Objective:To study the characteristic of hearing loss in essential hypertension. Method:Sixty-eight cases (136 ears) of patients with essential hypertension were divided into two groups, i. e. group A, patients without retinal alteriosclerosis (35cases, 70 ears ) and group B, patients with retinal alterioselerosis (33cases, 66 ears ). The control group consisted of 30 cases (60 ears) of the same sex and same age. AH people were measured by pure tone audiometry and distortion product otoacoustic emissions. Result:The pure tone thresholds measured in group B hypertensive patients were significantly higher than in the normal controls (P<0. 05) , whereas pure tone thresholds in group A were not different from those in the control group(P>0. 05). From 1000 to 8 000 Hz , DPOAE amplitudes of hypertensive group A and group B were lower than that in control group(P<0. 01). Only on the frequency points of 4 000 Hz , the detection rate of DPOAE in group B was lower than that in control group (P<0. 05). Conclusion: Hypertension is a risk factor of degeneration of the hearing apparatus. The hearing function of hypertensive patients has probability to be impaired, although they do not feel hearing loss.

Objective To study the expression of forkhead box Q1(FOXQ1)in non‐small cell lung cancer(NSCLC) ,then investi‐gate clinical pathological characteristics of NSCLC and its prognosis in patients .Methods The expression of FOXQ1 in 84 cases of NSCLC(selected from June 2007 to December 2008 )was detected by immunohistochemistry(SP) .The correlations of the expres‐sion of FOXQ1 with clinic pathological features and survival time of the NSCLC patients were analyzed .Results The positive ex‐pression rate of FOXQ1 was 91 .7% (77/84) ,closely correlated with patients`histological type and TNM stage(P<0 .05) .The Cox multivariate analysis demonstrated that histological type ,TNM stage and FOXQ1expression were independent factors of NSCLC (P<0 .05) .Conclusion The expression of FOXQ1 may be highly expressed in NSCLC and negatively correlated with prognosis .

AIM: Hydroxymethylglutaryl CoA (HMG-CoA) reductase inhibitors, such as simvastatin, have been shown to reduce atherosclerotic cardiovascular morbidity and mortality by mechanisms unrelated to its lipid-lowering effect. Several studies have shown that simvastatin induces apoptosis in a varieties of cell lines including vascular smooth muscle cells (VSMC). The aim of this study was to investigate the signal pathways involved in apoptosis induced by simvastatin. METHODS: Cultured VSMC were treated with simvastatin. Calpain activity was determined by measuring Ca 2+ ionophore-specific calpain substrate (suc-LLVY-AMC), caspase-3 activation was detected by Western blot, and apoptotic changes were distinguished by annexin Ⅴ binding and DNA laddering. RESULTS: After incubated with 30 ?mol/L simvastatin for 8 h, calpain activity had a marked increase ( P

Heart Failure ; diagnosis ; therapy ; Humans ; Phonocardiography ; methods

Objective To investigated the role of the autophagy lysosomal pathway in PD cells and the possible molecular mechanisms. Methods A dopaminergic neuronal injury model was induced by 6-OHDA in PC12 cells . Autophagosomes in PC12 cells were examined by transmission electronmicro-scopy( TEM ). The expression of LC3- Ⅱ , Cathepsin B were assayed by western blot analysis. Results TEM revealed that the autophagosomes were increased in PC12 cells after 6-OHDA treatment and appeared apoptosis. The LC3-Ⅱ (2h:52.57 ±2.27,4h:56.83 ±3.51,6h:73.43 ±5.41,12h:103.90 ±2.57,24h: 100.40 ±3.91 )and Cathepsin B expression ( model group: 113.80 ± 4.46; normal group 35.89 ± 3.40) were increased after 6-OH DA treatments (P ＜ 0.05 or P ＜ 0.01 ). Conclusion The results indicate that autophagy lysosome pathway is involved in 6-OHDA-induced cell death in PC12 cells.

Aged ; Carcinoma, Renal Cell ; pathology ; Carcinosarcoma ; pathology ; Chondroma ; pathology ; Chondrosarcoma ; complications ; metabolism ; pathology ; surgery ; Diagnosis, Differential ; Female ; Humans ; Kidney Neoplasms ; complications ; metabolism ; pathology ; secondary ; surgery ; Lung Neoplasms ; secondary ; Nephrectomy ; Pleural Effusion, Malignant ; etiology ; S100 Proteins ; metabolism ; Soft Tissue Neoplasms ; pathology ; Vimentin ; metabolism

Aim To investigate TY501′s role in bleo-mycin ( BLM )-induced pulmonary fibrosis in rats. Methods Forty rats were randomly divided into 5 groups, including the sham operation, BLM, PFD, TY501(high and low dose) groups. After administra-tion of BLM intratracheally, PFD and TY501 were giv-en in each group daily, according to the dosage de-signed during 21 days. Lung coefficient, PaO2 were tested before killing the rats. The contents of ALB, ALP, LDH, GSH, HYP were detected by regent kit respectively. PCⅢ and COL4 were determined by ELISA. Results ( 1 ) Some indicators of alveolitis in early stage of IPF: the contents of lung coefficient in three treatment groups were lower and PaO2 was higher than those in BLM group ( P<0. 05 ); compared with BLM group, the contents of ALB, ALP, LDH in the treatment groups reduced on 21 st day ( P<0. 05 );the expression of GSH in BLM group was increased for feedback regulation and higher than the treatment groups and the sham operation group (P<0. 05);(2) some indicators of pulmonary interstitial fibrosis in late stage of IPF:the expressions of HYP, PCⅢand COL4 were reduced after the treatment. There were signifi-cant differences compared with BLM group ( P <0. 05 ) . Conclusions TY501 is valuable for the ther-apy of IPF, the same as the positive drug pirfenidone. TY501 attenuates BLM-induced pulmonary fibrosis, which may be related to the affection of TGF-βpathway and inhibition of MMPs.

Objective:To investigate the protective effect of Yiqi Huazhi recipe Quqian granules on rat renal tubular cell apoptosis induced by lead poisoning. Methods:Totally 60 Wistar rats were divided into 2 groups, 12 in the control group and the others in the model group. Chronic lead poisoning model was made by drinking 0. 02% lead acetate water for 60 days. Then the lead poisoning rats were randomly divided into four groups, high-dose Quqian granules group (3. 0 g·kg-1·d-1), low-dose Quqian granules group (0. 6 g·kg-1 ·d-1 ) , positive control group ( calcium disodium edentate plus procaine, im, 50 mg·kg-1 ·d-1 ) and model group. Seven treatment courses were carried out in the first three groups with every 4-d as one course and 4-d withdrawal period between every two courses. After 60 days, the change of lead in blood and kidney was observed by atomic absorption spectrometry,the apoptosis of kidney tissues was studied by TUNEL, the expression of Bcl-2 protein was detected by immunohistochemical methods and the expression of p53 was studied by Western Blotting. Results:Compared with the control group, the body weight, hemoglobin and the expression of Bcl-2 in the model group were decreased significantly(P<0.01)those in, and Pb in blood(0.990 ±0.443)μg·ml-1, Pb in kidney(51.33 ± 5. 16)μg·ml-1 , the apoptosis of tubular epithelial cell(4. 148 ± 0. 414) and the expression of p53 protein (1. 868 ± 0. 139) were significantly higher (P<0. 05). Compared with the those in model group, the body weight, hemoglobin and Bcl-2 in high-dose group were increased significantly(P<0.01), and the blood lead level (0.082 ±0.015)μg·ml-1, the kidney lead level (6.38 ±0.97)μg ·ml-1 , the apoptosis of tubular epithelial cell(1. 412 ± 0. 109) and p53 protein expression(1. 164 ± 0. 172) were significantly lower (P<0. 05). Conclusion:Lead may induce high expression of p53,low expression of Bcl-2 and promote the apoptosis of renal tubular epithelial cells. It is proven that Yiqi Huazhi recipe Quqian granules can inhibit the expression increase of p53 and the expression de-crease of Bcl-2 resulting in the reduction of the renal tubular apoptosis to allivate the renal injury caused by lead.

Objective To evaluate the inhibitory effect of photocatalytic titanium dioxide (TiO2)on the growth of a human epidermal squamous cell carcinoma cell line A431 and its mechanism.Methods Cultured A431 cells were classified into various groups to remain untreated (blank control group),be treated with different concentrations (100,200,300,400,500,600 mg/L) of TiO2 nanoparticles alone or in combination with ultraviolet (UV,main wavelength 253.7 nm,power 30 W,distance 30 cm,exposure duration 15 min) irradiation.After additional culture for different durations,methyl thiazolyl tetrazolium (MTT) assay was performed to evaluate cell growth,annexin V-fluorescein isothiocyanate/propidium iodide (PI) double staining to observe cell apoptosis,and Rho123 staining to determine mitochondrial transmembrane potential.Statistical analysis was carried out using SPSS 13.0 software.Analysis of variance (AOV),t test and Student-Newman-Keuls (SNK) test were performed to assess the differences in these parameters between these groups.Results The growth of A431 cells was inhibited by pretreatment with TiO2 nanoparticles followed by UV irradiation,and the inhibitory effect was enhanced as the dose of TiO2 nanoparticles increased.As AOV and SNK test showed,there were significant differences in the growth inhibition rate among A431 cells treated with different concentrations of TiO2 nanoparticles at the three time points (24,48 and 72 hours) after UV irradiation (n =6,F =21.54,77.56,20.27,respectively,all P ＜ 0.05).No statistical inhibition was observed in the growth of A431 cells treated with TiO2 nanoparticles alone compared with untreated A431 cells (all P ＞ 0.05).Photocatalytic TiO2 nanoparticles also induced the apoptosis but decreased the mitochondrial transmembrane potential in A431 cells.In detail,the apoptosis rate was 8.86％ ± 0.22％,11.72％ ± 0.29％ and 31.24％ ± 0.78％ in A431 cells treated with TiO2nanoparticles of 100,200,400 mg/L followed by UV irradiation,respectively,compared to 2.69％ ± 0.28％ in the blank control group (n =3,F =256.61,P ＜ 0.05).Decreased mitochondrial transmembrane potential (expressed as total fluorescence intensity) was observed in A431 cells treated with TiO2 nanoparticles of 100,200,400 mg/L followed by UV irradiation compared with blank control group (758.48 ± 15.42,676.60 ± 14.35,557.71 ± 13.12vs.2943.65 ± 70.26,F =208.57,P ＜ 0.05,n =3),and SNK test also revealed statistical differences between these groups.Conclusions TiO2 nanoparticles combined with UV can inhibit the growth of but induce the apoptosis in A431 cells,which may be associated with the reduction in mitochondrial transmembrane potential in A431 cells,while TiO2 nanoparticles alone show no inhibitory effect on the growth of A431 cells.

Objective To investigate the expressions of c-Fos,5-HT and spontaneous activities in single prolonged stress (SPS) stress rats,and to study the possible mechanism of posttraumatic stress disorder(PTSD).Methods forty-eight male SD rats were randomly divided into 6 groups:Individual living + SPS group (IS group),Individual living+control group (IC group),Enriched environment+SPS group (ES group),Enriched environment+control group (EC group),control+SPS group(CS group),control group(C group),8 rats in each group,spontaneous activities were measured before the experiment and post experiment at week 1,2.And the expressions of c-Fos,5-HT in the hippocampus were examined by immunohistochemical staining.Results (1) Spontaneous activity:there were no differences of crossing number and distance among 6 groups before experiment (P＞0.05).On SPS 14 days the crossing number and distance of IS group (12.12±9.64,(2.71 ± 1.99)m) decreased compared with the CS group(45.25±8.37,(6.37± 1.18) m,P＜0.05),and ES group (69.75± 10.05,(10.69± 1.50) m)showed significant increase compared with CS group (P＜0.05).(2)5-HT:the expression of 5-HT in the hippocampus of IS group(0.1125±0.0095) was significantly higher than that in CS group(0.6138±0.0059,P＜0.05),menwhile lower in ES group(0.0495±0.0074,P＜0.05).(3)c-Fos:compared with CS group(0.3108±0.0074),the expression of c-Fos in the hippocampus of IS group(0.3585±0.0150,P＜0.05) significantly increased,but decreased in ES group (0.2613±0.0063,P＜ 0.05).Conclusion Enriched environmental can improve the level of activities in PTSD rats,and to reduce the the expression of c-Fos and 5-HT in the hippocampal neurons.