Adult ; Drug Therapy, Combination ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Humans ; Male ; Medicine, Chinese Traditional ; Peripheral Vascular Diseases ; drug therapy ; Phytotherapy ; Takayasu Arteritis ; drug therapy

Objective To explore the efficacy of transurethral resection of bladder neck(female)and urinary sphincter(male)to treat neurogenic urinary dysfunction. Methods Forty-one patients(28 women and 13 men)with neurogenic urinary dysfunction(dysuria)were retrospectively analyzed.All patients had sacral neurological damage.The mean patient age was 27(12-43)years.All patients had urinary retention and ureter dilation.Twenty-nine patients had renal function damage.Residual urine volume was 151-700 ml(mean 420 m1).MFR was 4-14 ml/s.After local anesthesia,bladder neck(female)was incised at 5,6,7 o'clock to the circle fiber.Urinary sphincter(male) was cut off at 11,1 o'clock and was dilated using sound(F24-F27).The catheterization time was 1-2 weeks. Results All 41 patients were followed up,from 2 months to 252 months,average 85 months.Thirty-six patients(88%)were completely recovered with no residual urine,no dilation of ureter and pelvis,no renal function damage.of these 36 cases,surgery was carried out once for 1 patient,twice for 20 and 3 times for 15.Five patients(12%)were not improved. Conclusion Transurethral resection of bladder neck(female)and urinary sphincter(reale)to treat neurogenic urinary dysfunction could be an effective method.

Objective To observe the influence of inactive FRMD4A gene′s expression on the biological behavior of tongue cancer CAL-27cell. Methods FRMD4A-siRNA was transfered into CAL-27 cell by lipidosome, to the expression of FRMD4A-siRNA in CAL-27 cell after transfection was detect by qRT-PCR cell proliferation , was checked by CCK-8,the influence of inactive FRMD4A gene on cell cycle distribution of CAL-27 cell was assayed by flow cytometry. Results Compared with the control group, FRMD4A mRNA expression significantly reduced in FRMD4A-siRNA interfering group (94%) and the cell proliferation index decreased(P<0.05). The cell cycle arrested in G1 period (P<0.05). Conclusion FRMD4A-siRNA could effectively inhibit FRMD4A mRNA expression in tongue cancer CAL-27cell, impact the distribution of cell cycle, and reduce cell proliferation.

Objective To explore acute toxicity of succimer on mice.Methods Twenty Kunming mice(10 males and 10 females) weighting approximately (21.2?2.3)g were acclimatized for 3 days prior to dosing,then were divided into control group and experiment group with 10 mice in each group according to body weight.Fasted for 12 hours,the mice in experiment group received intragastric administration of 160mg DMSA in deionized water in 24 hours,and the control group received the same volume of deionized water,and then they were observed for 7 days.Blood was collected into heparinized-tubes by removal of eyeball.All mice were sacrificed and brain,heart,liver and kidney were removed and washed with normal saline.The activity or amount of BUN,Scr,AST,ALT,SOD, GSH-PX and MDA were analyzed.Results (1)Given 160rag DMSA in 24 hours,gastrointestinal symptoms were main side effects.During the observation,experiment group lost weight due to the decrease of food-intake ,and some mice had slight hydroabdomen.(2)High dose of DMSA caused a significant inhibition of GSH-PX(P0.05).The hepatic cell was damaged accord- ing to the significant raise of MDA in liver(P0.05),which was related to acute toxicity on liver.Conclusion Succimer could inhibit the antioxidarrt systems and could do damage to liver and kidney.

BACKGROUNDThe classic glycine receptor (GlyR) in the central nervous system is a ligand-gated membrane-spanning ion channel. Recent studies have provided evidence for the existence of GlyR in endothelial cells, renal proximal tubular cells and most leukocytes. In contrast, no evidence for GlyR in myocardial cells has been found so far. Our recent researches have showed that glycine could protect myocardial cells from the damage induced by lipopolysaccharide (LPS). Further studies suggest that myocardial cells could contain GlyR or binding site of glycine.

METHODSIn isolated rat heart damaged by LPS, the myocardial monophasic action potential (MAP), the heart rate (HR), the myocardial tension and the activities of lactate dehydrogenase (LDH) from the coronary effluent were determined. The concentration of intracellular free calcium ([Ca(2+)](i)) was measured in cardiomyocytes injured by LPS and by hypoxia/reoxygenation (H/R), which excludes the possibility that reduced calcium influx because of LPS neutralized by glycine. Immunohistochemistry was used to detect the GlyR in myocardial tissue. GlyR and its subunit in the purified cultured cardiomyocytes were identified by Western blotting.

RESULTSAlthough significant improvement in the MAP/MAPD(20), HR, and reduction in LDH release were observed in glycine + LPS hearts, myocardial tension did not recover. Further studies demonstrated that glycine could prevent rat mycordial cells from LPS and hypoxia/reoxygenation injury (no endotoxin) by attenuating calcium influx. Immunohistochemistry exhibited a positive green-fluorescence signaling along the cardiac muscle fibers. Western blotting shows that the purified cultured cardiomyocytes express GlyR beta subunit, but GlyR alpha1 subunit could not be detected.

CONCLUSIONSThe results suggest that glycine receptor is expressed in cardiomyocytes and participates in cytoprotection from LPS and hypoxia/reoxygenation injury. Glycine could directly activate GlyR on the cardiomyocytes and prevent calcium influx into the cardiomyocytes.

Animals ; Blood Pressure ; drug effects ; Blotting, Western ; Calcium ; metabolism ; Cytoprotection ; Glycine ; pharmacology ; Heart ; drug effects ; physiology ; Heart Rate ; drug effects ; Immunohistochemistry ; L-Lactate Dehydrogenase ; secretion ; Lipopolysaccharides ; toxicity ; Male ; Rats ; Rats, Sprague-Dawley ; Receptors, Glycine ; analysis ; physiology

Child ; Electrocardiography ; Humans ; Male ; Ventricular Fibrillation ; physiopathology

OBJECTIVETo evaluate the effect of alpha-galactosidase A (Gla) deficiency on FV Leiden (FVL) associated thrombosis in vivo.

METHODSTo generate the mice carrying mutations in Gla and FVL and analyze the tissue fibrin deposition in organs and thrombosis.

RESULTSIn the presence of FVL, Gla deficiency greatly increased tissue fibrin deposition compared with that in wild-type [Gla(-/0) FV(Q/Q) vs. Gla(+/0) FV(Q/Q) = (0.24 +/- 0.07)% vs. (0.086 +/- 0.049)%, P < 0.0001; Gla(-/-) FV(Q/Q) vs. Gla(+/+) FV(Q/Q) = (0.32 +/- 0.03)% vs. (0.06 +/- 0.005)%, P < 0.05]. With Gla deficiency, the number of thrombi on organ sections in FVL mice was significantly increased [(Gla(-/-) FV(Q/Q) and Gla(-/0) FV(Q/Q)) vs. (Gla(+/+) FV(Q/Q) and Gla(+/0) FV(Q/Q)) = 1.9 +/- 0.7 vs. 0.3 +/- 0.1, P < 0.05].

CONCLUSIONSGla deficiency could be an important genetic modifier for the enhanced thrombosis associated with FVL.

Animals ; Fabry Disease ; genetics ; Factor V ; genetics ; Genotype ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mutation ; Thrombosis ; genetics ; pathology

OBJECTIVETo investigate the relationship between beta-catenin and matrix metalloproteinase-7 (MMP-7) expression and development/biologic behavior of human colorectal cancer.

METHODSImmunohistochemical study for beta-catenin and MMP-7 was carried out on colorectal adenoma-carcinoma tissue microarrays and results analyzed.

RESULTSThe nuclear beta-catenin expression rate was 35.9% in adenoma with malignant transformation, significantly higher than that in adenoma (16.7%) and carcinoma (19.7%) (both P < 0.05). The cytoplasmic and nuclear beta-catenin expression rate in adenoma with severe dysplasia was significantly higher than that in adenoma with mild dysplasia (both P < 0.05). The nuclear beta-catenin expression rate in adenocarcinomas of the ulcerative type, with lymph node metastasis and in the late tumor stages were all significantly higher than that in adenocarcinomas of the polypoid type, with negative lymph node and in the early tumor stages (P < 0.05 or P < 0.01). The MMP-7 expression rate in adenocarcinoma (69.2%) was significantly higher than that in normal colorectal mucosa (15.0%), adenoma (35.0%) and adenoma with malignant transformation (46.2%, P < 0.05 or P < 0.01). The MMP-7 expression rate in ulcerative type adenocarcinoma with lymph node metastasis and in late tumor stages was significantly higher than that in polypoid type adenocarcinoma with negative lymph node and in early tumor stages (all P < 0.05). The cytoplasmic and nuclear beta-catenin expression was thus in positive correlation with the expression of MMP-7 (both P < 0.01).

CONCLUSIONSThe cytoplasmic and nuclear beta-catenin expression, probably an early event, was related to the development of colorectal cancer. beta-catenin may enhance the degradative function of the target gene MMP-7 through nuclear translocation and may further facilitate local invasion and metastasis by the colorectal cancer cells.

Adenocarcinoma ; metabolism ; pathology ; Adenoma ; metabolism ; pathology ; Adult ; Aged ; Aged, 80 and over ; Cell Nucleus ; metabolism ; Cell Transformation, Neoplastic ; Colorectal Neoplasms ; metabolism ; pathology ; Cytoplasm ; metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Intestinal Mucosa ; metabolism ; Liver Neoplasms ; metabolism ; secondary ; Lung Neoplasms ; metabolism ; secondary ; Lymphatic Metastasis ; Male ; Matrix Metalloproteinase 7 ; metabolism ; Middle Aged ; Neoplasm Staging ; Precancerous Conditions ; metabolism ; pathology ; beta Catenin ; metabolism

OBJECTIVE To illuminate the adenoid bacteria distribution in children with adenoid hypertrophy. METHODS PubMed, Embash, Medline, CNKI, VIP Information and Wanfang data were searched for studies on the adenoid bacteria distribution and adenoid hypertrophy. Random effects meta-analysis was used to pool data. RESULTS Nine studies were included in this meta analysis. The pooled detection rates of haemophilus influenza, staphylococcus aureus and streptococcus pneumonia were 0.21 (95%CI, 0.09-0.32), 0.14 (95%CI, 0.09-0.20) and 0.15 (95%CI , 0.08-0.22) respectively. CONCLUSION Haemophilus influenzae, staphylococcus aureus, and streptococcus pneumoniae are three main kinds of pathogenic bacteria of adenoid hypertrophy in children.