Child, Preschool ; Epithelioid Cells ; Heart Atria ; pathology ; Heart Neoplasms ; Humans ; Perivascular Epithelioid Cell Neoplasms

Animals ; Neural Stem Cells ; metabolism ; Rats ; Rats, Wistar ; Semaphorins ; metabolism

The policies of healthcare big data and their common and respective characteristics in USA, Britain, France, Japan, Republic of Korea, and Singapore were analyzed in aspects of their strategic planning, infrastruc-ture construction, R&D of key technologies, professional training, and privacy protection with 5 suggestions put for-ward for improving the policies of healthcare big data in China , namely transforming thinking , establishing opera-tional systems, working out construction criteria, building platform for big data sharing, and attaching importance to professional training .

AIM:To analyze the expression profile of long non-coding RNA (lncRNA) in the liver tissues of drug-induced liver injury ( DILI) and immune liver injury ( ILI) .METHODS:The technique of lncRNA microarray was used to inspect the lncRNA expression profile in the mouse liver tissues that the liver injury was induced by acetaminophen or concanavalin A .The raw data of lncRNA were pretreated for normalization .RESULTS:Compared with normal hepatic tissue, the lncRNA which had more than 1.5-fold variation and significant difference (P<0.05) by statistical analysis were regarded as lncRNA with differential expression .A total of 68 lncRNA with differential expression were found in the hepatic tissues of DILI, with 21 increased more than 1.5 folds and 47 reduced more than 1.5 folds.A total of 60 lncRNA with differential expression in the liver tissues of ILI were observed , with 17 increased more than 1.5 folds and 43 reduced more than 1.5 folds.In all lncRNA, 8 was simultaneously up-regulated in 2 liver injury models , accounting for 38%and 47%respectively, while 28 was simultaneously down-regulated in 2 liver injury models, accounting for 59%and 65%re-spectively .CONCLUSION:lncRNA expression profiles of DILI and ILI change significantly in comparison with normal hepatic tissue , and there are also differences between 2 hepatic damage models .The simultaneous changes of lncRNA may participate in the same or similar pathophysiological process , while the differences may be involved in relatively particular mechanisms .

Objective To study the changes of serum endotheline(ET),D-dimer and fibrinogen(Fbg) in infants with pneumonia complicated with heart failure(HF) and explore the changes of blood coagulation,fibrinolysis,and endothelial cell function.Methods Eighty patients with infant pneumonia complicated with HF and 20 controls were studied.Serum ET,D-dimer,Fbg,activated partial thromboplastin time(APTT),prothrombin time(PT) and thrombin time(TT) were measured.Results ET,D-dimer,Fbg,APTT in every group had differences.With the disease deteriorating,the values of ET,D-dimer,Fbg increased,but the values of APTT decresed gradually.There were positive relations between ET and D-dimer(r=0.42 P

Background:Tripterygium glycosides(TG)is effective for treatment of ulcerative colitis(UC)in clinical practice, however,the underlying mechanism has not been clarified yet. Aims:To investigate the therapeutic effect of TG on dextran sulfate sodium(DSS)-induced experimental colitis in mice and its possible mechanisms. Methods:Sixty healthy male BALB/ c mice were randomly divided into six groups:model control group,low,medium and high-dose TG group,blank control group and normal control group. Mice in the first four groups drank 5% DSS freely for 7 days to induce experimental colitis;simultaneously,distilled water,9. 01,27. 03 or 81. 09 mg/(kg·d)TG were given intragastrically for 21 days in these four groups,respectively. Histopathological changes of colonic mucosal tissues were observed;expressions of TLR4 mRNA and protein were determined by RT-PCR and Western blotting;expression of NF-κB p65 was detected by immunohistochemistry;concentrations of IL-1α,TNF-α and IL-13 were measured by ELISA. Results:Tissue damage and inflammation in varying degrees were observed in colonic mucosal tissues in TG groups with different dosage,but all were less severe than those in model control group. Expressions of TLR4 mRNA,TLR4 protein,and NF-κB p65 in colonic mucosal tissues,as well as concentrations of IL-1α and TNF-α in supernatant of colonic homogenate were significantly lower in TG groups than those in model control group(P < 0. 01). These parameters in medium and high-dose TG groups were significantly lower than those in low-dose TG group(P < 0. 05),but higher than those in blank control group and normal control group(P < 0. 05). Except for TNF-α,no significant differences were seen between medium and high-dose TG groups(P > 0. 05). Conclusions:TG exerts a protective effect on DSS-induced experimental colitis in mice. The underlying mechanism of its anti-inflammatory effect might be related with the inhibition of TLR4 / NF-κB signaling pathway activation and subsequently suppressing downstream proinflammatory cytokines expression and secretion.

Liver fibrosis is a common pathological process for chronic liver injury caused by multiple etiological factors and an inevitable phase leading to liver cirrhosis. According to the previous studies, hesperidin (HDN) shows a very good protective effect on CCl4-induced chemical hepatic fibrosis in rats. In this experiment, based on the findings of the previous studies, a platelet-derived growth factor (PDGF)-induced HSC-T6 model was established to observe the inhibitory effect of HDN on HSC-T6 proliferation. The ELISA method was adopted to detect the content of collagen I in HSC-T6 supernatant. Transforming growth factor (TGF)-beta1, Smad2, Smad3, Smad7 and connective tissue growth factor (CTGF) mRNA expressions were measured by RT-PCR; TGF-beta1 and CT-GF protein expressions in HSC-T6 were determined by Western blot, in order to study HDN's effect on TGF-beta1 signaling pathway in HSC and its potential action mechanism. The results demonstrated that HDN could notably improve HSC-T6 proliferation, Collagen I growth and TGF-beta1, Smad2, Smad3 and CTGF mRNA.expressions. After being intervened with HDN, it could notably inhibit HSC-T6 proliferation and Collagen I growth, reduce TGF-beta1, Smad2, Smad3 and CTGF mRNA and TGF-beta1, CTGF protein expressions and increase Smad7 mRNA expression. HDN's antihepatic fibrosis effect may be related to the inhibition of HSC proliferation and activation by modulating TGF-beta/Smad signaling pathway.
Animals ; Cell Proliferation ; drug effects ; Cells, Cultured ; Connective Tissue Growth Factor ; physiology ; Hesperidin ; pharmacology ; Platelet-Derived Growth Factor ; pharmacology ; Rats ; Signal Transduction ; drug effects ; Smad Proteins ; physiology ; Transforming Growth Factor beta1 ; physiology

Objective To investigate the expression of Notch 1 receptor in renal tissues of patients with hepatitis B virus associated-glomerulonephritis (HBV-GN) and its role in the pathogenesis of HBV-GN.Methods A total of 48 patients with HBV-GN confirmed by renal biopsy during 2008-2010 were enrolled in the study.Distribution of Notch1 receptor in renal tissue of HBV-GN was detected by immunohistochemistry and the association between the distribution of Notch1 receptor and HBsAg was examined by double-label immunofluorescence assays.Correlations of Notch1 receptor expression with renal pathology and clinical parameters of HBV-GN were analyzed.Results Notch1 receptor distributed mainly in renal tubular epithelial cells and interstitial area as brownish red granules,and a few expression in glomerulus was also found.The positive score of Notch1 receptor expression in HBV-GN patients was significantly higher as compared to primary glomerulonephritis patients with serum HBsAg positive or negative and normal renal tissue controls.Notch1 receptor expression was more obvious in membrano-proliferative glomerulonephritis (MPGN) and mesangial proliferative nephritis (MsPGN) patients,but there was no significant difference among the different pathology groups.Distribution of Notch1 receptor was consistent with the distribution of HBsAg and its intensity was positively correlated with renal interstitial fibrosis (r=0.473,P=0.001),tubular atrophy (r=0.690,P=0.000),inflammatory cell infiltration (r=0.616,P=0.000).Negative correlation was found between renal function and the intensity of Notch1 receptor (r=-0.393,P=0.006).Conclusions Notch1 receptor expression increases in the renal tissues of HBV-GN patients and distributes mainly in renal tubular epithelial cells and interstitium,which is consistent with the distribution of HBsAg.Its intensity is closely correlated with renal interstitial lesions and renal function.Abnormal expression of Notchl receptor in renal tissue of HBV-GN may be involved in the progress of HBV-GN.

ObjectiveTo investigate the expression and distribution of Toll-like receptor 4 (TLR4) in renal tissue of HBV associated nephropathy (HBV-GN) and its role in the pathogenesis and clinical manifestations of HBV-GN.MethodsRenal tissues were sampled from 48 HBV-GN patients confirmed by renal biopsy and 154 non-HBV-GN patients.The distribution of TLR4 in renal tissue and the relationship between the distribution of TLR4 and HBsAg were detected by immunohistochemistry.Integrating case record,correlations between the expression of TLR4 with clinical parameters including pathology,glomeruli,kidney tubules lesions,renal interstitial inflammatory infiltration and blood serum HBV were analyzed.ResultsTLR4 mainly distributed in the renal tubular epithelial cells and interstitial areas as brownish red and granular,which was in consistent with HBsAg distribution.The TLR4 positive rate and score in HBV-GN group were higher than those in non-HBV-GN group (P ＜ 0.05 ).TLR4 positive score was slightly higher in mesangial proliferative glomerulonephritis group and focal segmental glomerulosclerosis group,which had no significant difference (P ＞ 0.05).Kidney tubules lesions were strongly associated with TLR4 expression (r =0.748,P ＜ 0.001 ) which increased with aggravation of renal interstitial fibrosis ( r =0.569,P ＜0.001 ),tubular atrophy ( r =0.577,P ＜ 0.001 ) and inflammatory cell infiltration ( r =0.684,P ＜0.001 ).No obvious correlation with glomeruli lesions was observed ( r =0.293,P =0.053 ).Negative correlation could be seen between TLR4 and the renal function ( R2 =0.784),systolic blood pressure ( R2 =0.869),high sensitivity C-reactive protein (R2 =0.979) and urinary protein (R2 =0.615 ) by regression analysis.Other clinical parameters had no statistical significances.ConclusionsThe expression of TLR4 is abnormal in the renal tissue of HBV-GN patients,mainly in renal tubular epithelial cells and interstitial,which is consistent with the distribution of HBsAg.Its intensity is closely related with renal interstitial lesions,renal function changes and inflammatory cell infiltration.A speculation,that HBV can promote abnormal expression of TLR4 in renal tissues of HBV-GN which may be involved in the lesion progress of HBV-GN,is made upon our study.

Objective To examine the effects of comprehensive family intervention on family function among HIV-infected injection drug users (IDUs). Methods Ninety-eight HIV-infected IDUs in 3 AIDS treatment sites in Hunan Province were selected by random cluster sampling and were randomly divided into the intervention group (50 cases) and the control group (48 cases). Subjects in the intervention group were given a 9-month comprehensive family intervention, while those in the control group received standard treatment and care. When the study was completed, APGAR questionnaire was used to analyze the effects of comprehensive family intervention. Results Before the intervention ,the scores of family function were not significantly different the intervention group and the control group. After the intervention, the scores of family function among the control group were(4.26± 3.73) points and the intervention group was (6.53± 4.29) points, the scores of family function were significantly different between the two groups. Conclusions The comprehensive family intervention is an effective model to improve the family function of HIV-infected injection drug users.