Purpose To study the clincal and pathological characterization of autoimnune hapatitis(AIH)cases. Methods The clinical data, the results of pathological examination, immtmofluorescence stainingobservation of the liver biopsy tissue of 8 AIH cases were investigated retrospectively. Results All of 8patients were female and were diagnosed as type Ⅰ AIH. The main symptoms included fever, arthrodynia,purpura or jaundice. Most of cases were companied with other autoimmune diseases and were positive for RFor/and ANA antibodies. The titer of ganna globulin, ALT and AST was increased. The chronic hepatitiswas the main histologic change, in which the minor to moderate degree was in most cases with spotty,piecemeal and bridging necrosis of liver tissue, inflammatory infiltration and fibrosis processing in portal area.In 5 cases IgG was detected by immunofluorescence assay,and in 2cases HBsAg was positive. ConclusionsThe histologic and immunofluorescence examination are necessary for the diagnosis of AIH and can behelpful especially in the diagnosis of the variant type of AIH.

Objective: To observe the alteration of type-　 Ⅰ collagen protein gene expression after arterial injury and investigate its effect on the development of restenosis. Methods: Firstly, thee xperimental carotid arterial injury rabbit model was constructed. Then, Norther n blot, in situ hybridization and histomorphometric analysis were used to de tect the expression of procollagen mRNA and the accumulation of collagen protein 1,2,4 weeks after injury. Results: Type-　Ⅰ collag en mRNA increased 1 week after injury, peaked 2 weeks later and decreased 4 week s later. The deposition of the collagen protein account for a high percentage o f space in neointima on histomorphometric analysis. Conclusion: Collagen protein may play an important role in the development of neointima and restenosis.

Objective: To observe the alteration of type Ⅰ collagen protein gene expression after arterial injury and investigate its effect on the development of restenosis. Methods: Firstly, theexperimental carotid arterial injury rabbit model was constructed. Then, Northern blot, in situ hybridization and histomorphometric analysis were used to detect the expression of procollagen mRNA and the accumulation of collagen protein 1,2,4 weeks after injury. Results: Type Ⅰ collagen mRNA increased 1 week after injury, peaked 2 weeks later and decreased 4 weeks later. The deposition of the collagen protein account for a high percentage of space in neointima on histomorphometric analysis. Conclusion: Collagen protein may play an important role in the development of neointima and restenosis. [

AIM: To investigate the role of proliferation and apoptosis in hypertensive left ventricular hypertrophy (LVH) and the effect of AT 1 blockade with losartan. METHODS: Left ventricles (LV) from 12, 24-week-old SHR (SHR 12 , SHR 24 ), 24-week-old SHR treated with losartan (15 mg?kg -1 ?d -1 , SHR-L 24 ) during 12 weeks, and age-matched WKY rats (WKY 12 , WKY 24 ) were studied. Expression of PCNA was examined by immunohistochemistry. Apoptotic cells in LV sections were assessed by TUNEL method. Levels of fas mRNA were quantitated by RT-PCR. RESULTS: Compared with age-matched WKY, SHR 12 and SHR 24 showed increased LV hypertrophied index (HI), increased apoptotic index (AI) of myocytes ( P

Prophylactic effect of magnesium sulfate on reperfusion-airhythmias was studied using a left anterior descending coronary artery occlusion followed by reperfusion in the isolated rat hearts. In the first part of the present work, we observed a bell-shaped relationship between the incidence of reperfusion-induced ventricular fibrillation (VF) and the duration of preceding ischemia. In the second part, the concentration of magnesium sulfate in perfusate was increased to 3.6, 4.8 and 6.0mmol/L, respectively, 1 min before coronary ligation, VF fell in a dose-dependent manner from its control total incidence of 100% to 82%, 73% and 18% (P

Objective To understand the pathogenic mechanism of ?-endorphin(?-EP) on infective brain edema(IBE).Methods Experimental IBE was induced by pertussis bacilli in rabbits.Forteen rabbits were divided randomly into two groups:Normal saline group(NS,n=7),pertussis bacilli group(PB,n=7).Water content(WC) in brain tissue and ?-EP were measured in plasma,cerebrospinal fluid(CSF),cortex and hippocampus in two groups respectively.Results WC was singnificantly higher in the PB group than those in the NS groups(P

Objective To investigate the levels of serum tumor necrosis factor-alpha (TNF-?琢) and soluble tumor necrosis factor receptor (sTNF-R) and sTNF-R/TNF-?琢 ratios in patients with severe lupus nephritis (SLN) and the impact of double pulse therapy with methylprednisolone (MP) combined cytoxan (CTX). Methods Serum TNF-?琢, soluble tumor necrosis factor receptor type Ⅰ(sTNF-RⅠ) and soluble tumor necrosis factor receptor type Ⅱ (sTNF-RⅡ) levels were determined in 38 cases of SLN patients and 35 health controls by double antibody sandwich enzyme-linked immunosorbent assay (ELISA) before and after the double pulse therapy with MP and CTX. Anti-dsDNA antibody was detected by ELISA. Antinuclear antibody (ANA) was detected by indirect immunofluorescence experiments. Complement C3 and complement C4 were detected by rate nephelometry. Results The serum levels of TNF-?琢, sTNF-RⅠ, sTNF-RⅡand ratios of TNF-?琢/sTNF-RⅠ, TNF-a/sTNF-RⅡ were significantly higher in SLN patients than those in normal control group (P

AIM: The present study is to investigate the inhibitory effect of the transfer of replication-defective retroviral recombinant plasmid encoding a wild-type P16 ink4a gene on the formation of restenosis after rabbit carotid arterial injury in vivo.METHODS:A replication-defective retroviral recombinant plasmid encoding wild-type gene P16 ink4a was constructed and the packaged high titer virus stock was obtained. It was transferred into the rabbit carotid arterial wall immediately after injury. The P16 ink4a mRNA expression in the arteries was examined by Northern blot and in situ hybridization. The effect of overexpression of the P16 ink4a gene on arterial intima hyperplasia was determined by pathophysiological method. RESULTS: The exogenous P16 ink4a could be effectively transferred into injured arterial wall by retroviral recombinant plasmid and the gene products could inhibit smooth muscle cells proliferation (11.80?3.54 vs 25.20?5.12,P

Objective: To investigate the effect of human vascular endothelial growth factor on restenosis after angioplasty. Methods: A rabbit model of injured carotid artery was established using percutaneous transluminal angioplasty. The pcDNA3/hVEGF165（500 μg,n=12） and pcDNA3 （500 μg,n=12） were separately transfected into injured arterial wall with 30 min incubation. The carotid artery was imaged by arotic angiography at the end of week 2 and week 4. Pathology analysis and Northern blot analysis were performed for harvested injured artery segment. Results: Arotic angiography showed carotid artery diameter narrowness were obviously lessened at week 2 and week 4 in experimental group than that in control group; H-E stains showed lumina narrow ratio were obviously reduced at week 2 and week 4 in experimental group than that in control group［（9.58±1.35）% vs (31.72±1.72)%；(18.09±2.93)% vs (44.05±3.28)%， P<0.01 ］; By Northern blot analysis, the expression of hVEGF165mRNA in experimental group were upregulated than in contol group. Conclusion: pcDNA3/hVEGF165 can be transfected into smooth muscle cell and continue to secret bioactivity protein at least for 4 weeks; it can accelerate reendothelialization and prevent restenosis.

Objective:To observe the effect of percutaneous tr ansluminal coronary angioplasty (PTCA) on coronary circulating tumor necrosis fa ctor-α (TNF-α) activity. Methods: Plasma TNF-α levls were measured with radioimmunoassay and bioactive assay respectively. Result s: Plasma TNF-α activity in femoral artery (AO) was significantly incr eased immediately after PTCA ［(15.86±3.75) U/ml vs （41.32±4.36） U/ml， P<0.01］, and plasma TNF-α activity in coronary sinus was remarkably incre ased immediately after PTCA　［(16.72±4.14） U/ml vs （65.61±6.25） U/ml, P<0.01］. There was no change in plasma TNF-α activity in AO 24 h after PT CA ［(18.32±5.12） U/ml vs （15.86±3.75） U/ml, P>0.05］. Conclu sion: The increase in plasma TNF-α activity after PTCA may be associat ed with the injury of coronary artery caused by PTCA, suggesting that TNF-α ma y be involved in the coronary occlusion and the development of coronary restenos is after PTCA.