Abdominal Pain ; etiology ; Child ; Female ; Humans ; Lung Diseases, Parasitic ; complications ; diagnosis

AIM: To develop a rat model of insulin resistance and observe the effect of puerarin injection on expression of GSK-3 in insulin resistance rats.METHEDS: 30 Wistar rats were divided into three groups randomly: control group,model group and puerarin group.The model group and puerarin group were given high fat diet(20% surcose,10% ard,(2.5)% chlesterol,1% cholic acid) for 4 weeks.Then the puerarin group was given abdominal injection puerarin 100(mg?kg~(-1)?d~(-1)) for six weeks.At the end of this experiment,we detect GSK-3 protein by western-blot analysis.Then computer image pattern analysis system was used to analyze the expression of GSK-3 in the hepatacyte.RESULTS: Tthe model group showed a hyperglycemia,hyperinsulinism,the ISI decreased and HOMA-IR increased.GSK-3 expression enhanced in the model group,but the expression of GSK-3 in puerarin group decreased compared to the model group.CONCLUSION: Puerarin injection can significantly decreased the expression of GSK-3 and improve insulin resistance.

20 normal males were examined by BIODEX isokinetic test and rehabilitation system,and data collected were used to observe the influence of angle and time on the isokinetic concentric constriction of knee joint. It was found that angle and time, especially angle factor obviously affected the testing results.

Objective To dynamic monitoring the changes of serum cortisol,adrenocorticotropic hormone (ACTH) in children with sepsis and servere sepsis,and to assess it's relationship with clinical features.Methods Thirty children with sepsis were enrolled in this study from Sep 2010 to Jan 2011 in our hospital,and were divided into severe sepsis group (n =10) and sepsis group (n =20).The serum cortisol and ACTH were analysed in acute and recovery period respectively in both two groups,and compared with 10 non-sepsis children as control group.Results In the acute period,the level of serum cortisol in severe sepsis group [ (33.97 ±6.83) μg/ml ] was significantly higher than those in sepsis group [ (26.30 ± 10.43) μg/ml]and control group [ ( 19.06 ± 6.91 ) μg/ml ] ( P ＜ 0.01 ) ; the level of serum ACTH in severe sepsis group [ (25.47 ± 9.41 ) pg/ml ] was significantly higher than those in sepsis group [ ( 15.52 ± 5.85 ) pg/ml ] and control group [ (9.16 ± 3.02 ) pg/ml ] ( P ＜ 0.01 ).Conclusion Stress response exists in the early period of sepsis,and the levels of serum cortisol and ACTH are increased significantly.The levels of serum cortisol and ACTH are positive correlation with the severity of diseases,and they could be used as serious index and a marker for evaluating prognosis in children with sepsis.

80 years.The 104 patients had hypertension and 63 no hypertension.Average Scr level was(104.3?14.1)?mol/L,in normal range.The correlation coefficients between Cockcroft-Gault equation and age was the best(r=0.665,P

Objective To explore the clinical feature and influencing factors of pneumonia in patients with lung cancer,in order to these patients might be timely diagnosed and treated correctly.Methods A series of 1495 cases of pneumonia in patients with lung cancer in recent 10 years were reviewed as their clinical characteristics, pathological cell types, imaging study, bacteriological monitoring, chemotherapy/radiotherapy, antibiotic treatment and prognosis.Results The infection rate of pneumonia in patients with lung cancer was 60.8%, most of them were occurred in patients treated after chemotherapy/radiotherapy, especially in patients being treated after glucocorticoid. The prognosis was poor.Conclusions The clinical situation of pneumonia in patients with lung cancer is not typical. The symptom of respiratory tract is not obvious. CT scan demonstrated obstructive pneumonia and atelectasis. Gram-negative bacteria were the mainly pathogen. The influencing factors are related to the smoking, chronic consumption, obstruction of bronchus, lower resistance after chemotherapy/radiotherapy and the basic diseases. The methods of treatment are also prelimilary discussed.

Background C57BL/6andB10R Ⅲareroutinemurinespeciesusedinexperimental autoimmune uveitis (EAU).The inflammation is light for mouse after immunization whereas it is prominent for B10R Ⅲ.ObjectiveThis study was to observe the killing effect of interphotoreceptor retinoid binding protein (IRBP) 1-20-specific T cells on mouse retinal astrocyte.Th1 and Th17 cells effect in the EAU mechanism was discussed.MethodsB10RllⅢ mice and C57BL/6 mice were immunized with IRBP 161-180 and IRBP 1-20 in complete Freund adjuvant (CFA).The infiltrating cells of diseased B10R Ⅲ eyes were analyzed by flow cytometry.IRBP 1-20-specific T cells were isolated from the drainage lymph node and spleen and cultured in IL-2 or IL-23 for Th1 and Th17 cells polarization,respectively.Th1 and Th17 cells cultured for 5 days were seeded on the mouse retinal astrocyte monolayer pretreated with gamma interferon.Cell interaction was observed and the quantity of TNF-α was tested by ELISA.Every test was repeated 6 times and the mean was calculated.The maintenance of experimental animals complied with the Statement of ARVO.ResultsThere were lots of infiltrating cells in the eyes of B10Rm mice after immunization,including 9.5％ IFNγ+ cells,5.1％ IL-17+cells and 41.4％ CD45+ cells.Six days after IRBP1-20 stimulation and cultured by IL-2 and IL-23,44.0％ and 8.0％ cells were IFNγ+,and 1.0％ and 26.0％ cells were IL17+.Twentyfour hours after the interaction between Th1 or Th17 and retinal astrocyte,retinal astrocyte died and detached.The killing effect of Th17 was stronger than Th1.48 hours after co-culture of Th1 or Th17T cells with astrocytes,the concentrations of TNF-α were ( 500± 10 ) and ( 801 ±24 μg/L) μg/L,respectively,with a significant statistical difference (t =-20.36,P =0.00).ConclusionsBoth Th1 and Th17 can kill retinal astrocyte,but Th17 plays a key role in the EAU pathogenesis process.The killing effect is caused by intercellular contact and interaction under the induction of cytokines.

Aim To investigate the toxicity of isopsor-alen in HepG2 cells and its effects on bile acid, bile acid synthesis and transport. Methods Cell viability was evaluated by MTT assay and bile acid was deter-mined inside HepG2 cells, with exposure to various isopsoralen for 24h. The mRNA transcription of BSEP, MRP2, MRP3, NTCP, OATP2, OSTα, CYP7A1, CYP27 A1 , FXR and PXR were assessed by real-time PCR. Results The cell viability was decreased dose-dependently with isopsoralen in HepG2 cells, and IC50 was 118. 1μmol·L-1 exposure to isopsoralen for 24h. Bile acid inside cells significantly increased with 100 and 400 μmol · L-1 isopsoralen. Isopsoralen caused the down-regulation of MRP2 , MRP3 , CYP7 A1 mRNA at 25 μmol · L-1 . Beside these, the up-regulation of OATP2,OSTα,CYP27A1,FXR,PXR with 100 μmol· L-1 isopsoralen, but there was no significant change of BSEP and NTCP. Conclusion The results show that isopsoralen induces bile acid accumulation and cytotox-icity which may be associated with the down-regulation of MRP2, MRP3 in HepG2 cells.