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.

Objective To summarize the clinical features of Budd-Chiari syndrome.Methods A total of 151 Budd-Chiari syndrome admitted in Peking University People's Hospital from 1996 to 2012 were analyzed retrospectively.Results Abdominal distension was the most common complaint,with 62.9％ (95/151)of lower extremity edema,53.0％ (80/151)of typical bottom-up flow of the abdominal wall longitudinal varicose veins and 60.9％ (92/151) with ascites.Laboratory tests results showed median of alanine aminotransferase (ALT) was 21.5 (15.0,30.0) U/L,aspartate aminotransferase (AST) was 30.0 (23.8,42.0) U/L,total bilirubin was 31.1 (23.3,47.8) μmol/L,blood albumin 37.5 was (31.8,41.5) g/L,prothrombin activity was 71％ (61％,84％).WBC was 5.2 (3.5,7.5) × 109/L,hemoglobin concentration was 126.5 (108.8,144.2) g/L,and platelet count was 117.0 (85.5,155.5) × 109/L.Abdominal B-ultrasound examination showed hepatomegaly existed in 68.9％ (104/151) patients.Intraoperative angiography and surgical exploration showed that 41.1％ (62/151) patients were simple inferior vena cava obstruction or stenosis,15.9％ (24/151)were simple hepatic vein obstruction or stenosis and 43.0％ (65/151) suffered from the inferior vena cava combined with hepatic vein stenosis or obstruction.Surgically confirmation of the lesions showed that inferior vena cava membrane-like structure combined with thrombosis was in 59.6％ (90/151) cases.Conclusions Liver congestion,inferior vena cava congestion and portal hypertension are the main clinical manifestations of Budd-Chiari syndrome.With slightly liver function injury,liver dysfunction of Budd-Chiari syndrome isn't parallel with its portal hypertension.

Objective To analyze the clinical characteristic of autoimmune gastritis (AIG).Methods From January 1990 to April 2010,the clinical data of 55 AIG patients were retrospectively analyzed,which included hemoglobin,lactate dehydrogenase (LDH),α-hydroxybutyrate dehydrogenase (α-HBDH),gastrin,intrinsic factor antibody (IFA),parietal cell antibody (PCA),gastrointestinal endoscopy examination and 24-hour esophageal pH recording.Another 31 megaloblastic anemia (MA) patients were selected as control.Statistical analysis was performed by independent-samples t test.Results Among 55 AIG patients,49 patients were associated with MA,and three out of four cases were identified of IFA.About 43.8％ (21/48) patients were PCA positive.Before treatment,the levels of LDH and α-HBDH of AIG patients with MA were (1045.50±853.46)U/L and (853.71±824.23) U/L which significantly increased,than those of patients without MA [(166.67±41.03) U/L,(133.67±27.90) U/L],the differences were statistically significant (t=-4.665,-2.120,both P＜0.05),however there was no significant difference when compared with the control group [(1047.52±1028.31) U/L,(1050.23±1264.37) U/L,both P＞0.05)].A total of 46 patients underwent gastroendoscopy examination,63.0％ (29/46) patients had gastric body atrophy while gastric antrum not involved; 34.8％ (16/46) patients had neither gastric body nor antrum atrophy; seven patients gastric mucosal showed intestinal metaplasia and one patient showed intestinal metaplasia with atypical hyperplasia and 2.2％ (1/46) presented both the antrum and the body atrophy.Conclusions The levels of LDH and α-HBDH increased in AIG patients might be related with MA caused marrow in-situ hemolysis.IFA is recommended as a routine test for AIG.There is still some limitations of AIG diagnosis according to histopathological features of gastric endoscopy specimen.The clinical features should be taken into consideration.

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.

SUMMARY The male patient reported here presented as gangrene and central diabetes insipidus ( CDI) , who had characteristics of vasculitis. The patient complained about polydipsia and polyuria half a year ago, and then developed tingling, pain and blackish discoloration of some fingers and toes 3 month ago. He also had Raynaud' s phenomenon. After admission, his laboratory examination showed the rise of erythrocyte sedimentation rate, C-reactive protein, immunoglobulin,β2-glycoproteinⅠand the activi-ty of rheumatoid factors, lupus anticoagulant test. his pituitary gland showed loss of posterior signal on magnetic resonance imaging. In addition, his vasopressin test was active. However, there was no suffi-cient evidence to diagnose any specific disease;as a consequence the patient was diagnosed as idiopathic systemic necrotizing vasculitis ( SNV) . For SNV, the patient was treated with glucocorticoid 40 mg/d and impact therapy of cyclophosphamide 0. 4 g every 2 weeks. He also received symptomatic treatment for gangrene and CDI. Cutaneous involvement leading to gangrene was widely reported in SNV, however pi-tuitary involvement in SNV leading to CDI was rare. The prognosis of this patient was poor.

Objective To evaluate the performance of the MAKER IS1200 automated chemiluminescence analyzer .Methods A series of experiments were designed to evaluate the precision ,reagent open bottle stability ,linearity range and reference interval of the MAKER IS1200 automated chemiluminescence analyzer in 8 items of hepatitis B 5 indexes ,AIDS ,hepatitis C and syphilis ac‐cording to the requirements of CLSI documents ,the detection results were performed the methodological comparison with those de‐tected by Abbott i2000 automated chemiluminescence analyzer .Results Except the total precision of HBEAG low value was slight‐ly higher than 15% of the judgment standard ,other indexes conformed to the requirements ;the open bottle stability of various items of reagent was better ;the quantitative item HBSAB had good linearity within the detection range (r2 >0 .95);in the verification of reference interval ,no outlier was found in each item ;in the methodological comparison ,the other items had good correlation with those detected by the ABBOTT i2000 except anti‐HCV .Conclusion The MAKER IS1200 automated chemiluminescence analyzer has good detection performance and meets the requirements of immunoassay detection in laboratory work .