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Unsuccessful randomized trial excluded from the main analysis; means of age, LDL-C value, and percentage of male gender at entry to study in all randomized patients; difference of the mean percentage LDL-C reduction during treatment period between active treatment A ; and control group C at the end of the study; $on the 2-year visit as published; 12 the median values are presented. A indicates active treatment; C, control group; ACAPS, Asymptomatic Carotid Artery Progression Study; AFCAPS TexCAPS, Air Force Texas Coronary Atherosclerosis Prevention Study; ALLHAT-LLT, Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial; ASCOT-LLA, Anglo-Scandinavian Cardiac Outcomes Trial-Lipid Lowering Arm; CARE, Cholesterol and Recurrent Events; CCAIT, Canadian Coronary Atherosclerosis Intervention Trial; HPS, Heart Protection Study; GISSI, Gruppo Italino per lo Studio della Sopravvivenza nell'Infarcto Miocardico; GREACE, GREek Atorvastatin and Coronary-Heart-Disease Evaluation; HTAS, HDL-Atherosclerosis Treatment Study; KAPS, Kuopio Atherosclerosis Prevention Study; KLIS, Kyushu Lipid Intervention Study; L-CAD, Lipid-Coronary Artery Disease; LIPID, Long-Term Intervention with Pravastatin in Ischemic Disease; LRT, Lovastatin Restenosis Trial; MAAS, Multicentre Anti-Atheroma Study; MARS, Monitored Atherosclerosis Regression Study; MIRACL, Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering; PLAC, Pravastatin Limitation of Atherosclerosis in the Coronary Arteries; PMNSG, Pravastatin Multinational Study Group; Post-CABG, Post-Coronary Artery Bypass Graft Trial; PROSPER, Prospective Study of Pravastatin in the Elderly at Risk; REGRESS, Regression Growth Evaluation Statin Study; SCAT, Simvastaitn Enalapril Coronary Atherosclerosis Trial; SSSS, Scandinavian Simvastatin Survival Study; WOSCOP, West of Scotland Coronary Prevention.
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There are ten rights set out in the code and these rights apply to all health and disability support services in New Zealand, both public and private services. The code gives rights to all people who use health and disability services and describes the obligations of all providers of health and disability services. The Health and Disability Commissioner contracts advocates in each region to ensure the code is upheld. To make a complaint to the advocate in your region, contact the office of the Health and Disability Commissioner. The Health and Disability Commissioner Freephone 0800 11 22 E-mail hdc hdc .nz Web hdc .nz AUCKLAND Level 10, Tower Centre 45 Queen Street PO Box 1791 Auckland Ph Fax 09 373 1060 The Privacy Act sets out general rules about the protection of our personal information. Extra rules have been developed to protect health information. These rules are set out in the Health Information Privacy Code, which is contained within the Privacy Act. The Health Information Privacy Code sets out 12 rules that agencies must follow when dealing with health information. These rules cover the collection, storage, use and disclosure of health information, and give you the right to access and correct your health information. The code applies to you whether you are receiving health services voluntarily or under the Mental Health Act. Under the code, health services can develop their own policies for dealing with health information. You are advised to ask for a copy of their policies. Health services must appoint a Privacy Officer, so find out who that person is in the service you are dealing with. You may request information from or make a complaint to the service's Privacy Officer and sporanox.
Narisawa T, Fukaura Y, Terada K, et al. Prevention of 1, 2-dimethylhydrazineinduced colon tumorigenesis by HMG-CoA reductase inhibitors, pravastatin and simvastatin, in ICR mice. Carcinogenesis 1994; 15: 2045 Agarwal B, Bhendwal S, Halmos B, Moss SF, Ramey WG, Holt PR. Lovastatin augments apoptosis induced by chemotherapeutic agents in colon cancer cells. Clin Cancer Res 1999; 5: 2223 Agarwal B, Rao CV, Bhendwal S, et al. Lovastatin augments sulindacinduced apoptosis in colon cancer cells and potentiates chemopreventive effects of sulindac. Gastroenterology 1999; 117: 838 Agarwal B, Halmos B, Feoktistov AS, et al. Mechanism of lovastatin-induced apoptosis in intestinal epithelial cells. Carcinogenesis 2002; 23: 521 Sacks FM, Pfeffer MA, Moye LA, et al. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events Trial investigators. N Engl J Med 1996; 335: 1001 Pederson TR, Berge K, Cook TJ, et al. Safety and tolerability of cholesterol lowering agents with simvastatin during 5 years in Scandinavian simvastatin survival study. Arch Intern Med 1996; 156: 3085 Bjerre LM, LeLorier J. Do statins cause cancer? A meta-analysis of large randomized clinical trials. J Med 2003; 110: 738 Greenberg ER, Baron JA, Tosteson TD, et al. A clinical trial of antioxidant vitamins to prevent colorectal adenoma. Polyp Prevention Study Group. N Engl J Med 1994; 331: 141 Baron JA, Beach M, Mandel JS, et al. Calcium supplements for the prevention of colorectal adenomas. Calcium Polyp Prevention Study Group. N Engl J Med 1999; 340: 101 Baron JA, Cole BF, Sandler RS, et al. A randomized trial of aspirin to prevent colorectal adenomas. N Engl J Med 2003; 348: 891!
We found that lovastatin and simvastatin inhibited cell proliferation by provoking g0 g1 phase arrest with concomitant depression of the proliferation antigen ki-67 mib- lovastatin at high concentrations of 20 micromol l caused cell death in the presence of serum but not under serum starved conditions, which was verified on the basis of increased dna strand breaks, decreased dna content and morphological alterations seen by electron microscopy and starlix.
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Variables Heart rate Systolic BP Diastolic BP Lipids, mg dL Total cholesterol Triglycerides LDL cholesterol Apolipoprotein B HDL cholesterol Apolipoprotein A-I Vasomotor function, % Flow-mediated dilation Nitroglycerin dilation Nitrate, mol L Malondialdehyde, mol L Cytokines and hemostasis MCP-1, pg mL C-reactive protein, mg L PAI-1, ng mL 194 8 1.9 ; 64 4 178 ; * 1.1 1.11.8 ; 0% ; * 63 4 7 ; 174 ; 1.1 1.12.2 ; 18% ; 53 3 17 ; 0.015 0.150 0.003 ; 13.01 0.60 10 ; 83 1.17 0.07 ; * 4.56 0.22 12.36 ; 12.83 0.57 6 ; 74 1.01 0.07 ; 0.001 0.379 0.115 ; 143 8 11 ; 154 4 8 ; * 247 6 202 ; 148 10 20 ; 153 4 6 ; * 0.164 0.145 0.211 Baseline 1 71 2 Simvastatin S ; 71 2 131 0 2 ; Baseline 2 72 2 Combination C ; 71 2 126 ; 0.819 0.048 0.021.
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However, prospective placebo-controlled trials of atorvastatin or simvastatin in definite ms are difficult to perform due to ethical and financial objections.
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On the domestic front, 3M completed its acquisition of Corning Precision Lens Inc., the largest worldwide manufacturer of lens systems for rear projection televisions, in December 2002. The Cincinnati-based company became a subsidiary of the 3M Optical Systems Division, operating under the name 3M Precision Optics Inc., and complementing the company's already-strong repertoire of display technology for mobile phones, palm devices and projectors. Another newsworthy acquisition came in April 2003, when 3M took over GuardiaNet Systems, Inc., a leading software company whose products manage access to and collect fees for the use of library resources, such as computers, printers, copiers, audiovisual equipment and meeting rooms. The transaction is expected to help 3M build on its ability to serve the public library market. In August 2004 3M acquired Info-X Inc., a medical coding compliance software and data provider that should bolster the services provided by 3M's Health Information Systems Division. In an effort to expand its line of safety products, 3M bought Gagnef, Sweden-based Hornell International for $100 million in January 2004. Hornell's products include Speedglas helmets, which filter light and protect welder's eyes, and Adflo respirators and
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Atorvastatin vs. Simvastatin In der CHESS Studie traten unter Atorvastatin mehr Therapieabbrche wegen unerwnschter Ereignisse auf als unter Simvastatin 14% vs. 6% ; . Unter Annahme vorliegender statistischer Signifikanz Fishers exact test, 2-seitig: p 0, 001 ; blieb dieses Ergebnis auch nach Durchfhrung einer best worst case Analyse robust. In der Studie von Illingworth et al. traten ebenfalls mehr Therapieabbrche wegen unerwnschter Ereignisse unter Atorvastatin als unter Simvastatin auf 6, 9% vs. 3, 1% ; . Unter Annahme vorliegender statistischer Signifikanz Fishers exact test, 2-seitig: p 0, 025 ; blieb dieses Ergebnis nach Durchfhrung einer best worst case Analyse nicht robust. Eine metaanalytische Zusammenfassung beider Studien zeigt, dass Therapieabbrche wegen unerwnschter Ereignisse statistisch signifikant hufiger unter Atorvastatin auftreten als unter Simvastatin Abbildung 6.
Comment: This was a four phase crossover study. Reference: Ducharme MP; Warbasse LH; Edwards DJ 1995 ; Disposition of intravenous and oral cyclosporine after administration with grapefruit juice Clin Pharmacol Ther. 57 5: 485-491 and
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In july 2001, the company acquired rosetta inpharmatics, inc, a publicly-held washington based informational genomics company that designs and develops unique technologies to efficiently analyze gene data to predict how medical compounds will interact with different kinds of cells in the body, for example, atorvastatin versus simvastatin.
Endothelial cell line treated with varying concentrations of simvastatin. As shown, endothelial cells transfected with the eNOS transgene were used as a positive control for the immunoblot Fig. 5A ; . These positive control cells were produced by incubating endothelial cells with 5 106 plaque-forming units of adenoviral construct that carries cDNA for eNOS and is driven by SV40 promoter as described previously by our laboratory 6 ; . As displayed in Fig. 5B, sjmvastatin increased eNOS protein levels in a dose-dependent manner. Treatment with 10 and 20 M zimvastatin increased eNOS levels by 114.7 39.9 and 212.0 75.0% II g protein, n 8; both P 0.05, respectively, compared with control. Effects of simvasstatin on hemodynamics in CHF. Changes in body weight, systolic and diastolic pressures, LV dP dt, and LVEDP after MI are listed in Table 1. The important changes in heart failure after MI were decreased LV dP dt and increased LVEDP. Right ventricular RV ; weight was increased, although LV weight-to-body weight was unchanged. These data are consistent with previous reports from our laboratory in the same model 8 ; . In normal rats, simvastatin treatment decreased both mean arterial pressure MAP ; and LV dP dt 116 4 vs. 105 6.7 mmHg and 7, 938 703 vs. 4, 289 673 mmHg s, respectively, n and terbinafine.
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Azie NE, Brater DC, Becker PA, Jones DR and Hall SD 1998 ; The interaction of diltiazem with lovastatin and pravastatin. Clin Pharmacol Ther 64: 369 377. Bensoussan C, Delaforge M and Mansuy D 1995 ; Particular ability of cytochromes P450 3A to form inhibitory P450-iron-metabolite complexes upon metabolic oxidation of aminodrugs. Biochem Pharmacol 49: 591 602. Buening MK and Franklin MR 1976 ; SKF 525-A inhibition, induction, and 452-nm complex formation. Drug Metab Dispos 4: 244 255. Eagling VA, Tjia JF and Back DJ 1998 ; Differential selectivity of cytochrome P450 inhibitors against probe substrates in human and rat liver microsomes. Br J Clin Pharmacol 45: 107114. Fonne-Pfister R and Meyer UA 1988 ; Xenobiotic and endobiotic inhibitors of cytochrome P-450db1 function, the target of the debrisoquine sparteine type polymorphism. Biochem Pharmacol 37: 3829 3835. Franklin MR 1991 ; Cytochrome P450 metabolic intermediate complexes from macrolide antibiotics and related compounds. Methods Enzymol 206: 559 573. Fukunaga Y, Miyashita A, Iwatsubo T, Noguchi K, Watanabe T and Higuchi S 1998 ; Identification of the human liver cytochrome P-450 isozymes involved in nicardipine metabolism. ISSX Proc 13: 124. Guengerich FP 1988 ; Oxidation of 17 -ethynylestradiol by human liver cytochrome P-450. Mol Pharmacol 33: 500 508. Halliday RC, Jones BC, Smith DA, Kitteringham NR and Park BK 1995 ; An investigation of the interaction between halofantrine, CYP2D6 and CYP3A4: Studies with human liver microsomes and heterologous enzyme expression systems. Br J Clin Pharmacol 40: 369 378. Hunt BA, Self TH, Lalonde RL and Bottorff MB 1989 ; Calcium channel blockers as inhibitors of drug metabolism. Chest 96: 393399. Kantola T, Kivisto KT and Neuvonen PJ 1998 ; Erythromycin and verapamil considerably increase serum simvastatin and simvastatin acid concentrations. Clin Pharmacol Ther 64: 177 182. Kelly JG and O'Malley K 1992 ; Clinical pharmacokinetics of calcium antagonists: An update. Clin Pharmacokinet 22: 416 433. Kirch W, Kleinbloesem CH and Belz GG 1990 ; Drug interactions with calcium antagonists. Pharmacol Ther 45: 109 136. Kroemer HK, Gautier J-C, Beaune P, Henderson C, Wolf CR and Eichelbaum M 1993.
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ORL J Otorhinolaryngol Relat Spec. 2007; 69 2 ; : 107-12. Porubsky C, Stiegler P, Matzi V, Lipp C, Kontaxis A, Klemen H, Walch C, Smolle-Juttner F Division of Thoracic Surgery and Hyperbaric Medicine, University of Medicine, Graz, Austria. christian. porubsky klinikum-graz.
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Antiplatelet drugs, together with antihypertensive and lipid-lowering agents, form part of the panoply of drugs that are used in the long-term management of patients who have experienced an episode of acs.
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Sphincter of Oddi. This state is accomplished simply by having the patient fast overnight. It ap pears reasonable not to pre-empty bile from the gallbladder by administering CCK-8 because it takes several minutes for the gallbladder to empty bile after the injection of CCK-8 and it takes sev eral hours for the gallbladder to refill, primarily because of slow pressure build-up as the sphincter of Oddi narrows gradually 17 ; . CCK-8 is a synthetic preparation that consists of only the last eight peptides of its parent mole cule CCK-33. Most of the injected CCK-8 mol ecules occupy the receptors in the normal gallbladder, which enables it to empty bile almost completely. In patients with chronic cholecystitis, the total number of receptors is reduced, which accounts for the decreased bile emptying that re sults when these patients receive CCK-8 Fig 2 ; . The widely used normal ejection fraction value of 35% or greater is established by infusing 3.3 ng kg min of CCK-8 for 3 minutes. Larger doses 20 40 ng often cause severe abdominal pain, with decreased or no bile emptying in healthy subjects. For gallbladder ejection fraction protocol, images are obtained up to 60 minutes after radiopharmaceutical injection or until the gallbladder is visualized. Data are collected for 20 minutes after slow 3 minutes ; intravenous infu sion of CCK-8. An ejection fraction of less than 35% is indicative of chronic cholecystitis with a greater than 90% positive predictive value 17, 18 ; . Compared with a 3-minute infusion and sporanox.
Vaginal discharge Vaginal discharge is most commonly caused by vaginitis but may also be the result of cervicitis. N. gonorrhoeae and C. trachomatis infection cause cervicitis, and T. vaginalis, C. albicans and a synergistic combination of Gardnerella sp. and anaerobic bacterial infection bacterial vaginosis ; cause vaginitis. Effective management of cervicitis is more important from a public health point of view, as cervicitis may have serious sequelae. However, clinical differentiation between the two conditions is difficult. Women attending for vaginal discharge should be asked if the partner has symptoms. They should automatically be treated for cervicitis if the partner complains of discharge. All women having complaints of discharge should be examined with a speculum. Other gynaecological pathology should be excluded by speculum and bimanual examination Fig. 11, 12.
Miner, L.L., Dmgo, J., Chamberlain, PM., Donovan, D., & Uhl, G.R. 1995 ; . Retained cocaine place preference in 01 deficient mice. Neummport. 6, 2314-2316. Milligan, G. 1983 ; . Agonist regulation of cellular G protein levels and distribution: mechanisms and fundional implications. Tmnds Pharmacul Sci. 14, 413-418. Milligan, G., Parenti, M., & Magee, AL. 1995 ; . The dynamic rote of palmitoylation in signal transduction. Trends Biochem Sci. 20, 181-186. Milligan, G., Wise, A., MacEwan, 0.J., Grassie, MA., Kennedy, F.R., Lee, T.W., Adie, E.J., Kim, G.D., McCallum, J.F., Burt, I., C m , C., Svoboda, P., Shah, B.H., & Mullaney, 1. 1995 ; . Mechanisms of agonist-induced G-protein elimination. B k Soc Trens. 23, 166-170. Miserendino, M.J.D., & Nestler, E.J. 1995 ; . Behavioral sensitization to cocaine: modulation by the cydic AM? system in the nudeus acaimbens. Brain Research. 674, 299-306. Missale, C., Nash, SR., Robinson, S.W., Jaber, M., & Caron, M.G. 1998 ; . Dopamine receptom: frwn structure to function. Physiol Rev. 78, 18922s.
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