Objective To investigate the influence of target controlled in-fusion of sufentanil on anesthesia quality in patients with heart mitral valve replacement.Methods The 60 patients with mitral valve replace-ment were randomly divided into control group ( n=30 ) and treatment group ( n=30 ).Anesthesia of patients in treatment group was induced and maintained using target-controlled infusion sufentanil at effect-site concentration of 0.8 ng · mL-1 and 0.4-0.8 ng · mL-1 ) , respective-ly.Anesthesia of patients in control group was induced by intravenous in-fusion of 10 μg · kg-1 sufentanil and maintained by injection of 10μg· kg -1 fentanyl.Extubation time after surgery, recovery time, visual analog scale ( VAS) score at extubation time, postoperative hemodyna-mics and the incidence of adverse drug reactions were compared between two groups.Results After surgery, the recovery and extubation time in the treatment group was significantly shorter than that in control group ( P<0.05).After surgery, VAS score between the two groups were not statistically significant ( P >0.05 ).After surgery, the mean arterial pressure, blood pressure, oxygen saturation in the treatment group were significantly higher ( P<0.05 ).The incidence of adverse drug reactions of treatment group was significantly lower than that in control group ( P<0.05 ).Conclusion For the patients with mitral valve replacement surgery, the treatment of target controlled infusion of sufentanil has a high anesthesia quality, rapid recovery and small adverse drug reactions.

OBJECTIVESTo study methodologies and relevant data-element specifications for basic dataset development in China public health information system construction

METHODSThe goals and scopes were determined through data-viewing analysis, while the function model was developed through information viewing analysis. The components and the structure of the data sets were also identified to distill data elements.

RESULTS50 basic datasets were developed and 1513 data elements were determined in 8 main domains and one public domain in China's public health information system. The 8 domains included Expanded Immunization Program (including 7 Basic Datasets and 326 data elements), Occupational Health and Poisoning (5 Basic Datasets and 158 data elements developed), Laboratory Management (9 Basic Datasets and 118 data elements included), Public Health Emergencies (including 3 Basic Datasets and 47 data elements), Infectious Disease Surveillance (4 Basic Datasets and 177 data elements developed), Non-Chronic Disease Surveillance (3 Basic Datasets and 64 data elements developed), Maternal and Child Health (totally 8 Basic Datasets and 368 data elements developed) and Environment Health (including 4 Basic Datasets and 72 data elements). One common domain consisted of 7 basic datasets and 183 data elements.

CONCLUSIONStandardizing basic datasets in public health information systems is an essential foundation in facilitating information system planning and the effective utilization of resources.

Objective To investigate the latent infection caused by enterovirus 71 (EV71) among healthy people in Tianjin and to provide evidence on prevention and control hand-food and mouth diseases (HFMD). Methods 1611 sera specimens were collected from healthy people in Tianjin while EV71 antibody was detected by neutralization test, and then the results were analyzed statistically. Results For determining positivity, the cut-point was set at 1:4. The positive rate was 66.79%( 1076/1611) for EV71 neutralizing antibody. The lowest positive rate was 32.71% in the 0-5 age group while the highest rate was 76.67% in the 16-25 age group. Significant difference was seen in the positive rates among different age groups. The lowest positive rate (59.05%) was seen in the city areas while the highest rate (72.35%) was seen in the surrounding counties. 5.71% of the people being tested showed their neutralizing antibody as ≥1:256. The difference was statistically significant on positive rates among different areas. We constructed logistic regression models with the EV71 neutralizing antibody positive rate as the dependent variable and age, sex, floating population, area etc. as independent variables. There appeared statistical significances in all the independent variables. Conclusion Age seemed a risk factor for recessive infection of EV71, and the neutralizing antibody against EV71 might not be kept permanently. In order to prevent and control the HFMD, more attention should be paid to the areas where more floating population were resided.

BACKGROUND: Peroxisome proliferator-activated receptor (PPAR)-gamma is a member of the nuclear receptor superfamily. PPAR-gamma plays an important role in numerous cellular processes including adipogenesis, insulin sensitivity, cell cycle progression, cell differentiation, inflammation, and extracellular matrix production. This study investigated the effect of a PPAR-gamma agonist on the progression of diabetic nephropathy in OLETF rats. METHODS: 30 week-old male OLETF rats were treated for 10 weeks as follows:diabetic control (DM), no treatment:pioglitazone therapy (DM+Pio). LETO rats were used as non-diabetic control (control). Body weight, blood pressure, blood sugar, creatinine, total cholesterol, triglyceride, and urinary protein excretion were measured. Histological analysis was taken with light microscope. Glomerular protein and mRNA expression of transforming growth factor (TGF)-beta1 and fibronectin were estimated by Western blot and RT-PCR. Kidney sections were stained for fibronectin by immunohistochemistry. RESULTS: Serum glucose, triglyceride and urinary protein excretion were decreased in DM+Pio rats compared to DM rats (p<0.05). PAS staining showed glomerular hypertrophy, mesangial expansion, nodular sclerosis, and glomerular basement membrane thickening in glomeruli of DM rats, but these changes were attenuated in glomeruli of pioglitazone-treated rats. Treatment with pioglitazone resulted in a significant decrease in TGF-beta1 protein and mRNA expression in diabetic glomeruli (80.6% and 78.4%, respectively). Glomerular expression of fibronectin protein and mRNA were also decreased in pioglitazone treatment group compared with DM group (93.1% and 98.6%, respectively). Immunohistochemical staining for fibronectin showed similar results. CONCLUSION: Increased TGF-beta1 and fibronectin mRNA and protein expressions in diabetic rat glomeruli were significantly ameliorated by pioglitazone treatment. These data suggest that activation of PPAR-gamma may play an important role in prevention and treatment of diabetic nephropathy.
Adipogenesis ; Animals ; Blood Glucose ; Blood Pressure ; Blotting, Western ; Body Weight ; Cell Cycle ; Cell Differentiation ; Cholesterol ; Creatinine ; Diabetic Nephropathies* ; Extracellular Matrix ; Fibronectins* ; Glomerular Basement Membrane ; Humans ; Hypertrophy ; Immunohistochemistry ; Inflammation ; Insulin Resistance ; Kidney ; Male ; Peroxisomes ; Rats ; Rats, Inbred OLETF ; RNA, Messenger ; Sclerosis ; Transforming Growth Factor beta1 ; Transforming Growth Factors* ; Triglycerides

BACKGROUND: Diabetic nephropathy (DN) is clinically characterized by persistent proteinuria. The underlying pathologic changes responsible for the nephropathy are the loss of size selective and/or charge selective properties of the glomerular filtration barrier. Size selectivity is maintained primarily by the slit diaphragm and ZO-1 is one of the basic components of it. However, the precise role of the ZO-1 in the pathogenesis of the glomerular diseases is not fully understood. We investigated the changes of ZO-1 expression in diabetic glomeruli in vivo, and by high glucose in cultured podocyte in vitro. We also evaluated the effect of angiotensin II type 1 receptor blocker (ARB) on the ZO-1 changes induced by diabetes or high glucose. METHODS: To determine the effect of ARB on podocytes ZO-1 protein and mRNA expression, immortalized mouse podocytes were incubated with RPMI medium containing normal glucose (NG, 5.6 mM) or high glucose (HG, 30 mM) with or without ARB (10-6 M, L-158, 809). For animal studies, rats were injected with diluent (Control, C, n=18) or streptozotocin. The latter were left untreated (DM, n=18) or treated with 1 mg/kg/day ARB (DM+ARB, n=18). Six rats from each group were sacrificed monthly, and Western blot and RT?PCR were performed for ZO-1 with sieved glomeruli. Renal sections were stained for ZO-1 by immunohistochemistry. RESULTS: The ZO-1 mRNA and protein expressions in podocytes exposed to HG conditions were significantly higher than those in podocytes exposed to NG media (p<0.05). ARB treatment inhibited the HG induced increase in ZO-1 mRNA and protein expression by 73% and 64%, respectively (p<0.05). Compared to the C rats (19.8+/-3.2 mg/day), 24 hour urinary protein excretion at 3 month was significantly higher in the DM rats (90.6+/-11.3 mg/day, p< 0.05), and ARB treatment partly reversed the increase in proteinuria in DM rats (51.6+/-6.6 mg/day, p<0.05). Glomerular ZO-1 mRNA and protein expressions were also significantly increased in DM than corresponding C at all duration (p<0.05). ARB treatment for 3 months in DM rats inhibited the increase in ZO-1 mRNA and protein expression by 57.5% and 70.6%, respectively (p<0.05). ARB treatment for 3 months significantly ameliorated increased glomerular ZO-1 expression in DM rats as assessed by immunohistochemistry. CONCLUSION: In conclusion, ZO-1 mRNA and protein expressions were increased in podocytes exposed to HG and in DM glomeruli, and this increment in ZO-1 expression was ameliorated with ARB. Taken together, these data suggest that change of ZO-1 expression in podocytes is implicated in the early changes of diabetic nephropathy and may contribute to the development of proteinuria.
Angiotensin II* ; Angiotensins* ; Animals ; Blotting, Western ; Diabetic Nephropathies ; Diaphragm ; Glomerular Filtration Barrier ; Glucose* ; Immunohistochemistry ; Mice* ; Podocytes* ; Proteinuria ; Rats* ; Receptor, Angiotensin, Type 1* ; RNA, Messenger ; Streptozocin

Previously, we reported that high glucose enhanced cytokine-induced nitric oxide (NO) production by rat mesangial cells (MCs), and that the enhanced expression of the iNOS pathway may promote extracellular matrix accumulation by MCs. The present study was designed to examine whether the iNOS pathway is pathologically altered in experimental diabetic nephropathy, and whether therapy with angiotensin converting enzyme (ACE) inhibitor (imidapril: I) or angiotensin II type I receptor (AT1) blocker (L-158,809: L), ameliorates these changes. Male Sprague-Dawley rats were injected with diluent (control: C) or streptozotocin. At sacrifice after 4, 8 and 12 weeks, rats underwent either a 4 hour placebo or an intraperitoneal lipopolysaccharide (LPS, 2 mg/kg) challenge. Systolic blood pressure (SBP) and urinary protein excretion (UPE) increased significantly in diabetic (D) rats compared with C. The basal expression of glomerular iNOS mRNA was increased in D rats compared with that of C rats, by reverse- transcription (RT)-polymerase chain reaction (PCR), whereas there was no significant difference in the level of protein by Western blot analysis. Upon LPS stimulation, the iNOS mRNA and protein expression was significantly elevated in D rats. In D rats, this up-regulation, of LPS-stimulated iNOS expression, was equally ameliorated both by I and L in mRNA and protein levels. From immunohistochemistry (IHC), there was a negative staining for the iNOS within the glomeruli of five C rats without LPS treatment, but one of four rats, with LPS treatment, showed minimal iNOS staining in the glomeruli. In D rats, the glomerular mesangium and podocytes were positive for iNOS in each of three out of five rats with, and without, LPS treatment. In conclusion, LPS-stimulated glomerular iNOS expression was enhanced in diabetic pnephropathy, and the activation of angiotensin II may play a role in this enhancement.
Angiotensin-Converting Enzyme Inhibitors/pharmacology ; Animal ; Kidney Glomerulus/*drug effects/*enzymology ; Lipopolysaccharides/*pharmacology ; Male ; Nitric-Oxide Synthase/*metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Angiotensin/antagonists & inhibitors

Adenoviridae ; Animals ; Axons ; Brain ; Cell Line ; Clone Cells ; Discrimination (Psychology) ; DNA Restriction Enzymes ; Enzyme-Linked Immunosorbent Assay ; Fluorescence ; Gene Library ; Half-Life ; HEK293 Cells ; Immunohistochemistry ; Lingual Nerve ; Microscopy ; Models, Animal ; Molar, Third ; Myelin Sheath ; Nerve Growth Factor ; Nerve Regeneration ; Neural Conduction ; Neurons ; Peripheral Nerves ; Rats ; Regeneration ; RNA, Messenger ; Schwann Cells ; Sequence Analysis, DNA ; Sucrose ; Tongue ; Transfection ; Transplants

Objective To investigate the effect of atorvastatin preconditioning on cerebral myelin basic protein (MBP),glial fibrillary acidic protein (GFAP) and neurospecific enolase (NSE) in rat model of cerebral ischemia reperfusion.Methods A total of 30 male SD rats were randomly assigned to test group,model group and sham group.The rats of test group received atorvastatin 5 mg · kg-1 · d-1 by gastric gavage for 5 consecutive days before modling while the other two groups received the same volume of 0.9％ NaC1.Right middle cerebral artery occlusion (MCAO) ischemia-reperfusion model was established in both model group and test group,while sham group was only subjected to right middle cerebral artery separation and suture.The expressions of cerebral NSE,MBP and GFAP were measured with immunohistochemistry after 24 h reperfusion.Results The expressions of NSE,MBP and GFAP were 0.11 ±0.03,0.11 ±0.02,0.14 ±0.04 in model group,had significant differences with those in sham group,which were 0.18±0.02,0.11 ±0.00,0.19 ± 0.02 (P ＜ 0.05).The expressions of NSE and MBP in test group were 0.14 ± 0.02,0.14 ± 0.02,had significant differences with those of model group (P ＜0.05).The expression of GFAP in test group had no statistical significance with model group (P ＞ 0.05).Conclusion Atorvastatin preconditioning can alleviate cerebral ischemia reperfusion injury in rats with MCAO,probably through protecting oligodendrocytes and neurons.

BACKGROUND: Proteinuria is a cardinal feature of glomerular disease including diabetic nephropathy, and glomerular filtration barrier is considered as a filter restricting protein excretion in urine. We tested whether the expression of P-cadherin, a molecule known to be located at the slit diaphragm, was altered by high glucose in cultured podocytes in vitro and by diabetes in vivo. METHODS: In vitro, immortalized mouse podocytes were cultured in media with 5.6 mM glucose (NG), NG+24.4 mM mannitol (NG+M), or 30 mM glucose (HG) for 7 days at 37dgrees C. Cell lysates were used for RT-PCR and Western blot. For animal studies, twelve Sprague-Dawley rats were injected with diluent (Control, C, N=6) or streptozotocin (DM, N=6) intraperitoneally, and were sacrificed after 6 weeks. RT-PCR and Western blot for P-cadherin mRNA and protein expression, respectively, were performed with sieved glomeruli, and immunohistochemistry with renal tissue. RESULTS: HG significantly reduced P-cadherin mRNA and protein expression in cultured podocytes by 47% and 62%, respectively (p<0.05). Twenty-four hour urinary albumin excretion was significantly higher in DM (12.80+/-1.12 mg/day) compared to C rats (3.15+/-0.24 mg/day) (p<0.05). Glomerular P-cadherin mRNA expression was significantly lower in DM than that in C rats (p<0.05). P-cadherin protein expression assessed by Western blot and immunohistochemistry showed a similar pattern. CONCLUSION: Exposure of podocytes to HG in vitro and diabetes in vivo reduced P-cadherin mRNA and protein expression. These findings suggest that the decrease in P-cadherin expression is connected to the early changes of diabetic nephropathy and thus may contribute to the development of proteinuria.
Animals ; Blotting, Western ; Cadherins* ; Diabetic Nephropathies* ; Diaphragm ; Glomerular Filtration Barrier ; Glucose ; Immunohistochemistry ; Mannitol ; Mice ; Podocytes* ; Proteinuria ; Rats ; Rats, Sprague-Dawley ; RNA, Messenger ; Streptozocin

BACKGROUND: The p38 mitogen-activated protein kinase (MAPK) pathway is activated by several stress factors, potentially leading to cellular apoptosis and growth. Little is known about the pattern of p38 MAPK pathway activation in mesangial cells under high glucose conditions. We examined the activity and expression of p38 MAPK members, p38 MAPK, MAPK kinase 3/6 (MKK3/6), c-AMP responsive element binding protein (CREB), and MAPK phosphatase-1 (MKP-1) in cultured mesangial cells exposed to high glucose. METHODS: Mesangial cells were subcultured from rat glomeruli isolated by sieving technique. After serum restriction for 48 hours mesangial cells were exposed to 5.6 mM glucose (low glucose, LG), 5.6 mM glucose+24.4 mM mannitol (LG+M), or 30 mM glucose (high glucose, HG) for 3 minutes to 48 hours with or without SB203580. Western blot was performed to determine the activity and protein expression of p38 MAPK members. RT-PCR and ELISA were performed for fibronectin mRNA expression and fibronectin synthesis, respectively. RESULTS: p38 MAPK and CREB activities were significantly increased in mesangial cells exposed to HG compared with LG or LG+M after 10 minutes and was sustained at higher levels to 48 hours (p<0.05), but total p38 MAPK and CREB protein expressions did not differ. MKP-1 showed a similar pattern as p38 MAPK and CREB (p<0.05). MKK3/6 acitvity was significantly higher in HG cells after 3 minutes and remained at higher levels throught the study period (p<0.05). Fibronectin mRNA expression and fibronectin synthesis were significantly increased in mesangial cells exposed to HG after 48 hours (p< 0.05). SB203580 (1 micrometer) pretreatment for 1 hour significantly reduced HG-induced fibronectin mRNA expression and fibronectin synthesis by 73% and 69%, respectively (p<0.05). CONCLUSION: p38 MAPK activity was increased in mesangial cells exposed to HG in parallel with increased MKK3/6 activity, resulting in CREB activation and increased fibronectin synthesis. This activated p38 MAPK may play a role in the pathogenesis of diabetic nephropathy.
Animals ; Apoptosis ; Blotting, Western ; Carrier Proteins ; Cyclic AMP Response Element-Binding Protein ; Diabetic Nephropathies ; Enzyme-Linked Immunosorbent Assay ; Fibronectins* ; Glucose* ; Mannitol ; Mesangial Cells* ; p38 Mitogen-Activated Protein Kinases* ; Phosphotransferases ; Protein Kinases ; Rats* ; RNA, Messenger