Objective To investigate the effect of atorvastatin on circulating endothelial progenitor cells (EPCs) and BP in hypertensive patients with normal lipid profiles.Methods Thirty-eight hypertensive patients were randomly to receive conventional anti-hypertensive drugs (n=18) or conventional anti-hypertensive drugs plus atorvastatin(20 mg QN)combination treatment (n=20).Eight healthy subjects were given atorvastatin (20 mg QN) for 8 weeks as control group.Before and after treatment,peripheral blood were drawn to isolate and culture EPCs.The circulating EPCs were identified by direct fluorescent staining under a laser scanning confocal micro- scope.EPCs populations were assessed using the colony forming unit assay (EPC-CFU) through a inverted phase contrast microscope 10 days after culture.Results After treatment,SBP was decreased (conventional treatment from 165.8?10.3 to 132.7?10.3 mmHg;combined group from 163.7?10.2 to 127.9?10.1 mmHg P

Objective To study the risk factors for ventilator associated pneumonia (VAP) in ICU and pathogens antimicrobial resistance.Methods 220 patients were selected and divided into observation group (88 patients) and control group(132 patients) depending on whetherhe has VAP or not.The clinical data were reviewed to explore the risk factors.And the secretions of respiratory tract were investigated by the routine bacterial culture and drag-resistance methods to analysis the distribution of pathogens.Results The risk factors associated with VAP were COPD,mechanical ventilation,the extensive use of antibiotics,age ＞ 60 years,APACHEII score ＞ 30(P ＜ 0.01).157 bacterial were cultured,68.9％ of pathogens was Gram-negative bacteria in which Pseudomonas aeruginosa was rated as the top one,and 26.1％ of pathogens was Gram-positive bacteria in which MRSA was the majority.The results of the antibiotic resistance monitoring indicated that all Gram-positive and Gram-negative bacteria showed high drugresistance to common antibiotics.Conclusion We should control these risk factors which are closely related to VAP,and select suitable antibiotics on the basis of etiological analysis and drug-resistance.

Anti-Bacterial Agents ; administration & dosage ; Child ; Child, Preschool ; Drug Administration Routes ; Drug Utilization ; standards ; Humans ; Infant ; Pediatrics ; Pharmaceutical Preparations ; administration & dosage ; Pharmacopoeias as Topic ; Pharmacy Administration

Dehydration ; therapy ; Fluid Therapy ; Humans

Humans ; Liver Diseases ; drug therapy ; prevention & control ; Oleanolic Acid ; analogs & derivatives ; therapeutic use ; Phytotherapy ; Saponins ; therapeutic use

Objective To investigate mechanisms of resistance to adriamycin(ADR)by human breast cancer cell line MCF-7 and to find the alteration of features and celluar behavior of MCF-7 after exposure to ADR.MethodsProliferation speed,population doubling time of MCF(wild type),MCF-7/ADR(exposure to adriamycin)and withdrawl group were respectively tested.Cell phenotype alteration was detected using SP immunohiatochemistry methods.Results No significant difference of proliferation speed was found between MCF-7/ADR and MCF cells.As exposure time prolonged,withdrawl group cells grew faster,thus population doubling time shortened.Differentiation of MCF-7/ADR and wthdrawl group was lower than wild group.The expression of drug resistance associated marker of MCF-7/ADR such as Pgp,LRP,GST-pi,TOPOⅡwas higher than that of MCF-7,ER turned to express negatively,and expression of PR gradually decreased as exposure continued.Conclusion MCF-7 cells exposed to ADR got drug resistant,their proliferation was not suppressed by withdrawl of ADR and even grew faster.Drug resistant cells gained dedifferentiation ability.Their heredity and biochemistry features changed,expression of target enzyme also altered and was reversible by drug withdrawl.

Objective This study examined the effects of Midazolum-ketamine oral solution (MKOS) on the expression of N-methyl-D-aspartate receptor 1 (NMDAR1) and gamma-aminobutyric acid (GABA)A receptors (GABAAR) mRNA in the cerebral cortex of rat, in order to investigate the sedation mechanism of MKOS. Methods Fifty Sprague-Dawley(SD) rats were divided into ten groups according to the observed time after MKOS administration (0,5,10, 15,30,60,90,120,240 and 360 minutes, n =5 each). The 0 minute group(control group) received 0.9% saline instead. Immunohistochemical staining and in situ hybridization were used to detect the expressions of NMDAR1 and GABAAR mRNA in the cerebral cortex. Results Both GABAAR and NMDAR1 all expressed in the glial cells of cerebral cortex. The expression of NMDAR1 in control group was strong. The expression of NMDAR1 became weaker during 15 to 90 minutes after administration of MKOS (P＜0.05). The expression of GABAAR mRNA in control group was weaker,while became stronger during 30 to 90 minutes after administration of MKOS (P ＜0. 05). Conclusion MKOS may play sedation by strengthening the expression of GABAAR and suppressing the expression of NMDAR1 in the cerebral cortex.

Objective To observe the changes of AGEs,NO and eyesight in patients with diabetic retinopathy(DR) treated by Aminoguanidine(AG) combined with Doxium.Methods 120 patients with DR were divided into treatment and control groups at random.Two groups were treated routinely with general treatment on DM and the treatment group was added routine dose of aminoguanidine(AG) and Doxium while the control group were treated with urokinasel.After 8 weeks,AGEs,NO and eyesight were determined.Results The level of NO and eyesight in treatment group were higher markedly than control group,AGEs in treatment group were lower most markedly than control group.Conclusion Aminoguanidine and Doxium can improve DR effectively.

Objective Sphingosine kinase 1 (SPK1) has been identified as a central mediator of ischemia preconditioning, and it has been shown to protect reactive oxygen species (ROS)-induced cardiomyocytes death. The present study aims at investigating the protective effects of adenovirus-mediated sphingosine kinase 1 gene (Ad-SPK1) transfer on ischemia-reperfusion induced cardiac injury. Methods Wistar rats were anesthetized and a left thoracotomy was performed. About 5?108 PFU of Ad-SPK1 in total volume of 100?l was injected intramyocardially into four separate sites of the left ventricular wall with a 30-gauge needle. The control rats received the same injection of adenovirus carrying green fluorescent protein gene (Ad-GFP). Three days later, hearts were isolated and subjected to ischemia/reperfusion (I/R) (30min/30min) ex vivo. Heart performance was evaluated by measuring the left ventricular systolic pressure (LVSP) and left ventricular end-diastolic pressure (LVEDP). The incidence of arrhythmia was recorded. Cardiomyocyte viability was detected by the detection of the release of creatine kinase (CK). The cardiac SPK1 activity was measured using an enzyme method. The forced and the total SKP1 expression was analyzed by immunoblotting with anti-FLAG and anti-SPK1 antibodies. Results The cardiac SPK1 activity was increased by about five-fold by injection of Ad-SPK1, compared to Ad-GFP control group. A more potent performance and a lower incidence of arrhythmia were observed in Ad-SPK1-injected hearts during the reperfusion period, compared with Ad-GFP-injected ones. Enzymatic activity assay showed that creatine kinase release was also less in Ad-SPK1-injected hearts. Conclusion Adenovirus-mediated SPK1 gene transfer efficiently protects heart from injury induced by ischemia-reperfusion.