Objective To investigate the regulatory effect of miR-21 on ADAMTS-1 expression in pulmonary fibrosis model. Methods A mouse model of pulmonary fibrosis was established using bleomycin (BLM) anda model of pulmonary fibrosis was constructed in vitro , the expression level of miR-21 was measured by quantitative real-time polymerase chain reaction (qRT-PCR), while the protein expression of ADAMTS-1 was measured by Western blot. NIH3T3 were transfected with miR-21 mimics and inhibitor in vitro and the cellular expression of ADAMTS-1 was measured by Western blot. Results Compared with the blank group , in mouse models of pulmonary fibrosis , the miR-21 expressions in lung tissues at three time points after BLM-treatment were significantly up-regulated while an evident decrease in ADAMTS-1 expressions were observed (P < 0.01). In vitro pulmonary fibrosis model , NIH3T3 cells after TGF-β1 in concentration 5 μg/L stimulation down-regulated ADAMTS-1 expression and up-regulated miR-21 expression (P < 0.01). NIH3T3 transfected with miR-21 mimics and inhibitor, up-regulated miR-21 expression, while down-regulated ADAMTS-1 protein expression. Conclusions Up-regulation of miR-21 and Down-regulation of ADAMTS-1 might be involved in the progression of pulmonary fibrosis model; miR-21 could negatively regulate ADAMTS-1 expression.

The evaluation of quality of life after stroke primarily includes body,psychology, society,and the ability of activities of daily living,and they can be mainly obtained from self rating quality of life by the patients,The commonly used evaluation methods include six generic measurement scales and four updated Stroke Specific Quality of Life Scales.The latter includes the Stroke Adapted Sickness Impact Profile,the Stroke Impact Scale,Stroke Specific Quality of Life Scales,and Stroke and Aphasia Quality of Life Scale.This article reviews the generic meas- urement scales,Stroke Specific Quality of Life Scales and the various factors that influencing quality of life after stroke.

OBJECTIVETo explore the effects of Feixin Decoction (FXD) on the hypoxia-inducible factor-1alpha (HIF-1alpha) and vascular endothelial growth factor (VEGF) in the rat model of hypoxic pulmonary hypertension (HPH), and to study its mechanisms for treating HPH.

METHODSForty healthy male SD rats were randomly divided into four groups, i. e., the normal control group, the HPH model group, the FXD group, and the Nifedipine group, 10 rats in each group. The HPH rat model was prepared using normal pressure intermittent hypoxia method. Except the normal control group, rats in the rest groups were fed in a self-made hypoxic plexiglass cabin, with the poor oxygen condition for 8 h daily for 14 successive days. Then the distilled water (at 30 mL/kg) was given by gastrogavage to rats in the normal control group and the HPH model group. FXD (at 28 g/kg) and Nifedipine (at 20 mg/kg) were given by gastrogavage to rats in the FXD group and the Nifedipine group respectively, once daily, for 14 successive days. Besides, hypoxia was continued for 14 days while medicating. The mean pulmonary artery pressure (mPAP) was detected on the second day after the last medication. The morphology of the pulmonary arteriole was detected. The ratio of pulmonary artery wall area and tube area (WA%) was determined. The protein and mRNA expressions of HIF-1alpha and VEGF were detected using immunohistochemistry and in situ hybridization technique.

RESULTSCompared with the normal control group, mPAP, WA%, and the protein and mRNA expressions of HIF-1alpha and VEGF significantly increased in the model group (P < 0.01, P < 0.05). Compared with the HPH model group, mPAP, WA%, and the protein and mRNA expressions of HIF-1alpha and VEGF significantly decreased in the FXD group (P < 0.01, P < 0.05).

CONCLUSIONSFXD down-regulated the expression of VEGF through decreasing the expression of HIF-1alpha. One of its mechanisms for treating HPH might be partially due to reversing the remodeling of pulmonary vascular smooth muscle.

Animals ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Hypertension, Pulmonary ; drug therapy ; etiology ; metabolism ; Hypoxia ; complications ; Hypoxia-Inducible Factor 1, alpha Subunit ; metabolism ; Male ; Phytotherapy ; Rats ; Rats, Sprague-Dawley ; Vascular Endothelial Growth Factor A ; metabolism

No abstract available.
Child* ; Hip* ; Humans ; Osteoma, Osteoid*

Sphingosine-1-phosphate(S1P) is an important bioactive lipid produced from cell membrane sphingomyelin metabolism process.S1P and cell membrane surface S1P receptors(S1PR1-5) are G protein coupled receptors(GPCRs), which influence the formation of new blood vessels in the immune system via combining the related inflammatory signaling pathway.This review describes briefly the effects of S1P and S1PRs on autoimmune disease angiogenesis through intracellular signal transduction, such as rheumatoid arthritis, multiple sclerosis, colitis, systemic lupus erythematosus.Further research will be a new therapeutic target on vascular inflammation of autoimmune diseases.

Objective To investigate the significance and safety of repeat transurethral resection(Re‐TUR) for treating stage T1 of non‐muscle invasive bladder cancer .Methods The clinical data were retrospectively analyzed on 41 cases of stage T1 of non‐muscle invasive bladder cancer in this department of our hospital from January 2013 to November 2014 .All cases underwent Re‐TUR at 4-6 weeks after primary surgery .Among them ,33 cases were male and 8 cases were female ,24 cases were single tumor and 17 cases were multiple tumors at first operation .The maximal tumor diameter was ≥ 3 cm in 13 cases and <3 cm in 28 cases . The first treatment was transurethral resection of bladder tumor(TURB‐t) .The pathological report was the stage T1 of urothelium cancer .Results All 41 cases were completed the operation smoothly ,and no serious complication occurred .In the postoperative pathological examination ,7 cases(17 .07% ) had tumor residue or tumor recurrence ,among them ,3 case had residue f tumor base and 4 cases were new onset tumor;the pathological grade at Re‐TUR in 1 case was increased from G2 to G3 .The follow up lasted for 3―27 months(average 13 .2 months) ,9 cases relapsed ,3 cases (42 .86% ,3/7) were positive at Re‐TUR and 6 cases(17 .65% , 6/34) were negative at Re‐TUR .Conclusion Re‐TUR for treating stage T1 of non‐muscle invasive bladder cancer is safe and feasi‐ble ,its significance to pick out high‐risk patient for conducting further active treatment ,which may have certain effect for reducing the recurrence rate of non‐muscle invasive bladder cancer .

0.05). The relative bioavailability of tested capsules to reference tablets was (99.3?13.1)% Conclusion Both formulations are of bioequivalence.

Objective To investigate the effect of microRNA(miR)-21 on proliferation and differentiation of murine pulmonary fibroblasts. Methods C57BL/6 mice of SPF grade (n=24) were randomly divided into Sham group and Pulmo?nary fibrosis model group with 12 mice in each group. Pulmonary fibrosis model was established by trans-tracheal jet ventila?tion of bleomycin into mice. The transcription levels of miR-21 were examined by quantitative real-time PCR in various pul?monary fibrosis tissues. Primary fibroblast were isolated and digested by Trypsin then inoculated into 6 well plate to reach confluence of 30%-50%. PBS (2.5μL), negative control stock solution and miR-21 mimic stock solution (20μmol/L) were added into Opti-MEM (50μL) as control group, blank group and miR-21 mimic group respectively.The cell viability was as?sessed by CCK-8. Expressions of ADAMTS-1 and TGF-β1 in the pulmonary fibroblasts were tested using Western blot. Re?sults The expression of miR-21 was significantly increased in lungs of mice in pulmonary fibrosis model group than that in sham group. Expression of miR-21 was higher in miR-21 mimic group than that in control group and blank group. Expres?sion of miR-21 was significantly higher with better cell viability in miR-21 mimic group than that in control group and blank group. The expression of ADAMTS-1 was significantly decreased in miR-21mimic group, while the expression of TGF-β1, a target gene of miR-21, was significantly increased in miR-21 mimic group compared with the other two groups. There is no significant different in expressions of ADAMTS-1 and TGF-β1 between control group and blank group. Conclusion Over?expression of miR-21 in pulmonary fibroblasts disrupts TGF-β1 signaling pathway by reducing expression of ADAMTS-1, which promotes the proliferation and differentiation of pulmonary fibroblast.

Atrial Fibrillation/surgery* ; Cardiac Tamponade/surgery* ; Catheter Ablation/adverse effects* ; Humans ; Radiofrequency Ablation ; Treatment Outcome ; Vena Cava, Superior/surgery*

OBJECTIVETo observe the expression and clinical implication of receptor for activated C kinase 1 (RACK1) in mononuclear cells and coronary atherosclerotic plaques from patients with coronary artery disease.

METHODSmRNA and protein expressions of RACK1 were detected in mononuclear cells from 29 patients with stable angina pectoris (SAP), 41 patients with acute coronary syndrome (ACS) and 30 healthy volunteers. RACK1 protein expression was also detected by immunohistochemistry in 17 coronary atherosclerotic plaques and 6 normal autopsy coronary samples.

RESULTS(1) mRNA expression of RACK1 was significantly upregulated in mononuclear cells from patients with ACS compared with those from patients with SAP (18.71 ± 5.45 vs. 12.18 ± 4.14, P < 0.05), and the latter was also significantly higher than in healthy controls (12.18 ± 4.14 vs. 3.65 ± 1.57, P < 0.05). (2) Similar changes were observed for protein expression of RACK1 for the three groups. (3) Increased expression of RACK1 was found in atherosclerotic plaques, especially in unstable plaques, positive RACK1 stain was evidenced in foam cells, inflammatory cells, smooth muscle cells and endothelial cells.

CONCLUSIONSThe expression of RACK1 is significantly upregulated in mononuclear cells from patients with coronary artery disease, especially in patients with ACS, and in coronary atherosclerotic plaques, especially in unstable plaques. Our results thus suggest that RACK1 might play an important role in the development and progression of coronary artery disease.

Adult ; Aged ; Case-Control Studies ; Coronary Artery Disease ; blood ; genetics ; pathology ; Female ; Gene Expression ; Humans ; Leukocytes ; metabolism ; Male ; Middle Aged ; Receptors for Activated C Kinase ; Receptors, Cell Surface ; genetics ; metabolism