Objective To observe the clinical curative effect of edaravone on treatment of acute lagre area cerebellar irdarction(ALACI). Methods 31 ALACI patients attacked within 72h were randomly assigned to therapygroup( n = 16) and control group( n = 15). Therapy group took the basic treatment as well as edaravone infused at a dose of 30mg,twice a day for 14 days. Control group took similar treatment to therapy group expect for edaravone.At 0th ,7th, 14th ,21th day after treatment, the C.SS and ability of daily living(ADL) were used to evaluate the recovery of neurological functions. Results Significant difference of CSS and ADL grading were detected between therapygoup and control group at 7th, 14th day( P < 0.05 ), with lower grading in therapy group ; there were significant differ-ence of CSS and ADL grading between therapy goup and control group at 21th day( P < 0.01 ), with lower grading in therapy group. No evident side effect was detected in edaravone therapy group. Conclusion Edaravone is a safe a-gent. It can effectively improve the neurological deficits and daily living ability of ALACI patients.

0.05 ). But CD8 +CD28 -T suppressor cells from colitis rats was significantly higher than that from controls (spleen: 11.3% ? 2.3% vs. 5.6% ? 1.0% ; colon: 6.5% ?5.4% vs. 1.1 %? 0.6% , P 0.05 ; colon: 7.5% ? 4.2% vs. 16.9% ? 4.1% , P

Objective To study the expressions of Toll-like receptor (TLR)2 and TLR4 in colonic mucosa of patients with irritable bowel syndrome (IBS) and in normal subjects. Methods Thirty patients with diarrhea predominant IBS and 12 healthy volunteers were enrolled. The expressions of TLR2 and TLR4 in colonic mucosa were examined by immunohistochemistry (IHC).TLR2 and TLR4 were semi-quantitative analyzed with average absorbence. Results Contrast to healthy controls, the lamina propria of IBS patients showed edema and looseness with lots of inflammatory cells infiltration. There was no difference in expression of TLR2 between healthy controls and IBS patients (P>0.05). Compared with healthy controls, TLR2 in crypt epithelium and TLR4 in luminal surface of IBS patients were significantly up-regulated (TLR2 : 6.7 % vs. 50.0 %,TLR4: 40.0% vs. 0, P<0. 05). The TLR4 expressed in intestine epithelial cell of both the apical surface and the basolateral surface in 86.7% of patients with IBS, and in 50% of healthy controls.The positive cells of TLR4 in lamina propria were higher in patients with IBS than those in healthy controls (70. 084 ± 21. 887 vs. 20. 577 ± 4. 546, P<0.01). The A values of TLR2 and TLR4 in colonic mucosa of the patients with IBS were higher than those in healthy controls (TLR2:0. 3079±0. 0283vs. 0.3886±0. 0510,TLR4:0. 3044±0. 0481 vs. 0. 3971 ±:010996,P<0. 01). Conclusions Inflammatory cells infiltrated into colonic mueosa in patients with IBS suggested that inflammation might participate in the pathogenesis of IBS. Up-regulated expressions of TLR2 and TLR4 in IBS patients supposed that they might contribute to the occurrence of IBS.

Objective To study the relationship between coagulation and inflammatory in 2,4,6- trinitrobenzenesulfonate (TNBS) induced colitis model as well as the therapeutic effect of warfarin.Methods Forty SD-rats were divided into 4 groups, including normal control group (received 0.9% HCI solution), colitis group, warfarin treated group (240 ng/kg daily) and salieylazosulfapyridine (SASP) treated group (100 mg/kg daily). The animal model was induced by injection with 20 mg TNBS. The blood and colon of the rats were removed and the rats was sacrificed at the 14th day. The index of coagulation such as prothrombin time (PT), activated partial thromboplastin time (APTT) and the activity of antithrombins (AT) and the level of tumor necrosis factor-α (TNF-α) were tested.The damage and inflammatory state of the colitis were evaluated by macroscopical score and histological score . The value of disease activity index (DAI) and the platelet counts were alsomeasured. Results The value of DAI was lower in warfarin (1.20±0.45) and SASP (1.78±0.90) treated groups as compared with colitis group (2. 25 ± 0. 89) with no difference (P>0. 05). The macroscopical score was lower in warfarin (1.40 ± 0.55) and SASP (3.14± 1.46) treated grouos as compared with colitis group (4.75 ± 1.66, P<0.01 ). The histological score in warfarin (4. 00± 1.41 ) and SASP (4.28 ± 1.49) treated groups were lower than that in colitis group (7. 75± 1.04, P<0.01). The level of TNF-α was lowest in normal control group (P<0. 01 ), and highest in colitis group. (P<0.01). The PT and APTT were shorter and the aetivity of AT was lower in colitis groupin comparison with warfarin treated group and normal control group (P<0.01). The platelet counts was highest in colitis group. P<0.01). Conclusion The abnormal coagulation in TNBS induced colitis can be effectively treated with warfarin.

Objective To explore the alterations of intestinal mechanical barrier during the nonalcoholic fatty liver disease (NAFLD) progression. Methods To establish NAFLD rats' model,ninety male SD rats were divided into three groups equally: normal-diet group, high-sucrose diet group and high-fat diet group. At the 4th, 8th and 12th week each time point, ten rats were sacrificed in each group. Another twenty SD rats were randomly divided into carbon tetrachloride (CCl4) group and control group. The liver injured model of CCl4 group was induced by CCl4 ; all the rats of these two groups were killed at the 4th week. The degree of liver steatosis was observed through HE staining of liver paraffin sections. The lipopolysaccharide (LPS) level of portal vein blood was measured by limulus test. The occludin expression in intestinal mucosal was detected by immunofluorescent assay,and the fluorescence intensity was scored. The morphology change of intestinal mucosa tight junction was observed through electron microscopy. Results The liver histopathology suggested that NAFLD and liver injured rats' model was successfully established. There was no statistical significance of LPS level between high-sucrose diet group and normal diet group at all the time point (P＞0.05). At the 4th and 12th week, there was no statistical significance of LPS level between high-fat diet group and normal diet group (P＞0.05), while it was significantly higher in high-fat diet group than normal diet group at the 8th week (P＜0. 05). There was no statistical significance of LPS level between CCl4 group and control group (P＞0. 05). At the 8th week, the expression of occludin in normal-diet group, high-sucrose diet group and high-fat diet group was 1.80±0. 42, 1. 50 ± 0. 53 and 1.30±0.67, respectively, the expression was a little bit lower in high-sucrose diet group and high-fat diet group than in normal diet group, the difference was statistical significance (P＜0. 05). At the 12th week, the expression of occludin was significantly lower in high-sucrose diet group and high-fat diet group than normal diet group. The expression of occludin was significantly lower in CCl4 group (0.60±0.16) than in control group (1.80±0. 42) (P＜0. 05). No obvious morphology changes of tight junction was found in high-sucrose diet group, high-fat diet group and CCl4 group at each time point.Conclusion The expression of occludin decreased gradually during the non-alcoholic fatty liver disease progression. So in the NAFLD treatment, besides improving insulin resistance and protecting liver function,the protection of intestinal mucosa barrier as early as possible may slow down the progression of liver injury.

Objective To study the expressions of TLR4, CD14, MD-2 and NF-kB in colonic mucosa in patients with diarrhea-irritable bowel syndrome (IBS-D) , and compared with normal subjects. The purpose of this study is to explore the role of TLR4 and TLR4 signal transduction pathway in the pathogenesis of IBS-D. Methods The expressions of TLR4, CD14, MD-2 and NF-kB in colon mucosa were examined by immunohistochemistry (IHC) in 30 IBS-D patients and 12 healthy volunteers separately. The average absorbance (A value) of TLR4 was analyzed. The positive expression rates of CD14, MD-2 and NF-kB of colonic mucosa were studied. Results Compared with healthy controls, significant upregulation of TLR4 expression relative to controls was found in colon mucosa of IBS-D. A value of TLR4 in IBS-D was significantly higher (0.3971 ±0.0996 vs 0. 3044 ±0.0481). The positive rate and intensity of NF-kB in IBS-D were significantly higher than those in healthy. The number of positive cells of MD-2 showed significant increase in lamina propria of IBS-D against controls. The percent of CD14 positive was upregulated in lamina propria in IBS-D. The expressions of MD-2 and CD14 in intestine epithelial cell were low or negative. Conclusions There is the activation of the signal transduction pathway of TLR4/NF-kB in the colonic mucosa of patients with IBS-D. Up-regulated expression of TLR4 in IBS patients suppose that it might contribute to occurrence of IBS-D.

Two hundred male and 200 female patients with type 2 diabetes mellitus admitted from January 2007 to April 2008 were enrolled in the study. Of them, 267 were diagnosed as non-alcoholic fatty liver disease (NAFLD) by ultrasonography. The measurements included:body mass index (BMI) ,waist-to-hip ratio (WHR) ,fasting blood glucose( FBG), ALT, AST, total bilirubin(TBIL), cholesterol(CHO),triglyceride(TG), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol ( LDL-C) ,serum creatinine (Cr), supersensitive C-reactive protein (hsCRP) and urine albumin/creatinine. The relationship of above factors with NAFLD was determined. Our data showed that male NAFLD patients were in general younger than female. The BMI ( t = 11. 361, P = 0. 000), waist circumference ( t = 9. 771, P =0. 000), hip circumference (t = 10. 469, P =0. 000) ,TG(t =7. 352, P =0. 000) and hsCRP (t =2. 242,P =0. 026) of NAFLD patients were significantly higher than those without NAFLD. The hsCRP of patients with central obesity was also significantly higher than those without central obesity (t = 0. 266, P = 0. 045 ).BMI and TG were positively correlated with NAFLD. Waist circumference was an independent factor of NAFLD in male patients, same as hip circumference with NAFLD in female patients. In conclusion, gender,central obesity and dyslipidemia may be risk factors for NAFLD in patients with type 2 diabetes mellitus.

Objective To study the relationship between coagulation abnormal and inflammatory in the TNBS induced rats colitis model as well as the therapeutic effect of heparin on this model Methods Forty SD-rats were separated into 4 groups randomly, including normal control group, colitis group, heparin group and SASP group. PT, APTT and the activity of antithrombin (AT)were chosen as indexs of coagulation. The level of damage ancl inflammatory state of the colitis rats were assessed by macroscopical score, histological score and the level of TNFα in each group. Results Compared with normal control group, TNBS induced colitis group has a shorter PT [(14.83±0.45)s vs(16.68±1.08 )s, P < 0.05] and APTT[(12.49±1.30)s vs(29.06±1.60) s, P<0.05] and a lower activity level of AT [(111.33± 8.50)% vs(122.13±3.52)%,P<0.05]. In heparin group, PT, APTT were prolonged [PT: (17.83± 0.78)s vs (14.83±0.45)s,P<0.05, APTT:(53.34±9.49)s vs (12.49±1.30)s,P<0.05] and AT activity was higher than colitis group [(131.67±6.92)% vs (111.33±8.50) %, P < 0.05]. SASP group has a similar data in PT, APTT compared with colitis group and no statistical significance(P>0.05). The activity of AT in SASP group is higher than in colitis group [(122. 33±5.82)% vs (111.33±8.50)%,P <0.05]. The heparin therapy group showed lower macroscopical score(2.50±0.55 vs 4.75±1.16, P< 0.05), histological scores(3.83±0.41 vs 7.75±1.04, P<0.05) and the level of TNFα[(84.75± 18.03) ng/L vs (149.93±23.52)ng/L, P < 0.05] compared with the colitis group. Conclusion Coagulation was abnormality in the rat colitis model induced by TNBS; heparin therapy is effective in the colitis model It seemed that the abnormality of coagulation plays an important role in the pathogenesis of the rat colitis model.

Jaundice is a common clinic presentation which can be caused by various benign or life-threating disorders.Charaterization by unconjugated(indirect)hyperbilirubinemia and conjugated(direct)hyperbilirubinemia may help clinic diagnosis and treatment.The reasons causing unconjugated hyperbilirubinemia include hemolytic anemias,ineffective hematopoiesis,malfunction of bilirubin absorption and combination by hepatocytes or hyperbilirubinemia after hepatitis.Moreover,liver excretion disfunction by inherited disease,hepatocellular jaundice,or various obstruction of the duct system can lead to conjugated hyperbilirubinemia.This article discusses the category of jaundice according to different serum bilirubin,which warrants to clarify the cause quickly so that treatment can begin as soon as possilble.

Objective To identify the factors that may influence the risk of relapse.Methods 122 patients were included in the study,and 12 clinicopathologic factors related to the relapse of ulcerative colitis were analyzed by univariate and multivariate Cox regression proportional hazards mode.Results Multivariate analysis showed the exatrointestinal manifestations,Induced factors,irregular therapy and the compliance of patients were independent prognostic factors for the relapse of ulcerative colitis.Conclusion The patients with UC should be treated regularly and avoid inducing factors.When patients have exatrointestinal manifestations,they should be monitored closely to prevent relapse.