The changes of lipid peroxidation in the ischemic (renal artery occlusion for 75 min) and ischemie/reperfusion (renal artery occlusion 60 min plus 15 min reflow) kidney was studied in 19 male SD rats. The results showed that malondialdehydc of renal cortex and medulla was increased, but in both groups SOD and GSH-Px were not changed significantly. Activity of xanthine oxidase activity in the ischemic/reperfusion kidney were increased as compared with normal. These results suggest that lipid pcroxidation was involved in the ischemic and ischemic/reperfusion renal injury, and xanthine-xanthine oxidase might be one of the major sources of oxygen free radical when oxygen supply to ischemic kidney was restored.

Objective To investigate the effects of tumor necrosis factor-alpha (TNF-?) on insulin sensitivity and glucose-lipid metabolism in TNF-?-induced IR mice. Methods Male C57BL/6J mice were given an intraperitoneal injection of TNF-? (H group,6?g/kg; M group,3?g/kg; L group,1?g/kg;twice daily) and saline (NC group) for 7 days. The plasma glucose and insulin were assayed during intravenous glucose tolerance test (IVGTT) and hyperinsulinemic-euglycemic clamp combined with 3-[3H] glucose as a tracer was carried out. Results After TNF-? treatment,fasting blood glucose (FBG),plasma insulin and free fatty acids (FFA) were significantly elevated in H group compared with NC,L and M groups (P

Objective To identify SEN virus and analyse the sequence of its partial gene in blood donors in China.Methods Two pair primers from ORF1 of SENV genome were designed and samples from blood donors were detected for SENV DNA by nested PCR.The isolates from blood donors were cloned and sequenced.Results 6 isolates were obtained in 329 sera from blood donors.The sequence analysis showed that there were about 52%～100% homology of deduced amino acid between SENV A～H genotypes and 6 isolates from blood donors. The Phylogenetic tree analysis showed that 6 SENV isolates from blood donors belong to SENVH genotype.Conclusion There exists SENVH genotype infection among blood donors in China. SENV may be transmitted through blood transfusion.

Objective To investigate chromosomal gains and losses in association with human papillomavirus status in the vulvar squamous cell carcinomas(VSCC). Methods We analyzed 21 VSCC with comparative genomic hybridization (CGH) and polymerase chain reaction.Results Each case had different degree of variances, including gains and losses of partial or whole chromosome. On average, each case had 4.9(102/21) abnormal regions; losses were more than gains, being respectively 2.6(54/21) and 2.3(48/21). Main variations were gains on chromosomes 3q(43%,9/21),8q(38%,8/21),12q(33%, 7/21 )and 9p(19%,4/21),and losses of 4p(52%,11/21),3p(43%,9/21)and 9p(10%,2/21).Gains of 3q(73%) and 12q(64%) were significantly more common in human papillomavirus (HPV)-positive VSCC compared to HPV-negative VSCC(10%,0;P

Objective To investigate the effect of pretreatment with dexmedetomidine alone or in combination with sufentanil on myocardial ischemia-reperfusion (I/R) injury in rats.Methods Fifty healthy male Sprague-Dawley rats,weighing 250-300 g,were anesthetized with intraperitoneal pentobarbital sodium 60 mg/kg.Myocardial I/R was induced by occlusion of anterior descending branch of left coronary artery for 30 min followed by 120 min of reperfusion.The rats were then randomly divided into 5 groups (n =10 each):sham operation group (group S),group I/R,dexmedetomidine pretreatment group (group DP),sufentanil pretreatment group (group SP),and dexmedetomidine + sufentanil pretreatment group (group DS).In group S the anterior descending branch was only exposed but not ligated.Dexmedetomidine 0.5μg/kg and sufentanil 0.1μg/kg were injected intraperitoneally 30 min before ischemia in groups DP and SP,respectively.Dexmedetomidine 0.5 μg/kg and sufentanil 0.1 μg/kg were injected intraperitoneally 30 min bbefore ischemia in group DS.Arterial blood samples were collected at 120 min of reperfusion for determination of serum creatine kinase (CK) and lactic dehydrogenase (LDH)concentrations.The rats were sacrificed at 120 min of reperfusion and hearts were removed for microscopic examination.Myocardial infarct size was calculated.The malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in myocardial tissues were measured.Results Compared with group S,the serum CK and LDH concentrations were significantly increased,the myocardial infarct size was enlarged,and SOD activity was decreased in the other groups,MDA content was significantly increased in groups I/R,DP and SP (P ＜ 0.05 or 0.01).Compared with group I/R,the serum CK and LDH concentrations,MDA content and myocardial infarct size were significantly decreased,and SOD activity was increased in groups DP,SP and DS (P ＜ 0.05).Compared with group DS,the serum CK concentration was significantly increased,the myocardial infarct size was enlarged,and MDA content was increased in groups DP and SP,and LDH concentration was significantly increased and SOD activity was decreased in group DP (P ＜ 0.05).The pathological changes were significantly attenuated in groups DP and SP compared with group DS.Conclusion Dexmedetomidine pretreatment can reduce myocardial I/ R injury in rats,dexmedetomidine combined with sufentanil pretreatment provides better efficacy than either alone,and inhibition of lipid peroxidation is involved in the mechanism.

Objective Establish a laboratory quality control system to ensure accurate and reliable test data and to contrapose the influence of error factors in current detection methods for urinary iodine measurement. Methods The results of reagent blank absorbance value and uric iodine standard materials were collected, then their relevant technical indexes such as mean, standard deviation, control limit, auxiliary line were worked out. Then the quality control chart of blank test and the relative error control chart were made base on these technical indexes. And different iodine concentrations (high, middle and low concentration) were tested and their mean,relative reduction difference value, weighted mean value and critical limit Rc value were calculated, and then critical limit Rc value precision control chart was made. Results The range of absorbance of blank control test was 1.183 to 1.553. And the limit of the accuracy control Rc value was 0.0883, 0.0572, respectively, when the concentrations of urinary iodine was 0～ < 150 μg/L and 150 ～ 300 μg/L. The control limit of the relative error was 9.3%. Conclusions The method of quality control chart could be satisfactorily applied to identify the quality of the analytical results of urine iodine, and ensure the results of the urine iodine reliable and authentic.

Immunohistochemistry was carried out for assessment of the expression of IgG4 and IgG in 29 patients with Hashimoto's thyroiditis (HT) and 26 other patients with subacute thyroiditis,thyroid adenoma,and thyroid carcinoma.HT group were divided into IgG4 HT (10/29) and non-IgG4 HT (19/29) groups.Statistical analyses of clinical and histological characteristics were also conducted in both groups.2 cases of subacute thyroiditis were IgG4 positive (2/26).The IgG4 positive plasma cells,IgG positive plasma cells,and ratio of IgG4 +/IgG + plasma cells in IgG4 HT cases were significantly higher than non-IgG4 HT ones(P＜0.05).The serum Fl4 in IgG4 HT cases were lower than non-IgG4 HT ones(P＜0.05).After operation,IgG4 HT had a greater proportion for accepting thyroxin treatment(P＜0.05).IgG4 HT is a new-found disease which has particular histological and immunological features and would have good response for cortical hormone therapy.Serum and tissue examination of IgG4 seems to be helpful to the diagnosis of IgG4 HT.

Objective To evaluate the effect of ulinastatin on oxidative stress injury to myocardial cells in diabetic rats in vitro.Methods The H9c2 cells were cultured in DMEM culture medium and the cells at the logarithmic growth phase were seeded in 96-well plates (density 1 × 104 cells/ml,200 μl/well) or in 6-well plates (density 1× 105 cells/m1,2 ml/well).The cells were randomly divided into 4 groups (n=18 each) using a random number table:normal control group (group C),high-glucose group (group HG),high-glucose + oxidative stress group (group HG+OS),ulinastatin +high-glucose+oxidative stress group (group U+HG+OS).The cells were cultured in high-glucose DMEM culture medium (25.0 mmol/L) for 48 h in group HG.After the cells were cultured in high-glucose DMEM culture medium for 24 h,H2O2 with the final concentration of 500 μmol/L was added to the high-glucose culture medium,and the cells were continuously cultured for 24 h in HG+OS and U+HG+OS groups.In group U+HG+OS,ulinastatin 400 U/ml was added to the high-glucose culture medium.The cells were collected for determination of cell viability,H9c2 apoptosis,activity of superoxide dismutase (SOD) and contents of malonadehyde (MDA).Apoptosis rate was calculated.The cell culture supernatant was collected for detection of lactate dehydrogenase (LDH) activity.Results Compared with group C,the cell viability and SOD activity were significantly decreased,and the apoptosis rate,MDA content and LDH activity were increased in the other groups.Compared with HG group,the cell viability and SOD activity were significantly decreased,and the apoptosis rate,MDA content and LDH activity were increased in HG+OS and U+HG+OS groups.Compared with group HG+OS,the cell viability and SOD activity were significantly increased,and the apoptosis rate,MDA content and LDH activity were decreased in group U + HG+ OS.Conclusion Ulinastatin can mitigate oxidative stress injury to myocardial cells in diabetic rats,and inhibited cell apoptosis is involved in the mechanism.

Objective To investigate the roles of myeloid differentiation factor 88 (MyD88) and TIR domain-containing adaptor inducing interferon-β (TRIF) in sepsis-induced myocardial dysfunction, and to analyze whether strain rate (SR) can be early sensitive evaluation for septic heart failure.Methods Sixty-four healthy male C57BL/6 mice were divided into four groups by random number table (n = 16 in each group): sham group, cecum ligation and puncture (CLP)-induced sepsis model group, anti-MyD88 group and anti-TRIF group. The anti-MyD88 group and anti-TRIF group were injected with 5μL/g of anti-MyD88 antibody or anti-TRIF antibody through the tail veins 2 hours before CLP. Eight animals in each group were used to observe the survival of 24 hours, and the other 8 myocardial tissues were harvested for examination. The cardiac function was evaluated by echocardiography before and 6 hours and 12 hours after operation. The mRNA expressions of MyD88, TRIF and inflammatory factors in myocardium were measured by polymerase chain reaction (PCR) at 24 hours after operation, and the degree of neutrophils infiltration was detected by myeloperoxidase (MPO) activity.Results The number of 24-hour survive in anti-MyD88 group and anti-TRIF group were higher than that in CLP group (number: 4, 3 vs. 2,P = 0.044,P = 0.047). Compared with sham group, the cardiac function was significantly decreased, the mRNA expressions of myocardial tissues MyD88, TRIF, interleukin (IL-1, IL-6) and tumor necrosis factor-α (TNF-α) were significantly increased, and the infiltration of neutrophils were obvious in CLP group. Compared with CLP group, the left ventricular short axis fractional shortening rate (FS) and SR were significantly increased after 12 hours in anti-MyD88 group and anti-TRIF group [FS: (49.52±1.78)%, (49.89±1.49)%vs. (41.11±1.63)%, SR (s-1): 17.63±2.16, 17.85±1.64 vs. 12.55±1.84]; the mRNA expressions of MyD88, TRIF and inflammatory factors were significantly decreased [MyD88 mRNA (A value): 0.463±0.046, 0.505±0.048 vs. 0.638±0.102, TRIF mRNA (A value): 0.413±0.031, 0.410±0.021 vs. 0.625±0.057, IL-1 mRNA (A value):0.569±0.101, 0.570±0.091 vs. 0.946±0.171, IL-6 mRNA (A value): 0.551±0.143, 0.431±0.157 vs. 0.850±0.194, TNF-α mRNA (A value): 0.471±0.082, 0.444±0.093 vs. 0.707±0.094]; and the infiltration of neutrophils were significantly decreased [MPO (U/L): 62.34±2.60, 60.87±2.40 vs. 73.83±4.90], with statistically significant differences (allP < 0.05). There was no statistical difference in above parameters between the anti-MyD88 group and anti-TRIF group (allP > 0.05).Conclusions Blocking MyD88 and TRIF expression play significant and similar roles in protecting cardiac deterioration from sepsis by attenuating cytokine release, reducing neutrophil infiltration. SR can sensitively assess septic cardiac dysfunction.

Objective To investigate the effect of cyclin-dependent kinase 2 (cdk2) recombinant lentivirus in rats with lipopolysaccharide (LPS)-induced acute lung injury (ALI).Methods Thirty-six adult SD rats were divided into control group, LPS model group and gene intervention group according to the random number table, with 12 rats per group.Rats with LPS-induced ALI were established by intratracheal injection of LPS.Saline solution (60 μL/kg) was injected in control group at the time point of 0, 24, 48 h respectively.Control-lentivirus (60 μL/kg) and cdk2 recombinant lentivirus (60 μL/kg) were injected respectively in LPS model group and gene intervention group at the time point of 0 h and 24 h.After 48 h, LPS (60 μL/kg) with isotonic saline solution were injected in both LPS model group and gene intervention group.Lung tissue samples from right-lower areas were collected at 24 h postinjury to evaluate the pathological changes with HE staining.Expressions of cdk2, clara cell secretory protein (CCSP), phospholipase A2(PLA2) and p-C/EBP β protein were detected by Western blot.Inflammatory factors of tumor necrosis factor-α(TNF-α), interleukin (IL)-1β, IL-6 and IL-10 in serum were measured with ELISA method.Results Inflammatory infiltration and damage to the alveolar structure were serious in LPS model group than control group, while inflammatory infiltration decreased significantly and alveolar structure tended to be normal in gene-intervention group.Expression of Cdk2 in control group (1.00±0.21) and LPS model group (0.93±0.17) were similar, but both were lower than that in gene intervention group (4.29±0.73) (P<0.05).Expression of CCSP in gene intervention group (3.19±0.38) was significantly higher than that in control group (1.00±0.20) and LPS model group (0.32±0.19) (P<0.05).Expression of PLA2 in LPS model group (4.49±0.51) was higher than that in control group (1.00±0.13) and gene intervention group (1.76±0.26) (P<0.05).Meanwhile, the variation of p-C/EBPβ concentration among the groups was similar to CCSP.Expression of TNF-α in LPS model group[(196.34±30.17)pg/ml] was higher than that in control group [(71.24±5.13)pg/ml] and gene intervention group[(86.32±11.02)pg/ml](P<0.05).Changes in IL-1β, IL-6 and IL-10 among the groups were similar to TNF-α.Conclusions Over-expression of Cdk2 plays a protective role for LPS-induced ALIby up-regulating CCSP and down-regulating inflammatory factors such as PLA2, TNF-α, IL-1β, IL-6 and IL-10, as may relate to the phosphorylation of C/EBPβ.