ObjectiveTo observe effects of modulated medium frequency low frequency current hydroelectric bath therapy on sequela of ankle fracture.Methods32 sequela patients of ankle fracture were treated with ZM-C type intellectual faculties intermediate frequency therapeutics instrument. Modulated medium frequency square all wave,the frequency of carry wave was 4 KHz,and the frequency of modulated wave was 100 Hz. The water temperature was 40℃. 30 minutes was a time,12 times was a course. Before and after treatment,results were contrasted themselves.ResultsAfter treatment,32 patients all got satisfactory effects,the shorter of the course,the better of the effect.ConclusionThe modulated medium frequency low frequency current hydroelectric bath therapy is a simple,safe and better effect method for sequela of ankle fracture.

Adult ; Bronchoalveolar Lavage ; methods ; Female ; Humans ; Male ; Middle Aged ; Pneumoconiosis ; therapy ; Respiration, Artificial ; Young Adult

Adhesives ; Anti-Bacterial Agents ; Dental Cements ; Dental Materials ; Humans

Objective Hyperglycaemia and hyperlipid are common in clinical cardiovascular disease .The article was to ob-serve the change of endothelial and the expression of Rho-kinase in the aorta of rats with hyperglycaemia and hyperlipid and the rela-tionship between them .Methods Healthy male Wistar rats were randomly divided into 3 groups:5 as normal control group , 10 as model group and 10 as drug intervention group .The latter two groups were given high-fat diets for 5 weeks after tail vein injection of streptozocin (STZ) to establish hyperglycaemia and hyperlipid models , then fasudil (inhibitor of Rho-kinases) or saline were respec-tively given intraperitoneally for 4 weeks.Venous blood glucose (VBG), blood lipid levels, ET-1 and eNOS were tested, along with the expression of MYPT-1(the protein substrates of ROCK)、mRNA of RhoA and ROCK. Results Compared with normal control group, the levels of VBG、ET-1、MYPT-1、mRNA of ROCK and Rho A were increased in model group[(6.18±1.14)mmol/L vs (26.36± 3.25)mmol/L,(72.13±6.13 )pg/mL vs (88.22±4.61) pg/mL, (0.54±0.08) v s (1.28±0.17),(0.16±0.20) vs (0.83± 0.12),(0.40±0.18) vs (0.78±0.13),P<0.05].TG、TC、LDL were also higher in model group(P<0.05), while eNOS level was lower in model group than in control group[(24.42±2.13)U/L sv (17.36±1.58)U/L,P<0.05].Compared with model group, the levels of VBG[(17.70±2.69)mmol/L]、TG、TC、LDL, ET-1 [(75.03±2.50)pg/mL]、MYPT-1(0.74±0.01)、mRNA of ROCK(04.0±0.08) and Rho A (0.25±0.07)in drug intervention group were lower(P<0.05), while eNOS level (0.74±0.11) was higher(P<0.05) in drug intervention group than in model group . Conclusion Endothelial dysfunction and over-expression of Rho kinase can be found in hyperglycaemia and hyperlipid rat models .Fa-sudil could improve endothelial function .

Acute Disease ; Adult ; Emergency Nursing ; First Aid ; Humans ; Male ; Nitriles ; poisoning ; Young Adult

Objective To determine the expression and clinical value of neuropilin-1 (NRP-1) in hepatocellular carcinoma (HCC).Methods One hundred and fifty-one cases of HCC tissues and 89 cases of healthy liver tissues were chosen to compare the expression of NRP-1 by immunohistochemistry.Then the relationships between different clinical factors and the expression of NRP-1 were analyzed by univariate and multivariate statistical analysis.Moreover,the survival rates were compared by survival analysis between different expressions of NRP-1 in HCC patients.Results Eleven cases were lost to follow-up or died for non HCC disease,and the effective cases in the final study were 140 cases.The positive expression rates of NRP-1 in HCC and normal liver tissues were 65.00％ and 35.96％ respectively,and the difference was statistically significant (x2 =18.843,P ＜0.001).According to the expression level of NRP-1,140 patients with HCC were divided into negative expression group (n =49) and positive expression group (n =91).Univariate analysis showed that the expression of NRP-1 in HCC was correlated with tumor number (x2 =8.025,P =0.005),TNM stage (x2 =26.467,P ＜ 0.001),differentiation degree (x2 =15.296,P ＜ 0.001),portal vein invasion (x2 =9.054,P =0.003) and hepatic vein invasion (x2 =5.928,P =0.015).Multivariate statistical analysis showed that TNM stage (OR =1.392,95％ CI:1.121-1.730,x2 =8.950,P =0.003),differentiation degree (OR =1.469,95％ CI:1.102-1.958,x2 =6.862,P =0.009),portal vein invasion (OR =1.829,95％ CI:1.157-2.893,x2 =6.665,P =0.010) and hepatic vein invasion (OR =2.161,95％ CI:1.172-3.987,x2 =6.084,P =0.014) were important factors for NRP-1 expression.The median survival time of NRP-1 negative HCC patients was significantly longer than that of positive group (44 months vs.23 months),and the difference was statistically significant (x2 =21.922,P ＜0.001).Conclusion NRP-1 is over-expression in HCC tissue and related to the malignant progress of HCC,and this suggests poor prognosis in patients with HCC.

ObjectiveTo determine whether the inhibition of caveolin-1 tyrosine residues 14 (Cav-1-Y14) phosphorylation with protein tyrosine kinase inhibitors (PP2) will upregulate heme oxygenase-1 (HO-1) activity to protect against ventilation induced lung injury in vivo of an animal model.Methods Fifty-four male Sprague-Dawley (SD) rats were randomly divided into nine groups (eachn = 6). Group A served as normal control group, in which rats did not receive ventilation but tracheotomy. Groups B1 and B2 received lung protective ventilation respectively for 1 hour or 2 hours. Groups C1 and C2 received high tidal volume (40 mL/kg) ventilation for 1 hour or 2 hours, respectively. The group D1 or D2 also received high tidal volume ventilation for 1 hour or 2 hour respectively, but they were given PP2 1 hour before high tidal volume ventilation. The groups E1 and E2 also received high tidal volume ventilation respectively for 1 hour or 2 hours, but tyrosine kinase inhibitor PP2 and HO-1 inhibitor zinc protoporphyrinⅨ(ZnPPⅨ) were given to animals 18 hours before high tidal volume ventilation. All the animals were sacrificed after ventilation, and the specimens of lung tissues and bronchoalveolar lavage fluid (BALF) were harvested. Then the changes in pathology of lung tissue was observed, and diffuse alveolar damage scores (DAD) were calculated, myeloperoxidase (MPO) activity was measured by colorimetric analysis, lung wet/dry ratio (W/D) was estimated. The expressions of phosphorylated caveolin-1 (P-Cav-1-Y14), caveolin-1 (Cav-1) and HO-1 were determined by Western Blot. The expressions of high mobility group B1 (HMGB1) and advanced glycation end product receptor (RAGE) in lung tissues were assayed with immunohistochemistry staining. The levels of tumor necrosis factor-α(TNF-α) in BALF were measured by enzyme linked immunosorbent assay (ELISA).Results There was no significant difference in all the parameters between group A and groups B. Compared with group B1, DAD score, W/D ratio, the activity of MPO and the concentration of TNF-α in BALF in group C1 were significantly increased [DAD score:7.97±0.59 vs. 0.55±0.13, W/D ratio: 5.70±1.61 vs. 5.04±0.63, MPO (U/g): 1.82±0.14 vs. 0.77±0.26, TNF-α(ng/L): 370.10±29.61 vs. 54.38±8.18, allP< 0.05], and the injury in ventilation 2 hours group was more serious than that in ventilation 1 hour group. Compared with groups C, all the parameters in groups D were significantly decreased. The parameters in groups E were significantly higher than those in groups A, B, and D, but no significant difference was found as compared with groups C. Compared with groups B, the protein expressions of Cav-1 and P-Cav-1-Y14 (gray value) in groups C were significantly increased (1 hour: 1.49±0.02 vs. 1.26±0.13, 1.34±0.02 vs. 0.87±0.04;2 hours: 1.58±0.02 vs. 1.27±0.27, 1.31±0.01 vs. 0.95±0.02, allP< 0.05), and the expression of HO-1 protein (gray value) was significantly decreased (1 hour: 0.59±0.02 vs. 1.10±0.01, 2 hours: 0.49±0.01 vs. 1.20±0.02, both P< 0.05). No significant difference in Cav-1 protein expression between groups D as well as groups E and groups C. The protein expression of P-Cav-1-Y14 in groups D and E was significantly lower than that in groups C. The protein expression of HO-1 in groups D was significantly higher than that in groups C, but the phenomenon was not found in groups E as compared with groups C. Compared with group A, the positive expression of HMGB1 and RAGE in lung tissue in groups C and E was significantly increased, but no significant difference was found between groups B as well as groups D and group A.Conclusion Cav-1-Y14 phosphorylation is the key factor for ventilator induced lung injury, which can not only lead to a decrease in vascular barrier function, but also inhibit the activity of HO-1 enzyme, thus further aggravates inflammatory injury of the lung as induced by mechanical ventilation.

Objective To investigate whether the inhibition of caveolin-1 (Cav-1) phosphorylation will regulate effectively nuclear factor-erythroid 2-related factor (Nrf2) signal pathway and downstream effector molecules and protest against ventilation induced lung injury (VILI) in an animal model in vivo. Methods Ninety male Sprague-Dawley (SD) rats were randomly divided into nine groups (each n = 10): sham group in which rats did not receive ventilation but received tracheotomy; lung protective ventilation (PV) for 1 hour or 2 hours group; mechanical ventilation (MV) at high volume tidal (VT, 40 mL/kg) for 1 hour or 2 hours group; protein tyrosine kinase inhibitor PP2 or rosiglitazone (Rsg) pretreatment + high VT ventilation for 1 hour or 2 hours groups. The two pretreatment groups were given intraperitoneal injection PP2 15 mg/kg or intragastric administration of Rsg 5 mg/kg 1 hour before ventilation respectively. The rats were sacrificed after model reproduction, and bronchoalveolar lavage fluid (BALF) was collected. Pulmonary vascular permeability was measured by Evans blue (EB). The levels of tumor necrosis factor-α (TNF-α), activator protein-1 (AP-1), nuclear factor-κB (NF-κB), and interleukin-8 (IL-8) in BALF were determined by enzyme linked immunosorbent assay (ELISA). Then the lung tissues were collected, the lung wet/dry ratio (W/D) was calculated, the changes in pathology was observed with light microscope, and myeloperoxidase (MPO) activity was determined by colorimetric analysis. Nrf2 mRNA was determined by reverse transcription-polymerase chain reaction (RT-PCR). The expressions of Cav-1 tyrosine residues 14 phosphorylation (pCav-1-Y14), Cav-1, peroxisome proliferators-activated receptor γ (PPARγ) and claudin-5 as well as Nrf2 in cytoplasm and nucleus were determined by Western Blot. The positive expressions of PPARγ and claudin-5 in lung tissues were assayed with immunohistochemistry staining. Results There were no obvious pathological changes in the lung tissue in sham group and PV groups, and there were no significant differences in all the parameters between the two groups either. However, the injury in lung tissue was severe in the high VT groups in which W/D ratio, EB contents, MPO activity, and TNF-α, AP-1, IL-8, NF-κB levels in BALF as well as the protein expressions of Cav-1 and pCav-1-Y14 were significantly higher than those of sham group and PV groups, and the protein expressions of PPARγ and claudin-5 were significant lower than those of sham group and PV groups with a dose-dependent manner; but Nrf2 expressions in cytoplasm and nucleus did not show a statistical increase. After pretreatment of PP2 or Rsg, W/D ratio, MPO activity, EB contents, TNF-α, AP-1, IL-8, and NF-κB in BALF were significantly decreased as compared with those of high VT group, and RT-PCR showed significant up-regulation of Nrf2 mRNA in lung tissues too. Moreover, there was a statistically significant increase in expressed Nrf2 proteins in nucleus in PP2 or Rsg groups as compared with those of high VT groups [Nrf2 in nucleus (gray value): 0.61±0.06, 0.56±0.06 vs. 0.31±0.02 at 1 hour, 0.38±0.06, 0.43±0.07 vs. 0.22±0.03 at 2 hours; all P < 0.05], but no significant difference was found in the expression of Nrf2 protein in the cytoplasm among all groups. The protein expressions of pCav-1-Y14 in PP2 pretreatment groups were significantly lower than those of high VT groups (gray value: 0.89±0.04 vs. 1.48±0.02 at 1 hour, 0.86±0.02 vs. 1.31±0.01 at 2 hours; both P < 0.05); but expressed PPARγ proteins and expressed claudin-5 proteins in PP2 or Rsg pretreatment groups were significantly higher than those of high VT groups [PPARγ (gray value): 0.34±0.07, 0.42±0.13 vs. 0.17±0.07 at 1 hour, 0.38±0.09, 0.33±0.07 vs. 0.16±0.03 at 2 hours; claudin-5 (gray value): 0.33±0.05, 0.38±0.07 vs. 0.14±0.03 at 1 hour; 0.30±0.06, 0.31±0.04 vs. 0.17±0.04 at 2 hours; all P < 0.05]. Conclusions The inhibition of Cav-1-Y14 phosphorylation can increase the expression of Nrf2 in the nucleus, then result in an increase in the protein expressions of PPARγ and claudin-5 of its effector molecules. This effect can reduce the inflammation and capillary permeability of lung tissue in the model of VILI.

OBJECTIVETo investigate the expression of long non-coding RNA-HOTAIR in prostate cancer cells and its effects on the growth and metastasis of the cells.

METHODSUsing quantitative reverse-transcription PCR (qRT-PCR), we determined the relative expression of HOTAIR in the normal human prostate epithelial cell line RWPE-I and prostate cancer cell lines PC-3 and DU145. We detected the effects of HOTAIR on the cell cycle and invasiveness of prostate cancer cells by RNA interference, flow cytometry, and Transwell mitration assay.

RESULTSThe expressions of HOTAIR in the PC3 and DU145 cells were increased 3.2 and 5.7 times, respectively, as compared with that in the normal RWPE-1 cells. After si-HOTAIR interference, the prostate cancer cells were arrested in the G2 phase and downregulated in the G1 phase. The invasive ability of the prostate cancer cells was evidently inhibited, with the inhibition rates of 32% and 44% of the PC3 cells and 43% and 34% of the DU145 cells for si-HOTAIR1 and si-HOTAIR2, respectively.

CONCLUSIONIncRNA HOTAIR is highly expressed in prostate cancer, which is associated with the growth and invasiveness of prostate cancer cells. HOTAIR is potentially a novel marker for the diagnosis and prognosis of prostate cancer.

Cell Cycle ; Cell Cycle Checkpoints ; Cell Division ; Cell Line, Tumor ; Cell Proliferation ; Down-Regulation ; G1 Phase ; G2 Phase ; Humans ; Male ; Neoplasm Invasiveness ; Prognosis ; Prostatic Neoplasms ; metabolism ; pathology ; RNA Interference ; RNA, Long Noncoding ; metabolism ; RNA, Untranslated ; metabolism

Objective To systematically evaluate the association between protein C and Legg -Calve -Perthes disease.Methods A literature research was performed through PubMed,Embase,Cochrane library,Web of Science,Chinese Biomedical Literature Database(CBM),China National Knowledge Infrastructure(CNKI)and Wan-fang Database from inception to February 201 6 on the association between protein C and Legg -Calve -Perthes disease.According to the Newcastle -Ottawa Scale(NOS)criteria,the quality of studies was evaluated and data were extracted.Meta -analysis was performed with Stata 1 1 .0 software.Results A total of 1 4 articles were included.Twelve articles on protein C and Legg -Calve -Perthes disease in the study group and the control group were compared.The results of Meta -analysis showed that there was no significant difference in protein C levels between the study group and the control group[odds radio(OR)=1 .41 ,95% confidence interval(CI)(0.87,2.28),P =0.1 47];five articles on protein C and the white race of Legg -Calve -Perthes disease between the study group and the control group were com-pared,The results of Meta -analysis showed that there was no significant difference in protein C levels between the whiteskin patients′group and the control group[OR =0.61 2,95%CI(1 .83,7.29),P =0.61 2];three articles on pro-tein C and the yellow race of Legg -Calve -Perthes disease between the study group and the control group were com-pared,and the results of Meta -analysis showed that there was no significant difference in protein C levels between the yellow skin patients group and the control group[OR =0.59,95%CI(0.05,6.72),P =0.080].Conclusion There is no significant correlation between protein C and Legg -Calve -Perthes disease.