Hepatic fibrosis models were induced by CCl4 in rats. To explore vascular endothelial growth factor (VEGF), transforming growth factor-beta1 (TGFβ1) mRNA expression and bcl-2, Bax protein expression levels of intervention and explore the mechanism of the Aralia chinesis anti-hepatic fibrosis. Sixty male Sprague-Dawlley (SD) rats were randomly divided into six groups: nomal group, model group, high-dose (10 mL x kg(-1)), medium-dose (7.5 mL x kg(-1)), low-dose (5.0 mL x kg(-1)) of A. chinesis treated group and colchicine treated group. The change of liver histopathology was observed by HE and Masson staining. The mRNA of VEGF, TGF-β1 were detected by RT-PCR. The protein of Bcl-2 and Bax were detected by Western blot. In the model group liver cell obvious degeneration, necrosis, a large number of collagen fibers of the cable hyperplasia, part visible pseudolobule formation. A. chinesis large, medium, low-dose group and colchicine group liver cell degeneration and necrosis reduced A. chinesis small, medium, and high-dose group was gradually reduced trend and A. chinesis large, middle dose group degree of reduction is particularly significant. Compared with model group, A. chinesis of large, medium and small dose group and colchicine group VEGF mRNA expression, A. chinesis of large, medium-dose group TGF-β1 mRNA expression reduce (P < 0.05); compared with colchicine group, A. chinesis of large, middle dose group of VEGF mRNA expression decreased (P < 0.05); A. chinesis of large, middle dose group of TGF-β1 mRNA expression decreased (P < 0.01), and compared with colchicine group, large dose group of of TGF-β1 mRNA expression decreased (P < 0.05). Compared with model group, A. chinesis of large, medium and small dose group and colchicine group Bcl-2 protein expression reduce (all is P < 0.05). But A. chinesis of large, medium and small dose group and colchicine group of Bax protein expression were increased (P < 0.05). A. chinesis regulation of VEGF, TGF-β1 may prevent the activation of hepatic stellate cells, liver tissue by up regulating the anti-apoptotic protein Bax and down pro-apoptotic protein Bcl-2 expression, thereby to improve the degree of liver fibrosis.
Animals ; Apoptosis ; drug effects ; Aralia ; chemistry ; Drugs, Chinese Herbal ; administration & dosage ; Hepatic Stellate Cells ; drug effects ; metabolism ; Humans ; Liver Cirrhosis ; drug therapy ; genetics ; metabolism ; Male ; Proto-Oncogene Proteins c-bcl-2 ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Transforming Growth Factor beta1 ; genetics ; metabolism ; Vascular Endothelial Growth Factor A ; genetics ; metabolism ; bcl-2-Associated X Protein ; genetics ; metabolism

Female ; Humans ; Neoplasms ; physiopathology ; Thoracic Neoplasms ; pathology ; physiopathology ; Thoracic Wall ; pathology ; Young Adult

Objective:To detect the effect of microRNA-7 ( miR-7 ) knockdown on pathology in murine acute lung injury ( ALI) model,and preliminarily explore its significance.Methods:Murine ALI model was performed by intraperitoneal injection of Li-popolysaccharide (LPS) (10 mg/kg) into miR-7KD mice and wild-type (wild type,WT) mice respectively.Then,the pathologic injury of lung tissue were observed by HE staining.And total cell count of bronchoalveolarlavage(BAL) was calculated.The relative expression of related cytokines in lung tissue was analyzed by Real-time PCR assay.Furthermore,the changes on proportion of innate immune cells (γδT cell and F4/80 macrophages cell) and adaptive immune cell ( CD4+T cell and CD8+T cell) were analyzed by FACS.Meanwhile, the expression of CD62L and CD69,as well as the absolute number,in CD4+T cell were also analyzed.Results: Compared with WT mice,pathological damage in lung tissues was significantly alleviated in miR-7KD mice.Real-time PCR analysis showed that the relative expression of IL-6 was obviously reduced (P<0.01),conversely,relative expression of IL-4 and TGF-βwere obviously increased (P<0.05).Furthermore,the total cell number in BAL also reduced significantly (P<0.05).Importantly,FACS analysis showed that the proportion and the absolute number of F4/80+Mφcells obviously reduced (P<0.05);however,the proportion of γδT cells increased (P<0.05).Moreover,the proportion and the absolute number of CD4+T cells and CD8+T cells were significantly reduced (P<0.05). Finally, the proportion and the absolute number of CD62L+in CD4+T cells were upregulated vigorously,contrastly,the proportion and the absolute number of CD69+in CD4+T cells were notably up-regulated (P<0.05).Conclusion:miR-7 defeciency could significantly ameliorate the pathology of murine ALI,suggesting that it may play an important regulatory role in the development of ALI.

Humans ; Forensic Pathology

Objective To study the relationship between TGF-?signaling pathway and pathogenesis of gastric carcinoma.Methods The expression of TGF-?RⅠ,TGF-?RⅡand Smad4 protein was deter- mined by immunohistochemistry in normal gastric mucosa(26 cases),intestinal metaplasia(22 cases),dysplasia (20 cases)and gastric carcinoma(43 cases).Results The positive expression rate of TGF-?RⅠ,TGF-?RⅡand Smad4 decreased following the malignant degree in gastric tissues(P

Objective To explore the current profile of drowning related high risk behaviors among the floating children inNingbo City and to identify the risk factors on these behaviors.Methods A total of 7 600 students from grade 1 -9 ineight urban migrant workers'children schools were recruited and surveyed by the questionnaires.And the logistic regressionmodel was used for the analysis of risk factors.Results In last one year,without adult supervision,the incidence rate ofdrowning related high risk behaviors was 27.53%.The results of multivariate logistic regression showed that males (OR =2.30,95%CI:1.99 ~2.65),senior grade (OR =1.23,95%CI:1.18 ~1.27),other juvenile companion on the way toschools (OR =1.26,95%CI:1.06 ~1.51),being able to swim (OR =2.09,95%CI:1.77 ~2.46)and there being theopen water around school and home (OR =1.75,95%CI:1.52 ~2.00)could increase the incidence of drowning relatedhigh risk behaviors.And higher awareness of drowning prevention (OR =0.99,95%CI:0.98 ~0.99),higher rate ofcorrect attitude (OR =0.99,95%CI:0.98 ~0.99),getting along well with schoolmates (OR =0.69,95%CI:0.51 ~0.95)and with family members (OR =0.33,95%CI:0.24 ~0.46)could reduce the incidence of drowning related highrisk behaviors.Conclusion The incidence rate of drowning related high risk behaviors was high among the floatingchildren in Ningbo City,and males,being able to swim might increase the occurrence of high risk behaviors.

OBJECTIVETo investigate the delayed cardioprotection induced by remifentanil in intact rat ischemia-reperfusion (I/R) models.

METHODSTotally 42 adult male Wistar rats weighing 200-300 g were randomly divided into 7 groups (n = 6 in each group): In Group I, rats were injected with normal saline via tail vein, performed with the regimen of 3 x 5-min intravenous (i.v.) infusion at a rate of 0.1 ml x kg(-1) min(-1) 24 h before I/R; In Group II, rats were treated according to the same experimental protocols as in Group I except receiving additional naloxone (0.1 mg/kg) 10 minutes before normal saline pretreatment; In Groups III, IV, V, and VI, rats were treated with remifentanil via tail vein, performed with the regime of 3 x 5-min i.v. infusion at a rate of 2 microg x kg(-1) x min(-1) 12 h, 24 h, 48 h, and 72 h before I/R; In Group VII, the rats were treated according to the same experimental protocols as in Group IV except that they received additional naloxone (0.1 mg/kg) 10 minutes before remifentanil pretreatment. Heart rate (HR), mean arterial pressure (MAP), and a lead II electrocardiogram were continuously monitored during IR process. To determine plasma concentration of creatine kinase myocardial isoenzyme-MB (CK-MB), arterial blood samples were obtained immediately before ischemia, and at the end of ischemia and reperfusion. After a 120-min reperfusion, heart was removed for the measurement of myocardial infarct size. Infarct size (IS) was expressed as percentage of the area at risk.

RESULTSHR, MAP, and rate-pressure product were not significantly different at each time points among all groups (P > 0.05). Compared with Group I, plasma concentrations of CK-MB at the end of ischemia and reperfusion and myocardial infarct size were significantly lower in Groups IV and V (P < 0.05). Compared with Group IV, plasma concentrations of CK-MB at the end of ischemia and reperfusion were significantly higher and myocardial infarct size was significantly larger in Group VII (P < 0.05).

CONCLUSIONRemifentanil preconditioning induces delayed cardioprotection in intact rat ischemia-reperfusion model, which may be triggered via opioid receptors.

Animals ; Disease Models, Animal ; Ischemic Preconditioning, Myocardial ; Male ; Myocardial Reperfusion Injury ; physiopathology ; prevention & control ; Piperidines ; pharmacology ; Rats ; Rats, Wistar

BACKGROUNDStudy of the relationship between mast cells and atherosclerosis is mostly dependent on pathological observation and cytology experiments. To investigate the effects of mast cells degranulation on plaque and their possible mechanisms we used apolipoprotein E knockout mice which had been placed perivascular common carotid collar with mast cells degranulator compound 48-80.

METHODSForty apolipoprotein E knockout mice were fed a western-type diet and operated on with placement of perivascular right common carotid collar. Four weeks after surgery, the mice were intraperitoneally injected with compound 48-80 (0.5 mg/kg) or D-Hanks every other day for 4 times. The serum lipids and activity of tryptase were measured. Tissue sections were stained with hematoxylin and eosin. Corresponding sections were stained with toluidine blue and immunohistochemically with antibodies against macrophage-specific antigen, alpha-smooth muscle actin, interleukin-1beta and von Willebrand factor. Simultaneously, basic fibroblast growth factor was detected by in situ hybridization and immunofluorescence.

RESULTSNo pathological change was observed in common carotid non-collar placement but atherogenesis in common carotid collar placement of both groups. There was a significant increase in plaque area ((5.85+/-0.75) x 10(4) vs (0.86+/-0.28) x 10(4) microm(2), P<0.05), the degree of lumen stenosis ((81+/-15)% vs (41+/-12)%, P<0.05), the activity of tryptase in serum ((0.57+/-0.13) U/L vs (0.36+/-0.10) U/L, P<0.05), and the percentage of degranulated mast cells ((80.6+/-17.8)% vs (13.5+/-4.1)%, P<0.05). The expressions of macrophage-specific antigen, alpha-smooth muscle actin, interleukin-1beta, basic fibroblast growth factor and the density of neovessel in plaque were more in the compound 48-80 group than in the control group.

CONCLUSIONSPerivascular common carotid collar placement can promote atherosclerotic plaque formation in apolipoprotein E knockout mice. Compound 48-80 increases plaque area and the degree of lumen stenosis by the mechanism that compound 48-80 promotes proliferation of smooth muscle cells and aggregation of macrophages. Compound 48-80 promotes angiogenesis in plaque. The mechanism is potentially that compound 48-80 increases the expressions of basic fibroblast growth factor mRNA and protein in plaque. Compound 48-80 enhances the expression of interleukin-1beta in plaque.

Animals ; Apolipoproteins E ; genetics ; Atherosclerosis ; chemically induced ; genetics ; metabolism ; pathology ; Carotid Arteries ; drug effects ; pathology ; Fluorescent Antibody Technique ; Immunohistochemistry ; In Situ Hybridization ; In Vitro Techniques ; Male ; Mast Cells ; drug effects ; metabolism ; Mice ; Mice, Knockout ; p-Methoxy-N-methylphenethylamine ; pharmacology

OBJECTIVETo compare the results of procedure for prolapse and hemorrhoids (PPH) and open hemorrhoidectomy.

METHODSA standard questionnaire was given to all patients after PPH or open hemorrhoidectomy from March 2001 to March 2004. In combination with proctological examination, the results including symptoms relief and recurrence were compared between the two groups.

RESULTSThere were 184 effective questionnaires, including 96 cases in PPH group and 88 in open hemorrhoidectomy group. PPH and open hemorrhoidectomy both relieved prolapse (92.7% vs 96.8%, P=0.282), bleeding (91% vs 81%, P=0.241) and pain (91.7% vs 91.5%, P=0.977). There were no statistical differences in the overall complication rate (30.2% and 29.5%, P=0.923) and recurrence rate (21.8% vs 20.5%, P=0.814) between the two groups. The overall satisfactory degree was 87.5% in PPH group and 84.8% in open hemorrhoidectomy group (P=0.218).

CONCLUSIONPPH is a safe and effective option for prolapsed hemorrhoids compared with open hemorrhoidectomy.

Adult ; Aged ; Digestive System Surgical Procedures ; methods ; Female ; Hemorrhoids ; surgery ; Humans ; Male ; Middle Aged ; Surveys and Questionnaires ; Treatment Outcome

The objective of this study is to examine the effects of ANISpm, a novel polyamine naphthalimide conjugate, with acetylsalicylic acid against hepatocellular carcinoma in vivo and in vitro and elucidate its potential molecular mechanism. The proliferation inhibition was detected by MTT assay. Cell apoptosis, intracellular fluorescence intensity and mitochondrial membrane potential (MMP) were detected by high content screening (HCS) analysis. Polyamines content was analyzed by reverse-phase high performance liquid chromatography Protein expression levels were quantified by Western blotting assay. The combination treatment strongly inhibited cell proliferation, induced cell apoptosis in HepG2 cells and H22 hepatoma cells, which was mediated by enhanced ANISpm uptake via up-regulation of spermidine/spermine N1-acetyltransferase (SSAT) and depression of intracellular polyamine. Furthermore, this synergistic apoptosis was involved in mitochondria and death-receptor signal pathway. All these findings demonstrated that the combination treatment with acetylsalicylic acid and ANISpm resulted in synergistic antitumor effects on hepatoma cells. Thus, combination therapy with these agents may be useful as a potential template for the development of better chemotherapeutic strategy against hepatoma.
Acetyltransferases ; metabolism ; Animals ; Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Aspirin ; pharmacology ; Caspase 8 ; metabolism ; Caspase 9 ; metabolism ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Drug Synergism ; Female ; Hep G2 Cells ; Humans ; Liver Neoplasms, Experimental ; pathology ; Membrane Potential, Mitochondrial ; drug effects ; Mice ; Naphthalimides ; chemical synthesis ; metabolism ; pharmacology ; Neoplasm Transplantation ; Polyamines ; chemical synthesis ; metabolism ; pharmacology ; Random Allocation ; Spermine ; chemical synthesis ; metabolism ; pharmacology ; Tumor Burden ; drug effects ; Up-Regulation