To observe the clinic effects and complication of Ahmed glaucoma valve(AGV) implantation in refractory glaucoma by using the 23G syringe needle direct puncture the sclerotic tunnel.METHODS: Forty-four cases ( 44 eyes ) of refractory glaucoma underwent AGV implantation by useing the 23G syringe needle direct puncture the sclerotic tunnel. The intraocular pressure ( lOP ) , visual acuity, and complication of post - operation were contrasted with those of pre-operation.RESULTS:The success rate was 84. 1%, the mean preoperative lOP in research group was 52. 1±10. 1mmHg, and the last follow up mean lOP was 15. 6 ± 6. 9mmHg. Compared with the preoperative visual acuity, 11 eyes increased, 27 eyes had no changes and 6 eyes decreased. The main post-operative complications included shallow anterior chamber ( 4 eyes ) , choroidal detachment ( 3 eyes), drainage tube shift (1 eye), hyphema (6 eyes), drainage tube blockage ( 1 eye ) , expulsive choroidal hemorrhage (1 eye), and fiber wrap of drainage tray (5 eyes) .CONCLUSlON:AGV implantation by direct puncture the sclerotic tunnel is feasible and easy. lt avoids of making sclerotic petal and the xenogenic sclera transplanting, simplified the operation technique, prevent the leakage of around tube. The shallow anterior chamber rate is lower. lt is an effective procedure for refractory glaucoma.

Objective To investigate the effects of peroxisome proliferator-activated receptor gamma (PPARγ) agonist pioglitazone on delayed neuronal death,apoptosis of neurocytes,and expression of intercellular adhesion molecule-1 ( ICAM-1 ) following traumatic brain injury (TBI) in rats.MethodsThirty-six Sprague-Dawley rats were randomized into sham injury group,control group and pioglitazone treatment group,with 12 rats in each group.TBI model was established by modified Feeney method.Treatment grouP received intragastric administration of pioglitazone at a dosage of 10 mg/kg,and the sham injury group and the control group were lavaged with isometric 0.2％ dimethyl sulphoxide.Paraffin sections of brain tissues collected at 48 hours after TBI were employed to observe delayed neuronal death,apoptosis of neurocytes and expression of ICAM-1 by Nissl staining,TUNEL staining and immunochemistry respectively.Results( 1 ) Cell loss rate of Nissl body in the treatment group [ ( 38.59 ± 1.97 ) ％ ]was significantly lower than that of the control group [ (51.25 ± 4.01 ) ％ ] ( P ＜ 0.05 ),but was higher than that of the sham injury group [ (8.65 ± 1.23 ) ％ ] ( P ＜ 0.01 ).(2) The number of apoptotic neurocytes of the treatment group (31.67 ± 4.76) was significantly lower than that of the control group (45.33 ± 4.68 ) ( P ＜ 0.05),but was higher than that of the sham injury group ( 16.83 ± 2.04 ) ( P ＜ 0.01 ).(3) The mean optical degree of ICAM-1 positive expression of the treatment group (0.26 ± 0.04) was significantly lower than that of the control group (0.31 ± 0.04) ( P ＜ 0.05 ),but was higher than that of the sham injury group (0.10 ± 0.02 ) ( P ＜ 0.01 ).ConclusionsThe PPARγagonist pioglitazone can reduce the apoptosis of neurocytes and protect neurons after TBI.Meanwhile,its suppression of ICAM-1 expression is probably a mechanism of the suppression of inflammatory reaction and neural protection.

BACKGROUNDChronic obstructive pulmonary disease (COPD) is usually complicated with mucus overproduction in airway. Recently the increased expression of the human calcium-activated chloride channel 1 (CaCC(1)) was found to play an important role in mucus overproduction in the asthmatic airways. To investigate the relationship of CaCC(1) and mucus overproduction in the airway of Chinese patients with COPD, the expressions of CaCC(1), MUC5AC and mucus in bronchial tissues were examined.

METHODSBronchial tissues were obtained from fiberoptic bronchoscopy and bronchial biopsy in West China Hospital from April to July in 2004. Twenty-five patients were diagnosed as the patients with COPD overproduction, and other 20 were the control subjects. The expressions of CaCC(1), MUC5AC and mucin in bronchial tissues were detected by reverse transcriptase-polymerase chain reaction (RT-PCR), in situ hybridization with digoxigenin (DIG)-labeled RNA probe, immunohistochemical and alcian blue-periodic acid Schiff (AB-PAS) staining, respectively.

RESULTSCompared with the control group, the stronger expressions of CaCC(1) were further detected throughout the bronchial tissues from patients with COPD (P < 0.01). Furthermore, the stronger expressions of the CaCC(1) mRNA were related to the severity of airflow obstruction. Samples from COPD showed a stronger staining for MUC5AC than those in control subjects (P < 0.01) and AB-PAS staining revealed more mucins in COPD patients' submucosal gland comparing with that in control subjects (P < 0.01). Expression levels of the CaCC(1) mRNA were respectively negatively correlated with the patients' forced expiratory volume in one second (FEV(1))/forced vital capacity (FVC) data, FEV(1)% predicted data, V(50)% predicted data, V(25)% predicted data (r = -0.43, r = -0.43, r = -0.35, r = -0.36, P < 0.01, P < 0.01, P < 0.05, P < 0.05). While the expression levels of the CaCC(1) mRNA were well correlated with the expression levels of the MUC5AC mRNA of airway epithelium and the PAS-AB stained area of submucosal glands (r = 0.39, r = 0.46, P < 0.05, P < 0.01). Expression levels of the MUC5AC mRNA were negatively correlated with the patients' FEV(1)/FVC data (P = 0.01), FEV(1)% pred data (P = 0.01), V(50)% predicted data, V(25)% predicted data (r = -0.53, r = -0.53, r = -0.48, r = -0.43, P < 0.01, P < 0.01, P < 0.01, P < 0.01). While the expression levels of the MUC5AC mRNA were well correlated with the positively PAS-AB stained area of submucosal gland (P < 0.05), and the correlation coefficients were 0.43.

CONCLUSIONThese results suggest that the stronger gene expression of CaCC(1) exists, complicated with mucus overproduction in the airway of Chinese patients with COPD.

Adult ; Aged ; Bronchi ; metabolism ; Chloride Channels ; genetics ; Female ; Forced Expiratory Volume ; Gene Expression Regulation ; Humans ; Male ; Middle Aged ; Mucin 5AC ; Mucins ; genetics ; Mucus ; physiology ; Pulmonary Disease, Chronic Obstructive ; metabolism ; physiopathology ; RNA, Messenger ; analysis ; Vital Capacity

OBJECTIVETo investigate the variance and drug resistance of pathogenic bacteria isolated from children with infectious diseases seen between 2001 and 2006 in Chengdu area.

METHODSA total of 2888 pathogenic bacterial strains isolated from children in Chengdu Children's Hospital from 2001 to 2006 were analyzed. Tests were performed according to the guidelines of National Committee for Clinical Laboratory Standards (NCCLS) of the United States.

RESULT(1) Of the 2888 strains, 1845 (63.9%) were Gram negative bacteria. The main pathogenic bacteria included Escherichia coli (Ec, 718 strain, 24.9%), Hemophilus (H, 476 strain, 16.5%), Streptococcus pneumoniae (Sp, 412 strain, 14.3%), Klebsiella pneumoniae (Kp, 369 strain, 12.8%), Staphylococcus aureus (Sa, 353 strain, 12.2%), Staphylococcus epidermidis (Se, 278 strain, 9.6%), Pseudomonas aeruginosa (Pa, 146 strain, 5.1%) and other non-zymocyte (Onz, 136 strain, 4.7%). (2) The common pathogens found in blood specimen were 158 strain, which included Se (78 strain, 49.4%), Ec (23 strain, 14.6%), Kp (17 strain, 10.8%), Sa (14 strain, 8.9%), Onz (14 strain, 8.9%), Sp (7 strain, 4.4%) and Pa (5 strain, 3.2%). (3) The number of common pathogens isolated from patients with lower respiratory tract infection was 2018, including Ec (441 strains, 21.9%), H (430 strains, 21.3%), Sp (368 strains, 18.2%), Kp (253 strains, 12.5%), Sa (207 strains, 10.3%), Se (149 strains, 7.3%), Pa (97 strains, 4.8%) and Onz (73 strains, 3.6%). (4) There were 120 strains of common pathogens isolated from urine specimens, including Ec (78 strains, 65%), Kp (25 strains, 20.8%), Onz (7 strains, 5.8%), Pa (5 strains, 4.2%) and Se (5 strains, 4.2%). (5) There were 497 strains of common pathogens found in pus specimens, including Ec 167 strains, (33.6%), Sa (126 strains, 25.4%), Se (46 strains, 9.3%), H (44 strains, 8.9%), Onz (37 stains, 7.4%), Kp (31 strains, 6.2%), Sp (26 strains, 5.2%) and Pa (20 strain, 4.0%). The trend of drug resistance of pathogenic bacteria to antibiotics deteriorated. The proportion of methicillin-resistant Staphylococcus aureus (MRSA) was 6.7% and the methicillin-resistant coagulase-negative Staphylococci (MRCNS) rate was 20% in 2001 - 2003. The total proportion of extended-spectrum beta-lactamase stains (ESBL(S)) in Ec and Kp was 21.8%, and the rate of beta-lactamase production stains of Hemophilus influenzae (Hi) was 19.4% in 2001 - 2003.The proportion of MRSA was 17.2% and the MRCNS rate was 70.2%, the total proportion of ESBL(S) in Ec and Kp was 43.8%, and the rate of beta-lactamase producing stains of Hi was 39.7% in 2004 - 2006.

CONCLUSIONThe distribution of common pathogenic bacteria seen in Chengdu Children's Hospital has changed and the trend of drug resistance of pathogenic bacteria to antibiotics deteriorated in recent three years. Regionally monitoring the changes in pathogenic bacteria and the trend of drug resistance to antibiotics is paramount in guiding the pediatric clinical treatment.

Anti-Bacterial Agents ; pharmacology ; Bacterial Infections ; epidemiology ; microbiology ; Child ; China ; epidemiology ; Drug Resistance, Multiple, Bacterial ; drug effects ; Humans ; Microbial Sensitivity Tests

Objective To investigate the changes of sex hormone and androgen receptor levels and evaluate the relationship of the sex hormones and androgen receptor with coronary heart disease (CHD) in elderly men. Methods A cross-sectional study was performed in 539 elderly men, including 400 healthy people aged 62-92 years and 139 CHD patients aged 60-88 years. The plasma concentrations of total testosterone (TT), free testosterone (FT), dehydroepiandrosterone sulfate (DHEAS), sex hormone binding globulin (SHBG), estradiol (E2), luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were measured. The androgen receptor (AR) level was tested by flow cytometry. Results The fluorescence intensity of DHEAS, TT, SHBG, FT and AR were significantly lower in CHD group than in healthy group (P<0.01);however, FSH and E2 in CHD group were higher(P(0.01). Age was negatively correlated with TT(r=-0.28,P<0.01) and FT (r=-0.17,P<0.05), and positively correlated with SHBG(r=0.14,P<0.05) and E2 (r=0.33, P<0.01). AR fluorescence intensity was negatively correlated with systolic blood pressure (r=-0.12,P<0.01). Logistic regression analysis indicated that TT (OR=1.065,9% CI: 1.012～1.121,P<0.05), SHBG(OR=0.994,95% CI:0.990～0.998,P<0.01) and AR (OR=0.971,95%CI:0.956～0.986, P<0.01)were significantly associated with CHD in elderly male patients. Conclusions The levels of DHEAS, TT, SHBG, FT and AR are lower in elderly men with CHD than in elderly healthy men;however, the FSH and E2 concentrations are higher. Low levels of TT, SHBG and AR may be the independent risk factors for CHD in elderly men.

To test the hypothesis that concentration polarization of atherogenic lipids may occur in the arterial system and play an important role in localization of atherosclerosis, we simulated and measured in vitro the luminal surface concentration of low density lipoprotein (LDL) in local stenosis at the distal end of carotid artery by number simulation and laser scanning confocal microscopy, then we designed carotid stenosis model to test the role of LDL concentration polarization in atherogenesis. The in vitro experiment showed that the luminal surface LDL concentration was higher than the bulk concentration as predicted by the concentration polarization theory. The relative luminal surface LDL concentration changed with the flow velocity and ratio of stenosis. The wall concentration of LDL was highest in the round tube with 40% stenosis at the same velocity, while the wall concentration of LDL was higher when Re was 250 than Re was 500 at the same extent of narrowness. The animal experiment also revealed that general atherogenic plaques obviously occurred at the distal end of local stenosis where concentration polarized. The results strongly support our hypothesis that concentration polarization of lipoproteins occurs in local stenosis at the distal end of carotid artery, and this in turn promotes the localization of atherosclerosis which develops in the arterial system.
Animals ; Atherosclerosis ; physiopathology ; Carotid Stenosis ; physiopathology ; Disease Models, Animal ; Lipoproteins, LDL ; metabolism

OBJECTIVE: To explore the protective effect of HSP72 on the acute injury of cardiomyocyte induced by oxidative stress. METHODS: Cardiomyocytes of neonatal rats treated with heat shock (42 degrees C, 30 min, recovery for 6 h) to induce the expression of HSP72 and HSP72 antisense oligonucleotide was transformed to block the expression of HSP72. 0.5 mmol/L (final concentration) H2O2 was added into the culture medium to mimic oxidative stress, and to induce the acute injury of neonatal cardiomyocytes. The release of LDH and the total protein synthesis were applied to evaluate the injury of cardiomyocyte of neonatal rats. RESULTS: Oxidative stress could significantly increase the release of LDH, and inhibit the total protein synthesis. By inducing the expression of HSPs, heat shock pretreatment significantly reduced the release of LDH and relieved the oxidative stress-mediated inhibition of total protein synthesis. Moreover, HSP7-2 anti-sense oligonucleotide could remarkably block the protective effect of heat shock pretreatment on the cellular injuries induced by H2O2. CONCLUSION HSP72 plays a most important role in the acute injury of cardiomyocyte mediated by oxidative stress.
Animals ; Animals, Newborn ; Cells, Cultured ; HSP72 Heat-Shock Proteins ; pharmacology ; L-Lactate Dehydrogenase ; metabolism ; Myocytes, Cardiac ; pathology ; Oligonucleotides, Antisense ; pharmacology ; Oxidative Stress ; Protein Biosynthesis ; Random Allocation ; Rats ; Rats, Wistar

BACKGROUND: Arteriosclerosis obliterans (ASO) is a major cause of adult limb loss worldwide. Autophagy of vascular endothelial cell (VEC) contributes to the ASO progression. However, the molecular mechanism that controls VEC autophagy remains unclear. In this study, we aimed to explore the role of the GRB2 associated binding protein 1 (GAB1) in regulating VEC autophagy. METHODS: In vivo and in vitro studies were applied to determine the loss of adapt protein GAB1 in association with ASO progression. Histological GAB1 expression was measured in sclerotic vascular intima and normal vascular intima. Gain- and loss-of-function of GAB1 were applied in VEC to determine the effect and potential downstream signaling of GAB1. RESULTS: The autophagy repressor p62 was significantly downregulated in ASO intima as compared to that in healthy donor (0.80 vs. 0.20, t = 6.43, P < 0.05). The expression level of GAB1 mRNA (1.00 vs. 0.24, t = 7.41, P < 0.05) and protein (0.72 vs. 0.21, t = 5.97, P < 0.05) was significantly decreased in ASO group as compared with the control group. Loss of GAB1 led to a remarkable decrease in LC3II (1.19 vs. 0.68, t = 5.99, P < 0.05), whereas overexpression of GAB1 significantly led to a decrease in LC3II level (0.41 vs. 0.93, t = 7.12, P < 0.05). Phosphorylation levels of JNK and p38 were significantly associated with gain- and loss-of-function of GAB1 protein. CONCLUSION Loss of GAB1 promotes VEC autophagy which is associated with ASO. GAB1 and its downstream signaling might be potential therapeutic targets for ASO treatment.
Adaptor Proteins, Signal Transducing ; Adult ; Arteriosclerosis Obliterans/genetics* ; Autophagy ; GRB2 Adaptor Protein ; Humans ; Phosphoproteins/metabolism* ; Phosphorylation ; Protein Binding ; Signal Transduction

Objective To study the changes of amplitude of low-frequency fluctuation (ALFF) in blood oxygenation level dependent functional MRI (BOLD-fMPI) in non-lesional epilepsy (NLE),and discuss its underlying neurophysiological mechanism. Methods The BOLD-fMRI data of 16 patients with NLE and 15 normal volunteers were analyzed by ALFF. The amplitude of the blood oxygenation level dependent activation of the resting state brain was investigated. The brain structures showing increased and decreased ALFF in NLE patients were demonstrated by comparing to normal subjects with 2-sample t-test with threshold of P＜0.05. Results As compared with those in normal subjects,the regions showing increased ALFF in NLE patients were distributed in the right temporal lobe (Montreal Neurological Institute [MNI] coordinates:x=15,y=90,z=21),medial frontal lobe (MNI coordinates:0,24,-24),ventral anterior cingulated (MNI coordinates:-12,30,27) and right cerebellar hemisphere (MNI coordinates:-51,-57,-4); while the regions showing decreased ALFF covered the areas of the left cerebellar hemisphere (MNI coordinates:-48,-15,39),posterior cingulum gyrus (MNI coordinates:60,-21,33) and precuneus (MNI coordinates:-6,-54,66). Conclusion NLE patients show abnormal brain functional organization in resting state; the increased ALFF is considered to be the facilitation such as epileptic activity generation and propagation,while the decreased ALFF might be considered as the functional inhibition in these regions.