Objective To investigate the mechanism of inter fe ron-? (IFN?) in preventing hepatic fibrosis in rat experimental model . Methods Thirty-six male Sprague-Dawley rats were divide d into three groups randomly: group A(normal controls)of 12 rats were given norm al food and water and received subcutaneous injection of peanut oil twice weekly ; group B (fibrotic model)and group C (IFN? prevention) with 12 rats in eac h were induced by carbon terrachloride, high cholesterol and low protein. Group C were treated with intramusclular injections of IFN? in saline, administered daily at the doses of 1?10 5U. At the end of the sixth week, all the rats in each group were killed, the liver function was examined and the samples of t he liver obtained by biopsy were submitted to histological liver fibrosis studie s. The expressions of ?-smooth muscle actin in hepatic tissues were detect ed with immunohistochemical methods. The effect of IFN? on apoptosis of hep atic stellate cells (HSC) were investigated under electron microscope. Results The level of hepatic collagen Ⅰand Ⅲ and serum PC Ⅲ, HA, and LN in group C was significantly lower than that of group B under lig ht microscope (P

ObjectiveTo study the diagnostic value of serum type IV collagen(IV-C) in hepatic fibrosis. MethodsSerum IV-C levels were detected by using radioimmunoassay(RIA) and were compared with serum type Ⅲ procollagen(PCⅢ ) levels in normal controls(NC) and patients with chronic liver diseases. ResultsSerum IV-C and PCⅢ levels in patients with chronic liver diseases were all much higher than those in NC(P < 0.01, totally). Serum IV-C level in severe chronic hepa titis(CH) group was significantly higher than those in mild and median CH groups (P<0.01 total ly), and that in active liver cirrhosis(LC) group was significantly higher than that in static LC group (P＜0.05). There were significant positive correlation between serum IV-C level and serum PcⅢ level both in CH group and in LC group ( in CH γ=0.7023, in LC γ=0. 5878, P＜0. 001).Conclusion Serum IV-C level could reflect the activity of hepatic fibrogenesis.

Objective To investigate the effects of high glucose on the proliferation of hepatic stellate cell-T6(HSC-T6) and the expressions of transformation growth factor-?1(TGF-?1),platelet-derived growth factor(PDGF) and precollagen Ⅲ(PCⅢ).Methods Based on glucose groups of different concentration,we observed the proliferation of HSC in 30min-16h time period,and used the methods of immunohistochemistry and radioimmunoassay to measure the expressions of TGF-?1,PDGF and PCⅢ in the supernatant at 48h and 72h.Results In 2-16h time period,the proliferation of HSC was increased stepwise over time in 1500-6000mg/L group,and was more visible in 4500-6000mg/L group.The expressions of TGF-?1 and PDGF increased at 48h,and the expression of PCⅢ in the supernatant increased at 72h in 4500-6000mg/L group compared with that in glucose control and hypertonic control groups.Conclusion High glucose can promote hepatic fibrosis by stimulating the expressions of TGF-?1,PDGF and PCⅢ in HSC-T6.

Objective To investigate the preventive effect of spironolactone on hepatic fibrosis. Methods Ninety SD rats were randomly divided into three groups. Control group consisted of 8 rats that , fed by normal food, were injected with peanut oil subcutaneously. Model group consisted of 42 rats whose liver fibrosis was induced by compound factors. Spiro nolactone-prevention group consisted of 40 rats that were given 100 mg?kg -1 spironolactone per day, by the same methods of making models as those of the model group. At the end of weeks 2, 4, 6 and 8, 8 rats were randomly taken out of model group and spironol actone group and then were sacrificed. The expressions of TGF- ? 1 , PDGF- BB and ? -SMA in hepatic tissues were detected with immunohistochemical met hods. Results The expressions of TGF- ? 1 , PDGF-BB a nd ? -SMA in spironolactone group decreased greatly than those in model gro up ( P

Objective To investigate and evaluate the curative effect of radioimmunological targeting drug on nude mice bearing breast cancer. Methods The anti-CEA monoclonal antibody C50 was combined with ~ 131 I to produce radioimmunological targeting drug. 16 nude mice inoculated subcutaneously with breast cancer cell MCF-7 with tumor diameter about 0.5 cm were randomly into 4 groups(n=4): group Ⅰ, injected in part with ~ 131 I-C50 18.5 MBq; group Ⅱ, injected in part with ~ 131 I-C50 3.7 MBq; group Ⅲ, injected in part with ~ 131 I-mIgG 18.5 MBq; group Ⅳ, injected in part with C50 0.75 ?g. The size of tumor volume and inhibitory rate (IR) after treatment for six weeks were calculated and compared with the control group. Results The tumor volume and curves for tumor growth and tumor weight had significant differences between group Ⅰ and the group Ⅲ as well as group Ⅱ (P0.05). Conclusion Anti-CEA monoclonal antibody C50 labeled with radionuclide ~ 131 I could inhibit the growth of the tumor when given locally. ~ 131 I-C50 has a potential value of clinical application

Objective To comfirm the anti-fibrotic effect of spironolactone and investigate the influence of spironolactone on concentration of angiotensinⅡ(AngⅡ) in rat hepatic fibrosis. Methods Ninety male Sprague-Dawly rats were randomly divided into three groups: control group (8 rats, subcutaneous injection of pure peanut oil, normal diet), model group (42 rats, subcutaneous injection of 40% CCl 4, 0.3 mL/100 g, twice a week, high cholesterol and low protein diet, 5% alcohol as the drink), and spironolactone group (40 rats, same dosage of CCl 4, high cholesterol and low protein diet, gastropufusion of spironolactone at the dose of 100 mg?kg -1?d -1). The animals were sacrificed at 2, 4, 6 and 8 weeks of administration. AngⅡ was assayed by radioimmunoassay. The liver tissues were stained, coded and examined. Results ① The general conditions of the rats of spironolactone group were better than those of the model group. The degree of fibrosis and the area of collagen in the liver of spironolactone group were less than those of the model group after the 4th week (P

Objective To investigate the expression of indu ci ble initric oxide synthase(iNOS) in gastric carcinoma and its relationship with angiogenesis and the prognosis. Methods Immunohistochemical staining method was used to det ect the expression of iNOS, VEGF CD34 in gastric carcinoma. Results The positive expression of iNOS in gastric carcinom a was 58.70% and iNOS was not detected in normal gastric tissue. The rate of the positive expression of iNOS in stage Ⅳ was higher than that in stageⅠ～Ⅲ. Th e positive expression of iNOS in gastric carcinoma with lymph node metastasis wa s higher than those with no metastasis. The MVD was 59.88? 18.02/HP and 55.5 9+ 19.39/HP in gastric carcinoma positive for iNOS and VEGF, repectively, obviou sly higher than those with negative expression of iNOS and VEGF, repectively ( P

Objective To evaluate the relationship between the expression of cyclooxygenase-2(Cox-2) and inducible nitric oxide synthase (iNOS) and the angiogenesis in gastric carcinoma. Methods Immunohistochemical stain was used to detect the expression of Cox-2, iNOS and MVD in 45 resected specimens of gastric carcinoma. The monoclonal antibody against CD34 was used for displaying vascular endothelial cells, and MVD was detected by counting the CD34-positive vascular endothelia cells. Paracancerous tissues were examined as the control. Results The expression rates of Cox-2, iNOS and MVD in gastric cancer were significantly increased, compared with those in the paracancerous tissues (77.78% vs. 33.33%, 68.89% vs. 17.78%, 58.13?19.99 vs. 24.02?10.28, P

Objective To assess whether the G870A polymorphism of cyclin D1 (CCND1)was associated with individual susceptibility to gastric cancer in China. Methods Case-control study of 214 individuals was conducted, including 108 controls (non ulcerative dyspepsia) and 106 cases of gastric cancer. The polymorphism analysis of CCND1 A/G was performed in blood samples by PCR-RFLP method. Results The frequency of GG genotype was 19.8% and 7.4% in patients with gastric cancer and controls, respectively. The risk for gastric cancer in patients homozygous (GG) for CCND1 genotypes was 3.5 times higher in comparison with patients carrying AA genotypes (P＜0.05, OR =0.281). Furthermore, the stratification analyses showed that the male, elderly (≥60 years) or H. pylori infected gastric cancer patients who carrying GG genotype were more susceptible to gastric cancer compared with those carrying AA or GA genotype. Conclusion GG genotype is associated with increased susceptibility to gastric cancer in high risk area of Xi'an.

Objective To investigate the clinical features of aortic dissection (AD) and emergency treatments. Methods Data from 784 patients with aortic dissection were collected in the Department of Emergency from January 2000 through December 2009. A retrospective analysis was carried out to determine the survival rate, mortality rate and treatment efficiency. Results Pain was the most common onset symptom (77.7% , 609/784). The majority of patients (86.5%) had essential hypertension (678/784). All the patients with preoperative diagnosis of aortic dissection underwent emergency medical intervention by internists resulting in 81.5% survival rate (639/784) and 18.5% mortality rate (145/784). There were 157 patients without improvement (20.0% ) and the total efficiency rate was (83. 1% ). The efficiency rate of conventional treatment was 76.4% , while the efficiency rate of triple four-procedure treatment was 89. 8% (P<0.05). Of them, 139 patients (17. 7% ) died in the hospital. Among them,. 26 patients died within 24 hours (18.4% ) and 47 cases died within 48 hours (33. 8% ) and 66 patients died within 72 hours (47.2% ). There were 92 patients who refused treatments after diagnosis, and among them, 81 patients died within 72 hours (88.04% ). The difference in mortality rate between two groups was significant (P<0.05). Conclusions The diagnosis of aortic dissection depends on detailed history, physical examination and CT or MRI imaging. Analgesia, sedation and control of blood pressure are essential for emergency treatments. Early diagnosis and effective emergency treatments are the critical strategy for the early surgical intervention and time window for further treatment to improve the survival rate of AD.