Double-balloon enteroscopy in detecting small intestinal bleeding.
Explore the source record for details and available documents.
Adolescent↗
Biomedical subjects
Li-hui Wang
Publications and source records attributed to Li-hui Wang.
[Effect of losartan on expression of Janus kinase 2 and signal transducer and activator of transcription 3 in glomeruli of diabetic rats].
OBJECTIVE: To investigate the effects of losartan on Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 in glomeruli of diabetic rats. METHODS: Sixty Wistar male rats were randomly divided into control group (n=20), diabetes group (n=20), and losartan treatment group (n=20). Diabetes was induced by intraperitoneal injection of streptozotocin (STZ, 65 mg/kg). Losartan (10 mg/kg) was administered daily by gavage from the day following the induction of diabetes. The animals were sacrificed in the weeks 2 and 4 after STZ injection. The renal cortical tissues were obtained and glomeruli were isolated. The protein expressions of JAK2, STAT3 and tyrosine phosphorylated STAT3 (p-STAT3) were assessed respectively by Western blot. Immunoprecipitation and Western blot analysis were used to determine tyrosine phosphorylated JAK2 (p-JAK2). JAK2 and STAT3 mRNA were assayed by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: Compared with the control group rats, the respective expression of JAK2, p-JAK2, STAT3, p-STAT3, JAK2 mRNA and STAT3 mRNA was significantly increased in the diabetic glomeruli without losartan treatment (all P<0.01). After treatment with losartan, the expression of p-JAK2 and p-STAT3 in the diabetic glomeruli was down-regulated (all P<0.05). However losartan had no effect on the expression of JAK2, STAT3, JAK2 mRNA and STAT3 mRNA in the diabetic glomeruli. CONCLUSION: JAK2 and STAT3 signal proteins may be involved in the kidney damage associated with diabetes. Regulation of phosphorylation of JAK2 and STAT3 may be responsible for the renal protective effects of losartan in diabetic rats.
Angiotensin II Type 1 Receptor Blockers↗
[Tubular epithelial-myofibroblast transdifferentiation and expressions of hepatocyte growth factor and Smad7 in renal tissues of rat with experimental diabetes].
OBJECTIVE: To investigate the relationship of tubular epithelial-myofibroblast transdifferentiation and the expressions of hepatocyte growth factor (HGF) and Smad7, and to elucidate the role of HGF and Smad7 in diabetic nephropathy. METHODS: Diabetes was induced in male Wistar rats with right nephrectomy and streptozotocin (STZ) administration. The expressions of cytokeratin 18 (CK18), alpha-smooth muscle actin (alpha-SMA), HGF and Smad7 were assayed with immunohistochemistry. The expressions of alpha-SMA, HGF were assayed with flow cytometry. The expression of Smad7 was assessed by Western blot. RESULTS: Compared with those in kidneys of the control group, diabetic kidneys showed down-regulated expression of CK18 and up-regulated expression of alpha-SMA. The expressions of HGF and Smad7 were increased significantly in the kidneys of diabetic rats at first, then they decreased gradually, but were still higher than those of control. CONCLUSION: The tubular epithelial cells may undergo phenotypic alterations and change to myofibroblasts. The absence of up-regulation of HGF and Smad7 may be related with the transdifferentiation of tubular cells in this animal model.
Actins↗
[Effects of lovastatin on renal function and expression of phosphorylating-p38 mitogen-activated protein kinase in experimental diabetic nephropathy in rats].
OBJECTIVE: To investigate the effects of lovastatin on renal function, activity and expression of the p38 mitogen-activated protein kinase (MAPK) and cAMP responsive element-binding protein (CREB) in experimental diabetic nephropathy in rats. METHODS: Eighteen uninephrectomized male Wistar rats were randomly divided into three groups: control (n=6), diabetic (n=6) and lovastatin treatment group (n=6). Diabetes was induced by intraperitoneal injection of STZ (65 mg/kg). Lovastatin (20 mg/kg) was administered daily by gavage from the next day of the induction diabetes for 4 weeks. Four weeks later, animals were sacrificed and samples were collected to determine various parameters, including protein and creatinine in urine (Upro and UCr), and glucose (Glu), creatinine (SCr), blood urea nitrogen (BUN) in serum. Immunohistochemistry and computer image-pattern analysis system were used to analyze activation of P-p38 MAPK and P-CREB, the expression of transferase growth factor-beta(1) (TGF-beta(1)), fibronectin (FN), laminin (LN) in renal glomeruli were also measured. RESULTS: Expression of P-p38 MAPK and P-CREB in diabetic glomeruli in diabetic rats were higher than the controls, the same as the expression of TNF-beta(1), FN, LN(all P<0.01). After lovastatin treatment, expression of P-p38 MAPK, P-CREB and TGF-beta(1), FN, LN were markedly decreased compared with diabetic group(all P<0.01). CONCLUSION: Inhibition of glomerular p38 MAPK signal transduction pathway may be responsible for the decrement of extracellular matrix accumulation and renal protective effects of lovastatin in uninephrectomized rats.
Animals↗
[Relationship between lymph node metastasis and the expressions of E-cadherin, N-cadherin, and matrix metalloproteinase in breast carcinoma].
BACKGROUND & OBJECTIVE: There is little ideal predictor available on evaluating the lymph node metastatic potential of breast carcinoma. This study was designed to determine the expression of gene products of E-cadherin (epithelial), N-cadherin (nerve), and matrix metalloproteinase-9 (MMP-9) in breast carcinoma tissue and investigate their association with the invasion and metastasis of breast carcinoma. METHODS: The authors examined the expressions of E-cadherin, N-cadherin, and MMP-9 in 72 cases of breast carcinoma(39 cases with lymph node metastasis and 33 cases without lymph node metastasis) by immunohistochemistry. Multivariable Cox proportional hazards model was used to analyze the patients' prognosis. RESULTS: The average ranks of E-cadherin in lymph node metastasis group and no lymph node metastasis group were 29.19 and 45.14, respectively, with significant difference (P < 0.001). The expression of E-cadherin was correlated inversely with the metastasis of breast carcinoma. The average ranks of N-cadherin and MMP-9 were 40.04 and 42.97 in lymph node metastasis group, and 32.32 and 28.85 in no lymph node metastasis group, both with significant difference (P < 0.05), and these expressions were positively correlated with the lymph node metastasis of breast carcinoma. The patients who had high expression of E-cadherin had a longer survival time. CONCLUSION: Expression of E-cadherin, N-cadherin, and MMP-9 are associated strongly with lymph node metastasis of breast carcinoma. These proteins are indicators of metastasis potential and prognosis of breast carcinoma.
Adult↗
[FAK antisense oligodeoxynucleotides inhibit vascular smooth muscle cell migration and adhesion mediated by FAK-ERK1/2 signaling pathway].
AIM: To study the effects of FAK-ERK1/2 signaling pathway and FAK antisense oligodeoxynucleotides (ODNs) on vascular smooth muscle cell (SMC) migration and adhesion stimulated by fibronectin (FN). METHODS: Migration and adhesion of cultured SMCs were stimulated by different concentrations of FN, FAK, ERK1/2. And their phosphorylation were detected by immunoprecipitation and Western blot. FAK antisense ODNs were transfected into SMCs by cationic lipid to investigate its modulatory effects on tyrosine phosphorylation, SMCs migration and adhesion were also measured by modifing Boyden Chamber and morphological enumeration, respectively. RESULTS: FAK were expressed when SMCs adhesion and migration were successfully simulated by FN (5, 10, 20, 40, 60 micrograms.mL-1), high contents of FAK and ERK1/2 phosphorylation were detected by 20 micrograms.mL-1 FN or more. FAK antisense ODNs were transfected efficiently by cationic lipid. FAK and ERK1/2 phosphorylation were inhibited magnificently after FAK antisense ODNs transfection. Cell migration stimulated by FN 10, 20, 40 and 60 micrograms.mL-1 were reduced by 23.26%, 21.63%, 19.31% and 17.88% respectively (P < 0.05). SMCs adhesive spreading in 5-60 micrograms.mL-1 FN groups were reduced by 17.89%-27.67% (P < 0.05). CONCLUSION: FAK-ERK1/2 mediated signal transduction play important roles in SMCs migration and adhesion stimulated by extracellular matrix. The process can be inhibited by FAK antisense ODNs effectively.
Animals↗