was 39 months while 54 months in the control group. According to the univariate analysis, largest tumor size ( P=0.030), UCGD ( P=0.003) and lymphovascular invasion (LVI) ( P=0.032) were associated with disease recurrence. UCGD ( P=0.036) and LVI ( P=0.011) were associated with progression. Additionally, Cox multivariate analysis revealed that UCGD ( P=0.001), LVI ( P=0.038) were the independent factors of disease recurrence. UCGD ( P=0.007) and LVI ( P=0.037) were also found to be the independent factors of disease progression. Conclusions:Patients with T1 stage UCB and UCGD are at higher risk of disease recurrence and progression. Therefore, these patients should be followed up closely after being diagnosed and undergo individual treatment according to the situation.

Objective To explore the effects of two different methods on the blood glucose variability (BGV) of patients with traumatic brain injury (TBI) who had performed the surgery.Methods A total of 100 patients with TBI after the surgery, who were admitted at intensive care unit ( ICU) from June 2013 to July 2014, were randomly assigned to the observation group ( n=50) and the control group ( n=50) . Patients in the control group received the routine treatment to adjust the BVG. Patients in the observation group received the modified Leuven′s adjustment processes. Blood glucose was continuously monitored in 5 days and all the data include mean blood glucose, incidence of hypoglycemia (level of blood glucose≤3.2 mmol/L), blood glucose standard deviation (SD), mean amplitude of glycemic excursions (MAGE) and glucose lability index (GLI) were performed statistical analysis. Results Mean blood glucose was stable in 5 days after operation in two groups (P>0.05). The blood glucose SD, MAGE and GLI in the observation group among the first 2 days [1st day:(4.7±1.2), (0.86±0.41), (255.9±213.7);2nd day:(4.0±1.7), (0.63±0.38), (202.7±163.5)] was higher than the control group [1st day:(1.1±0.68), (0.51±0.25), (112.7±92.8); 2nd day: (1.2±0.44), (0.41±0.17), (93.1±72.7)], and the difference was statistically significant (P<0.05). In the last 3 days, these data between two groups all fallen and the difference was insignificant ( P>0. 05 ) . The incidence of hypoglycemia in the observation group was lower than that of the control group in the 1st day ( P<0.05) . In the last 4 days, the data in two groups fell (P>0.05).Conclusions The modified Leuven′s adjustment processes has characteristics of early adjustment, accessible and operate simply. It is better than the routine adjustment processes in the BGV control at the early stage.

Objective To investigate the effect of fluoride exposure on expression of miRNA (miR)-200c and its target in human osteoblast Saos-2 cells.Methods Saos-2 cells were cultured in DMEM/F-12 medium and treated with fluoride (sodium fluoride,NaF).There were two groups including:control group (0 mg/L) and fluoride group (4 mg/L).Cells were harvested after 48 hours of culture with fluoride.The expression of miR-200c,the mRNA of alkaline phosphatase (ALP),osteocalcin (BGP),the target phosphatase and tensin homolog deleted on chromosome ten (PTEN) and dual-specific phosphatase 1 (DUSP1) of miR-200c was detected by qRT-PCR.The protein expression of PTEN and DUSP1 was detected by Western blotting.Results The expressions of ALP,BGP mRNA and miR-200c in Saos-2 cells in the fluoride group (23.60 ± 1.87,9.41 ± 0.94,8.61 ± 0.26) were higher than those in the control group (1.00 ± 0.11,1.00 ± 0.07,1.00 ± 0.12).The differences were statistically significant (t =-24.084,-18.388,-8.687,P ＜ 0.05).The mRNA expressions of PTEN and DUSP1 in the fluoride group (0.63 ± 0.02,0.38 ± 0.02) were lower than those in the control group (1.02 ± 0.24,1.02 ± 0.24).The differences were statistically significant (t =3.327,5.454,P ＜ 0.05).The protein expressions of PTEN and DUSP1 in Saos-2 cells in the fluoride group (1.19 ± 0.10,0.83 ± 0.07) were lower than those in the control group (1.81 ± 0.14,1.44 ± 0.25).The differences were statistically significant (t =6.250,4.171,P ＜ 0.05).Conclusion Exposure to fluorine may increase the expression of miR-200c in Saos-2 cells,and fluorine may act on PTEN and DUSP1 through miR-200c,downregulates the mRNA and protein expression levels of PTEN and DUSP1.

OBJECTIVE：To obs erve the protective effect of protoca techuic aldehyde（PAL）on neurovascular unit （NVU） homeostasis damage in rats after cerebral ischemia-reperfusion injury （CIRI）. METHODS ：SD rats were randomly divided into sham operation group ，model group ，PAL high-dose and low-dose groups （10，20 mg/kg），with 11 rats in each group. Administration groups were given relevant medicine intragastrically. Sham operation group and model group were given the same volume of normal saline intragastrically ，10 mL/kg once a day ，for 5 days. After last administration ，CIRI model was induced by suture method ；the ultrastructural changes of NVU were observed by transmission electron microscope. Western blot assay was used to detect the expression of NUV related proteins （MAP-2，GFAP，AQP-4）in cerebral tissue. Immunofluorescence staining was used to observe the positive expression of above proteins in cerebral cortex. RESULTS ：Compared with sham operation group ， blood-brain barrier （BBB）structure of model group was destroyed severely ，the vascular lumen became narrower ，lateral edema of endothelial cells was severe ，and the thickness of basement membrane varied ；the nuclei of neurons were pyknosis and there was a large area of edema in the surrounding tissues ；the structure of glial cells was seriously damaged ，the cell body was shrunk and organelles were lost ；protein expression （or positive expression ）of MAP- 2 in brain tissue （or cerebral cortex ）were significantly decreased （P＜0.05 or P＜0.01），while protein expression （or positive expression ） of GFAP and AQP- 4 were increased significantly（P＜0.01）. After PAL intervention ，the rats had less BBB damage ，and the morphology of vascular lumen and basement membrane were not completely destroyed ；the damage of neurons was alleviated ，the pyknosis of neurons was decreased ， the chromatin was homogeneous and the heterochromatin was decreased；the damage of glial cell structure was alleviated protein expression of GFAP and AQP- 4（except for low-dose group） in cerebral tissue and positive expression of MAP- 2 and GFAP protein in cerebral cortex were reversed @qq.com significantly （P＜0.05 or P＜0.01）. CONCLUSIONS ：PAL can protect the stability of NVU from damage in CIRI model rats； the mechanism may be related to up-regulating the expression of MAP- 2 protein in cerebral cortex and down-regulating the expression of GFAP and AQP- 4 protein in brain tissue.

Objective To study the effect of T-2 toxin on proliferation and cell cycle of rat chondrocytes,in order to provide a new idea in molecular mechanism of T-2 toxin-induced chondrocyte damage.Methods Primary chondrocytes of neonatal Wistar rats were isolated and stained by toluidine blue staining and type Ⅱ collagen immunofluorescence staining.The effects of different concentrations of T-2 toxin [0 (control),1,5,10,20,50,100 μg/L)] on proliferation of chondrocytes for 24 h were detected by cell counting kit-8 (CCK-8) method,and control,1 (low dose),5 (medium dose),and 10 μg/L (high dose) T-2 toxin were selected for subsequent experiment;cell cycle changes were detected by flow cytometry;Real-time PCR and Western blotting were used to detect the effects of T-2 toxin on mRNA and protein expressions of proliferating cell nuclear antigen (PCNA) and Cyclin D1 in chondrocytes.Results With increase of T-2 toxin concentration (control,1,5,10,20,50,100 μg/L),the cell survival rates [(100.00 ± 0.00)％,(93.12 ± 1.66)％,(77.12 ± 1.11)％,(59.44 ± 4.09)％,(46.64 ± 3.86)％,(38.15 ± 3.37)％,(33.79 ± 0.99)％] were decreased,and the differences were statistically significant (F =139.21,P ＜0.05).The percentages of quiescent phase/pre-DNA synthesis phase (G0/G1 phase) ceils in 1,5,10 μg/L T-2 toxin groups [(22.03 ± 0.42)％,(30.54 ± 2.61)％,(36.01 ± 1.51)％] were significantly higher than that in control group [(13.79 ± 1.65)％,P ＜ 0.05];the percentages of DNA synthesis phase (S phase) cells [(60.27 ± 3.53)％,(53.88 ±4.38)％,(49.55 ± 2.49)％] were significantly lower than that in control group [(76.72 ± 4.24)％,P ＜ 0.05].The differences of mRNA levels of PCNA and Cyclin D1 between groups were statistically significant (F =46.80,17.97,P ＜ 0.05),and 5,10 μg/L T-2 toxin groups (0.77 ± 0.13,0.79 ± 0.08,0.60 ± 0.07,0.56 ± 0.05) were lower than the control group (0.99 ± 0.02,1.01 ± 0.01,P ＜ 0.05).The expressions of PCNA protein in 5,10 μg/L T-2 toxin groups (0.69 ± 0.03,0.49 ± 0.03) were lower than that in control group (0.92 ± 0.05,P ＜ 0.05);the expressions of Cyclin D1 protein in 1,5,10 μg/L T-2 toxin groups (0.80 ± 0.06,0.60 ± 0.07,0.33 ± 0.13) were lower than that in control group (0.95 ± 0.07,P ＜ 0.05).Conclusion T-2 toxin can inhibit the proliferation of chondrocytes,which may be worked through influencing the expression of cell cycle protein,causing cell cycle arrest,thereby inhibiting DNA synthesis.