Brain Injuries ; blood ; Humans ; Hypoglycemia ; pathology ; Infant, Newborn ; Infant, Premature

Humans ; Infant, Newborn ; Jaundice, Neonatal ; diagnosis ; therapy

Objective To investigate the genetype distribution of mycoplasma pneumoniae(MP) by denaturing high-performance liquid chromatography(DHPLC).Methods A total of 300 cases nasopharyngeal aspirate were collected from our hospital.The MP genes of standard strains and clinical specimens isolates were amplified by PCR followed by DHPLC and genetype determination.Results A total of 110 cases were positive after 24 hours fermentation from 300 cases with pharyngeal swab.By the specific primers of MP-129,MP-FH standard strain and specimens,2 280 bp and 2 580 bp gene fragments were made out respectively.One hundred and ten strains of clinical isolates were detected by DHPLC.One hundred and seven strains of P1-Ⅰ were 1b subtype,3 were type P1-Ⅱ which were all 2a subtype.Conclusion The genetype of MP infection in children from our hospital is P1-Ⅰ,1b subtype by using DHPLC technology.

Objective： This study was designed to investigate the effects of HMG-CoA reductase inhibitors on proliferation and growth of gastric cancer cells. Methods： MTT colorimetric assay and flow cytometry were used to measure the proliferative activity and the cell cycle progression of gastric cancer MNK450 cells. Results： Gastric cancer cells treated with Simvastatin had reductions in proliferative activity, S-phase fraction and proliferative index in a dose dependent manner with statistical significance at the concentrations of more than 1 μ mol/L as compared with normal control. The inhibitory rate ranged from 8.0％ to 51.5 ％ when cells were treated with Simvastatin at the concentrations of 0.2 -100 μ mol/L for 72 hours. Inhibition induced by Simvastatin was reversed by simultaneous addition of mevalonic acid at the concentation of 10 mmol/L. Gastric cancer cells were arrested by Simvastafin in G1 at the concentations of 1-20 μ mol/L. The fraction of S-phase cells was reduced from 32.1％ to 15.0％ after exposure to 20 μ mol/L Simvastatin for 36 hours. The addition of 10 mmol/L mevalonic acid overcome G1 arrest induced by 5 μ mol/L Simvastatin. Otherwise, the percentage of cells in G2 plus M2 remained rather constant throughout the treatment. Meanwhile, Pravastatin had no significant effect on the proliferatiive activity of gastric cancer MNK450 cells. Conclusion： Simvastatin could inhibit the proliferation and growth of gastric cancer cells, which suggests that Simvastatin has the effect of antitumor.

Cholesteatoma, Middle Ear ; Humans ; Male ; Young Adult

UNLABELLEDObjective: In order to assess the integrative cardiopulmonary function after percutaneous coronary intervention (PCI) in patients with stable coronary artery disease (CAD), we used symptom limited maximum cardiopulmonary exercise testing (CPET).

METHODSAll 59 patients diagnosed stable CAD by coronary angiography and echocardiography from August to December of 2014 in our hospital, were divided two groups. PCI group, 31 patients received PCI and drugs. Control group, 28 patients received drugs therapy only. All patients performed CPET before and after the treatment.

RESULTSAll patients safely completed CPET without any complications. The control group, all functional parameters were unchanged (P > 0.05). PCI group, the anaerobic threshold, peak oxygen uptake and peak oxygen pulse increased significantly (P < 0.05) from baseline,but not for others (P > 0.05). For individual analysis, PCI group had higher rates of increase (≥ 10% of baseline) in both peak oxygen uptake and peak oxygen pulse than those of control group (P < 0.05).

CONCLUSIONCPET is an objective, quantitative, safe and effective method to evaluate the clinical therapeutic efficiency. PCI can improve the integrative cardiopulmonary function in CAD patients.

Anaerobic Threshold ; Coronary Angiography ; Coronary Artery Disease ; surgery ; Exercise Test ; Heart Rate ; Humans ; Oxygen ; Oxygen Consumption ; Percutaneous Coronary Intervention

Anti-Arrhythmia Agents ; therapeutic use ; Cardiomyopathies ; drug therapy ; etiology ; Child, Preschool ; Female ; Humans ; Moricizine ; therapeutic use ; Tachycardia ; complications ; drug therapy ; Treatment Outcome

Objective: To explore the apoptosis-inducing effect of salvianolate on hepatoma SMMC-7721 cells and the underlying mechanism. Methods: SMMC-7721 cells were co-cultured in vitro with different concentrations (0.5, 1, 2 mg/ml) of salvianolate for 24 h. The apoptotic SMMC-7721 cells were examined by flow cytometry, and the changes of mitochondrial transmembrane potential were examined by mitochondrial transmembrane potential JC-1 kit. The activities of caspase-8, caspase-9, and caspase-3 were detected by spectrophotometry in the hepatoma SMMC-7721 cells after co-cultured with 1 mg/ml salvianolate. The changes of apoptotic SMMC-7721 cells induced by salvianolate in the presence or absence of caspase-9 inhibitor or caspase-3 inhibitor were measured by flow cytometry. The expressions of pro-apoptotic protein Bax and anti-apoptotic protein Bcl-2 were detected by Western blotting analysis. Results: Salvianolate significantly induced apoptosis of hepatoma SMMC-7721 cells (P<0.05), and the decline of mitochondrial membrane potential increased with the increase of salvianolate concentration (P<0.05). The activities of caspase-9 and caspase-3, but not caspase-8, were increased in hepatoma cells after treatment with 1 mg/ml salvianolate for 24 h (P<0.05). The apoptosis-inducing effect of salvianolate was significantly decreased in the presence of caspase-9 or caspase-3 inhibitors (P<0.05). Western blotting results showed that salvianolate increased pro-apoptotic protein Bax expression and decreased anti-apoptotic protein Bcl-2 expression. Conclusion: Salvianolate can induce the apoptosis of human hepatoma SMMC-7721 cells in a dose-dependent manner, which is probably mediated by mitochondrial apoptosis pathway.

Objective To evaluate the protective effect of hydrogen-rich saline on renal ischemia/reperfusion (I/R) in mice. Methods Thirty C57BL/6 mice were randomly divided into 3 groups: sham-operated (SO) group, I/R group (mice were injected with 5 ml/kg saline by tail vein just before ischemia induction) and hydrogen-rich saline group (mice were injected with 5 ml/kg hydrogen-rich saline). At the 6th h after reperfusion, the sera and renal samples subject to IR injury were collected. The Scr and BUN levels in serum were determined and renal histological changes were also examined. The apoptosis of renal tubular epithelial cells was measured by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling assay. Malondialdehyde (MDA) contents in renal samples were measured using specific kits. The infiltration of F4/80 positive macrophages and neutrophils was assayed by using immunohistochemistry. The mRNA expression of TNF-α, IL-6, IL-1β and IL-17 was detected by using real time reverse transcription PCR. Results As compared with LR group, at the 6th h following reperfusion the levels of Scr and BUN were significantly reduced (P<0.05), histological changes obviously alleviated (P<0.01), apoptosis of renal tubular epithelial cells and MDA contents was decreased (P<0.05) in hydrogen-rich saline group. Moreover, the infiltration of macrophages and neutrophils, and the mRNA expression of TNF-α, IL-6, IL-1β and IL-17 in renal tissue in hydrogen-rich saline group were also declined as compared with IR group (P<0.05). Conclusion Hydrogen-rich saline can ameliorate renal IR injury to some extent, which is associated with inhibition of inflammatory response induced by reperfusion.

Objective To investigate the adiponectin levels in non-obese first-degree relatives (FDR)of type 2 diabetic subjects and its relation to insulin sensitivity and the intima-media thickness of the common carotid artery (IMT) during 5-year follow-up. Methods Fifty-three FDR subjects and 37 control subjects who were free of type 2 diabetes were enrolled. Plasma adipenectin, lipid profile, blood glucose, fasting insulin, and blood pressure were determined at baseline and after 5-year follow-up. IMT and endothelial-dependent vasodilation (EDVD) were measured by high-resolution B-mode ultrasound imaging. Homeostasis model assessment was used to evaluate insulin resistance (HOMA-IR)and β-cell function (HOMA-β). 29 FDR subjects and 20 control subjects completed the follow-up. Results Comparing with the control, plasma adiponectin levels in non-obese FDR subjects were lower at baseline [(10.06±5.79)vs (14.43±7.91) mg/L, P< 0.05]. Plasma adiponectin were decreased 24.0% in non-obese FDR and 36.7% in control duning 5 year follow-up (both P<0.05). Adiponectin levels were negatively correlated with waist-to-hip ratio (r = -0. 397), fasting blood glucose (r = -0. 373), IMT (r = -0. 372), and HOMA-IR (r=-0. 40)in the non-obese FDR. After adjusting other relevant risk factors,adiponectin was associated with age, high-density lipoprotein-cholesterol, and IMT in multiple regression analyses in non-obese FDR group. In the control group, a similar analysis revealed that low-density lipoprotein-cholesterol and IMT explained 25% of the variability in the adiponectin concentration. Conclusion Plasma adiponectin levels were decreased after 5 years in both non-obese FDR and control subjects. Decreased adiponectin level may be related to IMT increment.