Objective To analyze the relationship between hepatitis B virus (HBV)DNA load and serum alanine aminotransferase (ALT) level and to investigate the reason that ALT level changes in patients with HBV infection.Methods ALT level (dependent variable)and HBV DNA load (independent variable)were subjected to curve fitting using SPSS 16.0 to establish a curve regression equation and analyze the curve regression equation.Results A power model was established by software analysis,with the following results:R2 =0.107,F=85.887,P=0.000,b0 =47.785,b1 =0.075,b2 =0.The curve analysis showed that as the HBV DNA load increased,the ALT level kept rising,but at a decreasing rate;within a certain range,the increase in HBV DNA load led to little change in ALT level,which was infinitely close to a certain value.Conclusion ALT level is correlated with HBV DNA load,but HBV DNA may not be the most direct cause of change in ALT level.

Objective The Study the difference of miRNA expression of AIDS patients with toxic heat accumulation syn -drome with healthy control group .Methods This research used Agilent miRNA chip to test the miRNA of blood preparation ,and used SAS system to screen the differences between groups ,then analyzed the significance function of target gene .Results Compare the heat-toxic accumulation group and the healthy control group ,100 cases of obvious expression difference and of which the differ-ence was 2 times and greater were screened out (in which 64 cases showed up-regulation and 36 showed down-regulation) .Differen-tially expressed miRNAs function involves the role of IL-21 receptor in T cell activation ,C reactive protein ,and the positive regula-tion of the immune response .Conclusion AIDS toxic heat accumulation syndrome patients and healthy control groups exist differ -ences in miRNA expression profiles ,the biological basis of syndrome maybe related to T cell activation and IL-21 receptor .

Objective To observe changes of motilin(MTL) levels in gastric body, duodenum and plasma in rat model of acute incisional pain.Methods A total of 156 healthy male adult SD rats,weighing 180-220 g,were randomized into two groups:control group (group C,n=78) and incisional pain group (group P,n=78),Rats in P group received incision on the right plantaris. Values of paw withdrawal mechanical threshold (PWMT) and paw withdrawal thermal latency (PWTL) at dif?ferent time points of 24 hours before operation (T0) and 1 hour (T1),6 hours (T2),24 hours(T3),48 hours (T4) and 72 hours (T5) after operation were measured in six rats chosen randomly from each group. Twelve rats were chosen from each group at T 0-5, and sacrificed. The MTL levels in plasma, the mucosal tissues of gastric body and duodenum were detected by ELISA. Re?sults Compared with group C, PWMT and PWTL were significantly decreased at T1-4 in group P. The MTL levels were sig?nificantly decreased in plasma and gastric body (P<0.05).The MTL level was significantly increased at T1-4 in duodenum (P<0.05),and no significant changes were found at T0 and T5 in P group(P>0.05). The plasma MTL levels were positively correlated with PWMT and PWTL (r=0.952,r=0.879,respectively,P<0.01) in P group. The MTL levels in gastric body were positively correlated with PWMT and PWTL(r=0.970,r=0.931,respectively,P<0.01) in P group. The MTL levels were neg?atively correlated with PWMT and PWTL(r=-0.991,r=-0.975,respectively,P<0.01) in duodenum in P group. Conclu?sion The MTL levels in plasma and gastric body are decreased in rat model of acute incisional pain, and increased in duo?denum.

AIM: To investigate the effect of high glucose concentration on serum and glucocorticoid induced protein kinase (SGK) mRNA and protein expressions in human proximal tubular epithelial cells (HKC) and the possible role of SGK in the production of extracellular matrix (ECM) of HKC under the condition of high glucose. METHODS: HKC was divided into 3 groups: control glucose group (CG group, 5 5 mmol/L D-glucose); high glucose group (HG group, 25 mmol/L D-glucose) and osmotic control group (MG group, 19 5 mmol/L mannitol and 5 5 mmol/L D-glucose). The expressions of SGK mRNA and protein were assessed by semi-quantitative RT-PCR and Western blotting respectively. The level of secretary and cytoplasmic fibronectin (FN) were detected by enzyme-linked immunoabsordent assay (ELISA) and indirect-immunofluorescence. RESULTS: HKC expressed SGK1, SGK2 and SGK3 at mRNA and protein levels. Their mRNA level were up-regulated since 2 hours after cells exposed to D-glucose and this up-regulation persisted to the end of 8th hour, and SGK1 protein level elevated simultaneously. On the other hand, the increased FN secretion by high glucose was in a time-dependent manner and its improved secretion threshold was just followed by the high expression of SGK1. CONCLUSIONS: In response to high glucose, the expression of SGK1, SGK2 and SGK3 in human proximal tubular epithelial cells were up-regulated which was accompanied with FN accumulation. The high expression of SGK may mediate overproduction of ECM in proximal tubular epithelial cells and contribute to the diabetic nephropathy.

The role of serum and glucocorticoid-induced kinase 1 (SGK1) pathway in the connective tissue growth factor (CTGF) expression was investigated in cultured human mesangial cells (HMCs) under high glucose. By using RT-PCR and Western blot, the effect of SGK1 on the CTGF expression in HMCs under high glucose was examined. Overexpression of active SGK1 in HMCs transfected with pIRES2-EGFP-S422D hSGK1 (SD) could increase the expression of phosphorylated SGK1 and CTGF as compared with HMCs groups transfected with pIRES2-EGFP (FP) under high glucose or normal glucose. Overexpression of inactive SGK1 in HMCs transfected with pIRES2-EGFP-K127N hSGK1 (KN) could decrease phosphorylated SGK1 and CTGF expression as compared with HMCs groups transfected with FP under high glucose. In conclusion, these results suggest that high glucose-induced CTGF expression is mediated through the active SGK1 in HMCs.
Cells, Cultured ; Connective Tissue Growth Factor/genetics ; Connective Tissue Growth Factor/*metabolism ; Glucose/*pharmacology ; Immediate-Early Proteins/metabolism ; Immediate-Early Proteins/*physiology ; Mesangial Cells/cytology ; Mesangial Cells/*metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Protein-Serine-Threonine Kinases/*physiology ; Signal Transduction/drug effects

Objective To compare inter-hospital transport and clinical outcome in severe acute respiratory distress syndrome(ARDS)patients whom were transported either on extracorporeal membrane oxygenation(ECMO) or on conventional ventilation,and to investigate the optimal means of inter-hospital transport. Methods Eleven patients with severe ARDS who were invalid under conventional ventilation and were transported from other hospitals to Tianjin Third Central Hospital from November 2009 to January 2014 were analyzed. Five patients were transported on ECMO(observation group)and 6 on conventional ventilation(control group). The clinical characteristics,outcomes, transportation,vital signs before and after transportation,respiratory parameters,and Murray score between two groups were compared. Results Patients in observation group were significantly older than those in control group〔years:73(46,77)vs. 34(23,46),Z=-2.293,P=0.022〕. There was no significant difference between observation group and control group in acute pathologic and chronic health evaluationⅡ(APACHEⅡ)score,Murray score,oxygenation index(PaO2/FiO2)before transportation,transit time,and transit distance〔APACHEⅡscore:36(33,39)vs. 27(23,35),Z=-1.830,P=0.067;Murray score:3.5±0.3 vs. 3.4±0.2,t=0.667,P=0.524;PaO2/FiO2(mmHg, 1 mmHg=0.133 kPa):61±14 vs. 63±14,t=-0.249,P=0.809;transit time(minutes):24(18,74)vs. 79(41, 86),Z=-1.654,P=0.098;transit distance(km):12.9(8.3,71.8)vs. 72.4(39.5,86.8),Z=-1.651,P=0.099〕. There was no significant difference between two groups in vital signs and respiratory parameters before transportation. When arrived in ECMO centre,heart rate,respiratory rate,fractional inspired oxygen,inspiratory pressure and Murray score in observation group were significantly lower than those in control group〔heart rate(beat/min):102±16 vs. 136±8, t=-4.374, P=0.002;respiratory rate(beat/min):23±3 vs. 37±2,t=-7.967,P=0.000;fractional inspired oxygen:0.40±0.05 vs. 0.96±0.09,t=-12.152,P=0.000;inspiratory pressure(cmH2O, 1 cmH2O=0.098 kPa):21±1 vs. 34±4,t=-6.887,P=0.000;Murray score:2.7±0.2 vs. 3.8±0.2,t=-8.573, P=0.000〕,but PaO2/FiO2 was higher than that of control group(mmHg:278±65 vs. 41±5 ,t=8.075,P=0.001). Four patients were survived in observation group,and one died from the shortage of oxygen induced lung injury deterioration during transportation. Three patients died in control group,which was directly associated with lung injury deterioration. Conclusion For patients with severe ARDS who need the support of ECMO,ECMO-assisted transfer is safer than conventional ventilation,but transfer should be implemented by experienced team.

To investigate the expression and the role of three isoforms of Serum and Glucocorticoid-inducible Kinase (SGK) in experimental diabetic nephropathy (DN), 12 male C57BL/6 mice of 8-weeks-old were divided into two groups. Streptozotocin (STZ)-induced diabetic nephropathy and normal controls were analyzed at the end of the 4th week after the induction of diabetes. Renal hemodynamics and histological studies were performed. The expression of SGK1 mRNA, SGK2 mRNA and SGK3 mRNA of kidney cortex were measured by RT-PCR, and the cortical SGK1 protein was detected with Western blotting. Our results showed that the blood glucose, blood HbA1c, 24h urinary protein, creatinine clearance and the renal index were all increased in DN group. More extracellular matrix (ECM) accumulation was observed. The level of cortical SGK1 mRNA and protein were up-regulated in DN group in comparison with control group. SGK2 and SGK3 mRNA were elevated in DN mice. In DN, mRNA level of three SGK isoforms and SGK1 protein were increased significantly. It is concluded that SGKs may contribute to the early renal injury of DN.

Objective Transesophageal echocardiography (TEE) guided, minimally invasive perventricular device occlusion of ventricular septal defects ( VSDs) without cardiopulmonary bypass ( CPB) has been applied in multiple centers. We reported experiences and the mid-term results. Methods Four hundred and thirty-two cases from 4 cardiac centers were involved in the study. There were 235 males and 197 females, aged from 3 months to 15 years, with a body weight varying from 4.0 to 26.0 kg. Three hundred and fifty-one patients had perimembranous VSDs, 57 had intracristal or supracristal VSDs and 24 had muscular VSDs (17 had multiple muscular VSDs). The diameter of the VSD ranged from 3 to 12 (5.3 ±1.6 ) mm.For those with perimembranous or muscular VSDs, a 3 to 5 cm inferior sternotomy was made, but for those with intracristal or supracristal VSDs, a 2 to 3 cm incision was made parastemally through the left third intercostal space. Being monitored and guided with TEE, the device was deployed to occlude the VSD through the puncture at the free wall of the right ventricle. TEE was used for assessing the residual shunting, the left and right ventricular outlet tracts, valvular function and for detecting any arrhythmia, The devices would be released if the heart rhythm was normal, as well as the residual shunting and valvular regurgilalion were not detected. Results The procedure was completed successfully in 417 cases(96.5% ) and converted to traditional surgical closure with CPB in the other 15 cases(3.5% ). Concentric devices were used in 238 cases(57.1% )and eccentric devices were used in 179 patients(42.9% ). Successful procedures finished in less than 90 minutes, and the deployment and evaluation of the devices were completed in 5 to 60 (18. 2 ± 8.6) minutes. No residual shunt and detectable aortic or tricuspid insufficiency and arrhythmia was observed. Patients were extubated within 2 hours and discharged 3 to 5 days after the operation. During fellow-up period from 3 months to 2 years, no clinically significant complications occurred. Conclusion The minimally invasive device closure of VSD under TEE guidance without CPB is proved to be a simple, safe and effective treatment for a considerable number of children with VSD. Its use in the clinical practice should be encouraged.

To investigate the expression and the role of three isoforms of Serum and Glucocorticoidinducible Kinase (SGK) in experimental diabetic nephropathy (DN), 12 male C57BL/6 mice of 8-weeks-old were divided into two groups. Streptozotocin (STZ)-induced diabetic nephropathy and normal controls were analyzed at the end of the 4th week after the induction of diabetes. Renal hemodynamics and histological studies were performed. The expression of SGK1 mRNA, SGK2 mRNA and SGK3 mRNA of kidney cortex were measured by RT-PCR, and the cortical SGK1 protein was detected with Western blotting. Our results showed that the blood glucose, blood HbA1c, 24-h urinary protein, creatinine clearance and the renal index were all increased in DN group. More extracellular matrix (ECM) accumulation was observed. The level of cortical SGK1 mRNA and protein were up-regulated in DN group in comparison with control group. SGK2 and SGK3 mRNA were elevated in DN mice. In DN, mRNA level of three SGK isoforms and SGK1 protein were increased significantly. It is concluded that SGKs may contribute to the early renal injury of DN.

Summary: The role of serum and glucocorticoid-induced kinase 1 (SGK1) pathway in the connective tissue growth factor (CTGF) expression was investigated in cultured human mesangial cells (HMCs) under high glucose. By using RT-PCR and Western blot, the effect of SGK1 on the CTGF expression in HMCs under high glucose was examined. Overexpression of active SGK1 in HMCs transfected with pIRES2-EGFP-S422D hSGK1 (SD) could increase the expression of phosphorylated SGK1 and CTGF as compared with HMCs groups transfected with pIRES2-EGFP (FP) under high glucose or normal glucose. Overexpression of inactive SGK1 in HMCs transfected with pIRES2-EGFP-K127N hSGK1 (KN) could decrease phosphorylated SGK1 and CTGF expression as compared with HMCs groups transfected with FP under high glucose. In conclusion, these results suggest that high glucose-induced CTGF expression is mediated through the active SGK1 in HMCs.