1.Optimization of initial antibacterial drug regimens for treating common staphylococcal infection in ICU
Xinkai YAO ; Yaling WU ; Ren LIU ; Qixin ZHOU ; Changqing LI
Chongqing Medicine 2015;(10):1300-1304
Objective To optimize the antibacterial drug regimen in ICU common staphylococcal infection.Methods The pharmacokinetic and pharmacodynamic parameters of antibacterial drugs were collected in combination with the hospital ICU anti-microbial drug resistance monitoring reports from the national antimicrobial resistance investigation net (Mohnarin)of the Ministry of Health and the performance standards for antimicrobial susceptibility testing (2013)issued by the clinical and laboratory stand-ards institute (CLSI),the minimum inhibitory concentration (MIC)of staphylococci was set by using the discrete uniform distribu-tion method and 16 kinds of administration regimens with 6 antimicrobial agents were worked out.The best initially antimicrobial regimen was optimized by using the pharmacokinetic and pharmacodynamic models and Monte Carlo simulations of cumulative frac-tion of response (CFR)from 5 000 patients.Results The alternative initially drug regimens to the infectious bacteria were:linezolid 0.40 g twice daily and vancomycin 0.75 g twice daily for staphylococcus aureus;amikacin 0.60 g once daily and linezolid 0.40 g twice daily,and vancomycin 0.75 g twice daily for hemolytic staphylococci and staphylococcus epidermidis;linezolid 0.40 g twice daily and vancomycin 0.75 g twice daily for methicillin-resistant Staphylococcus aureus;ampicillin/sulbactam 1.50 g 4 times daily, cefuroxime 0.75 g 4 times daily,amikacin 0.60 g once daily,moxifloxacin 0.40 g once daily for methicillin-sensitive staphylococcus aureus.Conclusion In the Staphylococcus aureus infection occurred in ICU,if which being methicillin-sensitive could be deter-mined,ampicillin/sulbactam,cefuroxime,amikacin and moxifloxacin could be selected for treatment,and linezolid or vancomycin could be selected for treating possible methicillin-resistant Staphylococcus aureus infection or undetermined whether being methicil-lin-resistant Staphylococcus aureus infection.
2.17β-Estradiol up-regulates the expression of insulin receptor-α in ovariectomized rats with insulin resistance induced by fructose
Donghua TANG ; Qixin YAO ; Zhuqing QI ; Guang WANG ; Shouhong ZHOU
Chinese Journal of Endocrinology and Metabolism 2010;26(8):695-698
Objective To investigate the effect of 17β-estradiol on insulin resistance and the expression of insulin receptor-α in skeletal muscle of ovariectomized rats with insulin resistance induced by high fructose.Methods Forty-eight mature female Sprague-Dawley (SD) rats were randomly divided into four groups: the normal control group (NC, n= 12) rats were fed with the normal diet for 8 weeks; the model group (M, n= 12)rats were ovariectomized and fed with the high fructose diet for 8 weeks, meanwhile the physiological-dose of 17βestradiol (30 μg · kg-1 · d-1 ) was injected subcutaneously every day; the vehicle control group (VC, n= 12) rats were ovariectomized and fed with the high fructose diet for eight weeks, meanwhile equivalent alcohol was injected subcutaneously every day. Systolic blood pressure (SBP), fasting blood sugar (FBS), and fasting serum insulin (FSI) were measured and insulin sensitivity index (ISI) was calculated. The expressions of mRNA and protein of insulin receptor-α in quadriceps femoris were measured by RT-PCR and Western-blot. Results Compared with the normal control group, SBP (P<0.05), FBS (P<0.05) and FSI (P<0.01) were increased significantly while ISI was decreased significantly (P < 0. 05) in the model group. The expressions of mRNA and protein of insulin receptor-α and phosphorylated Akt were decreased significantly in quadriceps femoris in the model group (P<0.05), compared with the normal control group. However, these effects were reversed by 17β-estradiol in the 17βestradiol replacement group. Conclusions 17β-Estradiol inhibits insulin resistance, and up-regulates the expression of insulin receptor-α and the level of phosphorylated Akt in ovariectomized rats with insulin resistance induced by high fructose diet.
3.Arecoline improved glucose and lipid metabolism in type 2 diabetic rats
Qixin YAO ; Zhuqing QI ; Guang WANG ; Wei ZHANG ; Shouhong ZHOU ; Hongyan LING ; Bi HU
Chinese Pharmacological Bulletin 2003;0(11):-
Aim To investigate the effects of arecoline on glucose and lipid metabolism in type 2 diabetic rats and its mechanisms in glucose metabolism.Methods A type 2 diabetic rat model was established by fed with high fructose-high fat diet.The animals were randomly divided into 7 groups: control group,high fructose-high fat diet group(HF)and high fructose-high fat diet+arecoline(1 mg?kg-1,5 mg?kg-1,10 mg?kg-1,20 mg?kg-1,50 mg?kg-1)groups.The blood glucose,lipid level,hepatic function and liver histology were measured.The mRNA expression of liver glucose-6-phosphatase(G6Pase),phosphoenolpyruvate carboxykinase(PEPCK),Forkhead Box O1(FoxO1)and peroxisome proliferator-activated receptor-? coactlvator-1? (PGC-1?)were observed through RT-PCR.Results In comparison with the high fructose-high fat diet group,the fasting blood glucose and TC of the rats were significantly decreased by arecoline in a dose-dependment manner in high fructose-high fat diet+arecoline group.But hepatic function was damaged by 10 mg?kg-1,20 mg?kg-1 and 50 mg?kg-1 arecoline.The mRNA expression of hepatic G6Pase,PEPCK,FoxO1 and PGC-1? was decreased by treatment with 1 mg?kg-1 and 5 mg?kg-1 arecoline compared with the high fructose-high fat diet group.Conclusions Low dose arecoline can decrease fasting blood glucose and TC in type 2 diabettic rats,and the mechanism in glucose metabolism may be related to its effect on the inhibition of hepatic gluconeogenesis.
4.Study on sugarcane alkane alcohol to quail hyperlipidemia and atherosclerosis model.
Zhongfeng SHI ; Qixin YAN ; Jinhua ZHAO ; Guanghui YAO
China Journal of Chinese Materia Medica 2009;34(16):2092-2096
OBJECTIVETo study on pharmacologic actions on quail hyperlipidemia and atherosclerosis model.
METHODTo duplicate quail hyperlipidemia model by ectogenesis cholesterol and high fat forage, induce to atherosclerosis model, observe influence of sugarcane alkane alcohol to model animals' blood fat level, formation of atherosclerosis plaque, pathological changes of coronary vessels and vascular intimal.
RESULTTC, TG, LDL-C level in blood serum of quail hyperlipidemia markedly decreased after administered sugarcane alkane alcohol by dose of 30, 15, 7.5 mg x kg(-1), proliferation of aorta and brachiocephalic artery tunica intima foam cells was suppressed.
CONCLUSIONSugarcane alkane alcohol has satisfactory pharmacologic actions on hyperlipidemia and atherosclerosis animal model by regulating blood fat.
Alkanes ; chemistry ; therapeutic use ; Animals ; Atherosclerosis ; drug therapy ; Cholesterol ; blood ; Disease Models, Animal ; Ethanol ; chemistry ; therapeutic use ; Hyperlipidemias ; drug therapy ; Male ; Plant Extracts ; chemistry ; therapeutic use ; Quail ; Random Allocation ; Saccharum ; chemistry