ObjectiveTo explore the effects of propofol combined with remifentanil in different ratios for intravenous anesthesia. Methods63 patients were randomly divided into three groups,each group 21 cases,different target plasma concentration of propofol and remifentanil were dosed for every group.Hemodynamic parameters such as MAP,HR were recorded at different time.so as to stop time for the zero time of local anesthetic.The extubation time,the quality and time of awakening were compared as well. ResultsThe MAP and HR value of all patients after induction of general anesthesia were lower than that before intubation,which showed significant difference(all P＜0.05),and the MAP and HR value of all patients after intubation reseal and decannulation showed significant difference compared with that before intubation reseal.The resurgence time and decannulation time of group A were the shortest,and the postoperative detubation revive quality score was also the best when compared with that of group B and C. ConclusionThe target plasma concentration of propofol(2.5mg/L)and remifentanil(μg/L)was the best.With the increasing of target plasma concentration of remifentanil and the decreasing of target plasma concentration of propofol,the resurgence time,decannulation time and the postoperative detubation revive quality score were improved gradually.

Objective To identify the outcomes and effect of applying the health check-up nursing quality control system developed as supervised by JCI quality assessment standards.Methods The monitoring system for nursing quality in the health check-up department is established within the framework of the hospital quality improvement committee and in line with characteristics of the department.Quality improvement tools may be called into play for analysis and decision making to revolve critical problems found in health check-up nursing,upgrading nursing quality and customer satisfaction.Results Significant rise of health check-up quality and customer satisfaction for nurses,and the nurses are trained in quality control knowledge and get further involved in quality management of their department.Conclusion Health check-up nursing management system under the JCI standard is conducive to raising the nursing quality,and helps nurses with problem analysis and solution.

Objective To investigate the correlation between matrix metalloproteinase-3 (MMP-3)serum level and polymorphism(5A/6A) and the stability of carotid plaque in Chinese Han population.Methods Two hundred and eighty acute cerebral infarction patients from the department of neurology of Taizhou Hospital were divided into carotid vulnerable plaque group and carotid stable plaque group according to the results of carotid B-mode uhrasonngraphy.Serum MMP-3 level waa measured by means of enzyme-linked immunosorbent assay (ELISA).At the same time, genotype was determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) for the common 5A/6A functional promoter polymorphism of the MMP-3 gene.The serum MMP-3 level and genotype frequencies of the MMP-3 gene between the two groups were analyzed.Results The genotype frequencies of the MMP-3 gene 5A/6A polymorphism of the two groups were in Hardy-Weinberg equilibrium The genotype distribution of the MMP-3 promoter 5A/6A polymorphism between the carotid vulnerable plaque group and the carotid stable plaque group was significantly different(χ2 =6.13, P =0.01, OR = 1.90, 95% CI 1.14-3.15).The frequencies of 5A allele were 20.6% and 12.8% in the carotid vulnerable plaque group and the carotid stable plaque group respectively (χ2=6.09, P=0.01, OR =1.76, 95%CI 1.12-2.77).Serum level of MMP-3 in the carotid vulnerable plaque group was higher than that in the carotid stable plaque group (t = 3.39, P =0.00).Conclusion The present findings suggest that serum level of MMP-3 and genetic polymorphism of 5A/6A in MMP-3 promoter are related with carotid vulnerable plaque in Chinese Han population and 5A allele may be a susceptible predictor of carotid vulnerable plaque.

ObjectiveTo evaluate prognosis and its clinical factors in patients with primary pontine hemorrhage. Methods Patients with primary pontine hemorrhage who were hospitalized in the First Affiliated Hospital of Wenzhou Medical College within 24 hours after stroke onset between April 2007 and April 2009 were registered conscutively. The patients were followed up for one year. Kaplan-Meier methods were used to analyze survival rate. Cox proportional hazards model was used to study risk factors for 1-year mortality. ResultsA total of 41 patients with primary pontine hemorrhage were studied. Their mean age was (63.5 ± 10. 1 ) years.The overall 1-year mortality rate was 61.0％, the median survival time was (80. 0 ±54.4) days (95％ CI 0-186. 64). After one-year follow-up, the mortality rate in patients with primary dorsal pontine hemorrhage( 18.2％ ) was significantly lower than that in patients with primary ventral pontine hemorrhage(72. 7％ ; x2 = 8. 800, P = 0. 003 ). Patients with massive primary pontine hemorrhage had significantly higher mortality rate than patients with dorsal primary pontine hemorrhage( x2 = 8. 927, P =0. 003). The average hematoma volume of the survivor group and mortality group was (3. 043 ± 1. 718) ml and (5. 984 ± 2. 707) ml, respectively, showing statistical significance (t = 3. 661, P = 0. 001 ). Analysis with Cox proportional hazards model showed that the risk factors associated with mortality were hematoma location ( RR = 2. 428, 95 ％ CI 1. 055-5. 587 ), hematoma volume ( RR = 1. 283, 95 ％ CI 1. 044-1. 577 ),GCS score on admission(RR =3. 389, 95％ CI 1. 177-9. 756). Patients with pontine hematomas in dorsal had a significantly better outcome than in other locations.Conclusions The survival and prognosis in primary dorsal pontine hemorrhage are better than with hemorrhaging in other parts of pontine. A significant correlation was observed between poor prognosis and hematoma volume, hematoma location and GCS score on admission.

OBJECTIVETo investigate the association of matrix metalloproteinase-3 (MMP-3) serum level and the promoter 5A/6A polymorphism of the MMP-3 gene with atherosclerotic cerebral infarction (ACI) in a Chinese Han population.

METHODSTwo hundred and fifteen patients with acute ACI from the Department of Neurology of Taizhou Hospital and 226 healthy controls were included in the study. Serum MMP-3 level was measured by enzyme-linked immunosorbent assay (ELISA). Genotype was determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) for the common 5A/6A functional promoter polymorphism of the MMP-3 gene.

RESULTSThe genotype distribution of the MMP-3 promoter 5A/6A polymorphism between the ACI patients group and the control group was significantly different (chi (2)= 9.389, P= 0.002). The frequencies of the 5A allele were 14.2% and 7.7% in the ACI patients group and the control group respectively (chi (2)= 9.430, P= 0.002). Serum level of MMP-3 in the ACI patients group was significantly higher than that in the control group (t= 24.867, P= 0.000). Among the ACI patients group, serum MMP-3 levels also had significant difference between the 5A/6A+ 5A/5A and the 6A/6A genotype (t= 2.057, P= 0.041).

CONCLUSIONThe present findings suggest that serum level of MMP-3 obviously increased within 48 hours of ischemic stroke and the genetic polymorphism of 5A/6A in the MMP-3 promoter is associated with ACI and MMP-3 expression in the Chinese Han population.

Adult ; Aged ; Aged, 80 and over ; Asian Continental Ancestry Group ; genetics ; Case-Control Studies ; Cerebral Infarction ; blood ; complications ; genetics ; Ethnic Groups ; genetics ; Female ; Gene Frequency ; Genotype ; Humans ; Intracranial Arteriosclerosis ; blood ; complications ; genetics ; Male ; Matrix Metalloproteinase 3 ; blood ; genetics ; Middle Aged ; Polymorphism, Genetic ; Promoter Regions, Genetic ; genetics

Objective:To investigate the regulation effect of endogenous nicotinamide phosphoribosyl transferase (Nampt) on the Vimentin expression of glomerular cells in high concentration glucose,and to clarify the mechanism of formation of diabetic kidney inflammation fibrosis.Methods:The C57/BL6 diabetic mice were selected and the kidney tissues were collected,and the wild C57/L86 mice were used as control group;the pathological section and tissue fluorescence staining were performed.The expression and location of endogenous Nampt and Vimentin in the glomerular cells were detected by immuno-focused technology.The HBZY-1 cells were randomly divided into 4 groups:low concentration of glucose (LG,0.56 mmol · L-1) control group,high concentration glucose (HG,200 mmol · L-1) group,HG +-FK866 group and HG+nicotinamide mononucleotide (NMN) group.In HG group,the cells were treated with FK866 (10 μmol · L-1) and NMN (1 mmol · L-1) for 24 h after cultured with HG for 5 d.The expression levels of Nampt,Vimentin,nuclear factor-kappa B p65 (NF-κBp65) and sirtuin type 1 (Sirt1) were detected by immunofluorescence and Western blotting methods.The expression levels of Nampt and Vimentin were detected by RT-PCR and Western blotting methods.Results:The shape and size of glomerulus had obvious atrophy of the mice in severe diabetic group compared with normal C57/BL6 mice group.The expression level of Vimentin in glomerular cells was increased with the increasing of endogenous Nampt (P＜0.01).When the HBZY-1 cells were cultured in HG condition,the exprssion levels of Nampt,Vimentin and NF-kB p65 were obviously increased while the Sirt1 expression levels was significantly decreased compared with control group (P＜ 0.01).The expression levels of Nampt,Vimentin and NF-κB p65 in glomerular cells in HG+FK866 HG+ NMN groups were singnificartyly decreased compared with control group (P＜0.01).Conclusion:The endogenous Nampt over-expression in glomerular cells can enhance the expression of Vimentin under high concentration of glucose stress through NF-κBp65 and Sirt1 signal pathway.

Objective:To explore the resistance of common clinical isolates to chlorhexidine gluconate (CHG) and the clinical characteristics of patients with the infections.Methods:A total of 1 000 isolates from the First Affiliated Hospital of Wenzhou Medical University in 2018 (from January to May) were collected, which included 200 strains each of Escherichia coli ( E. coli), Acinetobacter baumanii ( A. baumanii), Pseudomonas aeruginosa ( P. aeruginosa), Staphylococcus aureus ( S. aureus), and Enterococcus spp.. Minimum inhibitory concentration (MIC) of CHG against 1 000 isolates were determined by the agar dilution method. The correlation between the resistance of isolates and clinical characteristics of infected patients was analyzed. Chi-square test or Fisher exact probability test were used for statistical analysis. Results:A total of 57 CHG resistant strains were detected in 1 000 clinical isolates. These CHG-resistant strains were mainly isolated from sputum and intensive care unit ward, accounting for 49.1%(28/57)and 38.6%(22/57), respectively. The resistance rates of P. aeruginosa, A. baumanii, Enterococcus spp., S. aureus, and E. coli to CHG were 16.0%(32/200), 7.0%(14/200), 3.0%(6/200), 1.5%(3/200) and 1.0%(2/200), respectively. The CHG-resistant rates of P. aeruginosa to ceftazidime, ciprofloxacin, levofloxacin and gentamicin were 53.1%(17/32), 78.1%(25/32), 65.6%(21/32) and 50.0%(16/32), respectively, which were all higher than those of CHG-sensitive P. aeruginosa (25.0%(8/32), 25.0%(8/32), 21.9%(7/32) and 15.6%(5/32), respectively), with statistical significance ( χ2=5.317, 18.080, 12.444 and 8.576, respectively, all P<0.05). The hospital mortality was 22.8%(13/57) in patients infected with CHG-resistant bacteria, which was higher than that in patients infected with CHG-sensitive bacteria ((7.0%(4/57); Fisher exact probability test, P=0.018)). CHG-resistant group had a higher history of CHG exposure and antimicrobial treatment (61.4%(35/57) and 70.2%(40/57), respectively), which were both higher than those with CHG-susceptible isolates (17.5%(10/57) and 47.4%(27/57), respectively), the differences were both statistically significant ( χ2=22.947 and 6.118, respectively, both P<0.05). In addition, the multi-drug resistance rate of CHG-resistant strains was 54.4%(31/57), which was higher than that of CHG-susceptible strains (35.1%(20/57)), the difference was statistically significant ( χ2=4.293, P=0.039). Conclusions:CHG resistant strains have higher antimicrobial resistance. Hospital mortality in patients infected with CHG-resistant bacteria is higher than patients infected with CHG-sensitive bacteria. The important risk factors are CHG exposure and antimicrobial therapy.

AIM:To investigate the activation of Cl-channels by sodium taurocholate(NaTC)in mouse pan-creatic acinar cells.METHODS:The single isolated pancreatic acinar cells from FVB/N mice were prepared using colla-genase digestion method.Whole-cell patch clamp technique was performed to record the currents.Intracellular adenosine triphosphate(ATP)dependence of the channels was examined via eliminating ATP from the pipette solution.Anion per-meability of the channels was investigated with ion-exchange method.The pharmacological characteristics of the channels was confirmed by two Cl-channel blockers.The volume sensitivity of the channels was detected using 47%hypertonic bathing solution.Extracellular Ca2+dependence of activating the channels was examined through eliminating Ca2+from the bathing solution.Intracellular reactive oxygen species(ROS)level was detected by an oxidation-sensitive fluorescent probe,2',7'-dichlorofluorescin diacetate.The experiment was repeated 6 times in each group.RESULTS:Extracellular application of 5 mmol/L sodium taurocholate induced a Cl-current,exhibiting the properties of outward-rectification,a se-lectivity sequence of I->Br-≥Cl->gluconate-and intracellularATP dependence(P<0.01).The currents were inhibited by chloride channel blocker 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid disodium salt hydrate(DIDS)and tamoxifen and by 47%hypertonicity stimulation(P<0.01).When ROS production was scavenged by N-acetyl-L-cysteine,the sodi-um taurocholate-induced Cl-currents were unaffected.The effect of sodium taurocholate on ROS production did not alter with the treatment with DIDS.Sodium taurocholate failed to induce Cl-currents when Ca2+was absent in extracellular bath-ing solution(P>0.05).CONCLUSION:Sodium taurocholate activates Cl-channels in mouse pancreatic acinar cells,which is dependent on extracellular Ca2+but not ROS pathway.