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Results Study population A total of 264 women were randomized in six centres, of whom 257 were subsequently treated with rFSH Figure 1 ; . The number of patients treated per centre ranged between 15 and 76. The 150 IU daily dose treatment was given to 131 women low-dose group ; , compared with 126 women in the 200 IU group high-dose group ; . Both groups had comparable demographic and infertility characteristics Table I ; . The main causes of infertility were male and tubal infertility. Early follicular serum FSH concentrations were 6.3 IU l SD 1.8 ; and 6.1 IU l SD 1.6 ; in the low- and high-dose groups, respectively. Cycle cancellations In the 150 IU group, the cycle was cancelled prior to oocyte retrieval in four women 3.1% ; because of insufcient ovarian response n 3 ; and premature luteinization n 1 ; . the 92.
Summary of patient demographic and clinical characteristics at baseline for all randomised patients Fluvastatin XL 80 mg n 370 ; 193: 177 58 + 12 2187 ; 27 + 3 42% 30% n 369 7.19 + 0.85 4.94 + 0.80 1.29 + 0.31 4.0 + 1.1 2.07 + 0.81 3.88 + 0.65 4.63 + 0.62 Fluvastatin IR 40 mg n 185 ; 88: 97 57 + 1885 ; 28 + 4 41% 27% n 183 7.21 + 1.01 5.02 + 0.96 1.27 + 0.31 4.2 + 1.3 2.11 + 0.81 3.83 + 0.70 4.68 + 0.78.
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2.23 to .29 ; in all managed care plans from January 1999 to December 2000, evaluated using February 2001 wholesale acquisition cost WAC ; prices. The contribution of each brand is broken out into a dosage effect, based on the dosage mix of the brand, and a share effect, based on the brand's share of market. The investigators compute the dosage effect by holding the brand's market share constant and computing the change in overall statin cost per dose resulting only from changes in the brand's dosage mix. Conversely, the investigators compute the share effect by holding the brand's dosage mix constant and computing the change in overall statin cost per dose resulting only from changes in the brand's market share. Based on the results shown in Table 5, fluvastatin made the greatest contribution to the change in overall statin cost per dose, a 5.2-cents-perdose increase, due to its drop in share and relatively low WAC price. The other brands contributed to the overall change in cost per dose in differ.
For certain analyses included anti-human glycophorin A GlyA ; -PE 10F7 ; , anti-human CD33-PE BD ; , anti-human CD41a-PE Pharmacia Biotech, Quebec, Canada ; and anti-human CD38-PE BD ; . Frequencies of lympho-myeloid stem repopulating referred to as competitive repopulating units or CRUs ; 6-7 were calculated from the proportions of mice in a given experiment, or set of identical experiments, that were negative for lympho-myeloid engraftment using Poisson statistics and the method of maximum likelihood with the assistance of the L-calc software StemCell.
11: 48AM NF.00002 Capillary self-assembly of floating bodies , SUNGHWAN JUNG, PAUL THOMPSON, JOHN BUSH, Department of Mathematics, Massachusetts Institute of Technology -- We study the self-assembly of bodies supported on the water surface by surface tension. Attractive and repulsive capillary forces exist between menisci of, respectively, the same and opposite signs. In nature, floating objects e.g. mosquito larvae ; thus interact through capillary forces to form coherent packings on the water surface. We here present the results of an experimental investigation of such capillary pattern formation. Thin elliptical metal sheets were designed to have variable shape, flexibility and mass distribution. On the water surface, mono-, bi-, or tri-polar menisci could thus be achieved. The influence of the form of the menisci on the packings arising from the interaction of multiple floaters is explored. Biological applications are discussed and focalin.
| Fluvastatin takingThe high prevalence of obesity in New Zealand and its associated co-morbidities suggests that obesity is likely to command a significant portion of the total health care costs incurred by any government agency. Three component costs have been identified: the direct treatment cost to the individual and the service provider the opportunity costs to the individual and society arising from premature death or attributable morbidity the indirect costs to the individual and society of lost work production due to absenteeism from work and premature death.
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University of Washington S.M.O. ; , Seattle, Washington 98195; University of Colorado Health Sciences Center W.E.H., P.D.M. ; , Denver, Colorado 80262; and Emory University School of Medicine G.C. W., N.B. W. ; , Atlanta, Georgia 30322 ABSTRACT and follistim.
Bioinformatics and applied genomics for identifying targets for drugs and elucidation of pathogenesis and risk factors * Genetic and entomological studies on vectors e.g. mechanisms of resistance, adaptation to ecological changes.
| Compared with angioplasty in stable coronary artery disease. N Engl J Med 341: 70 76 Jacobson TA 2000 "The lower the better" in hypercholesterolemia therapy: a reliable clinical guideline? Ann Intern Med 133: 549 554 Fazio S, Linton MF 1998 On the relationship between cholesterol lowering and coronary disease event rate. Circulation 98: 26452646 Iso H, Jacobs DR, Wentworth D, Neaton JD, Cohen JD 1989 Serum cholesterol levels and six-year mortality from stroke in 350, 977 men screened for the Multiple Risk Factor Intervention Trial. N Engl J Med 320: 904 910 Yano K, Reed DM, MacLean CH 1989 Serum cholesterol and hemorrhagic stroke in the Honolulu Heart Program. Stroke 20: 1460 1465 Crouse III JR, Furberg CD 2000 Treatment of dyslipidemia. Room for improvement? Arterioscler Thromb Vasc Biol 20: 23332335 Ridker 1999 Evaluating novel cardiovascular risk factors: can we better predict heart attacks? Ann Intern Med 130: 933937 Oparil S, Oberman A 1999 Nontraditional cardiovascular risk factors. J Med Sci 317: 193207 Gotto Jr 2001 Low high-density lipoprotein cholesterol as a risk factor in coronary heart disease. A Working Group report. Circulation 103: 2213 2218 Havel RJ 2000 Remnant lipoproteins as therapeutic targets. Curr Opin Lipidol 11: 615 620 Rubins HB, Robins SJ, Collins D, Fye CL, Anderson JW, Elam MB, Faas FH, Linares E, Schaefer EJ, Schectman G, Wilt TJ, Wittes J 1999 Gemfibrozil for the secondary prevention of coronary heart disease in men with low levels of high-density lipoprotein cholesterol. N Engl J Med 341: 410 418 The Expert Panel 1988 Report of the National Cholesterol Education Program Expert Panel on detection, evaluation, and treatment of high blood cholesterol in adults. Arch Intern Med 148: 36 69 The Expert Panel 1993 Summary of the second report of the National Cholesterol Education Program NCEP ; Expert Panel on detection, evaluation, and treatment of high blood cholesterol in adults Adult Treatment Panel II ; . JAMA 269: 30153023 Frick MH, Elo O, Haapa K, Heinonen OP, Heinsalmi P, Helo P, Huttunen JK, Kaitaniemi P, Koskinen P, Manninen V 1987 Helsinki Heart Study: primary-prevention trial with gemfibrozil in middle-aged men with dyslipidemia. N Engl J Med 317: 12371245 Boden WE, Pearson TA 2000 Raising low levels of high-density lipoprotein cholesterol is an important target of therapy. J Cardiol 85: 645 650 Thompson GR, Barter PJ 2000 Therapeutic approaches to reducing the LDLand HDL-associated risks of coronary heart disease. Curr Opin Lipidol 11: 567570 Robins SJ, Collins D, Wittes JT, Papademetriou V, Deedwania PC, Schaefer EJ, McNamara JR, Kashyap ML, Hershman JM, Wexler LF, Rubins HB; VA-HIT Study Group. Veterans Affairs High-Density Lipoprotein Intervention Trial 2001 Relation of gemfibrozil treatment and lipid levels with major coronary events: VA-HIT: a randomized controlled trial. JAMA 285: 15851591 Ruotolo G, Ericsson CG, Tettamanti C, Karpe F, Grip L, Svane B, Nilsson J, de Faire U, Hamsten A 1998 Treatment effects on serum lipoprotein lipids, apolipoproteins and low density lipoprotein particle size and relationships of lipoprotein variable to progression of coronary artery disease in the bezafibrate coronary atherosclerosis intervention trial BECAIT ; . J Coll Cardiol 32: 1648 1656 Herd JA, Ballantyne CM, Farmer JA, Ferguson 3rd JJ, Jones PH, West MS, Gould KL, Gotto Jr AM, for the LCAS Investigators 1997 Effects of fluvastatin on coronary atherosclerosis in patients with mild to moderate cholesterol elevations [Lipoprotein and Coronary Atherosclerosis Study LCAS ; ]. J Cardiol 80: 278 286 Syvanne M, Nieminen M, Frick MH, Kauma H, Majahalme S, Virtanen V, Kesaniemi YA, Pasternack A, Ehnholm C, Taskinen MR 1998 Associations between lipoproteins and the progression of coronary and vein-graft atherosclerosis in a controlled trial with gemfibrozil in men with low baseline levels of HDL cholesterol. Circulation 98: 19931999 Brown G, Albers JJ, Fisher LD, Schaefer SM, Lin JT, Kaplan C, Zhao XQ, Bisson BD, Fitzpatrick VF, Dodge HT 1990 Regression of coronary artery disease as a result of intensive lipid-lowering therapy in men with high levels of apolipoprotein B. N Engl J Med 323: 1289 1298 Brown BG, Zhao XQ, Chait A, Fisher LD, Dowdy A, Cheung M, Morse JJ, Serafini L, Huss-Frechette E 2000 Niacin plus simvastatin, but not antioxidant vitamins, protect against atherosclerosis and clinical events in CAD patients with low HDLC. Circulation 102 Suppl II ; : II506 Oberman A, Kreisberg RA 2000 Hypertriglyceridemia and coronary heart disease. J Clin Endocrinol Metab 85: 2098 2105 Miller M 1999 The epidemiology of triglyceride as a coronary artery disease risk factor. Clin Cardiol 22: II-1II-6 Sacks FM, Alaupovic P, Moye LA, Cole TG, Sussex B, Stampfer MJ, Pfeffer MA, Braunwald E 2000 VLDL, apolipoproteins B, CIII, and E, and risk of recurrent coronary events in the cholesterol and recurrent events CARE ; trial. Circulation 102: 1886 1892 Thompson GR, Barter PJ 1999 Clinical lipidology at the end of the millennium. Curr Opin Lipidol 10: 521526 and formoterol.
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1991: 48-9 ; analyses the contribution of information encoded by mood to the interpretation of 32 ; : John, you are calm Clark's 35 According to Clark, what the hearer of 32 ; is licensed to assume, given the semantically encoded information in declarative syntax, is 32' ; : 32' ; The proposition that John Smith has the property of being calm represents a thought entertained as a description of an actual or possible state of affairs. This encoded information is then combined with contextual assumptions as the hearer infers the speaker's intended message. Compare this with how the utterance would be interpreted on the current account. The decoding of the utterance would make the following assumption manifest to the hearer: 32'' ; The speaker has said that John Smith is calm The fact that indicative mood has been used to express the proposition that John Smith is calm would mean that two inferential routes for the interpretation of the utterance were open: one exploring the implications of 32'' ; and another exploring the implications of the proposition that John Smith is calm. If this second route resulted in adequate cognitive effects for expectations of relevance to be fulfilled, then the main relevance of the utterance would lie down this route and the speaker would be taken to have asserted the proposition that John Smith is calm. If, however, the first route proved the more fruitful then an alternative interpretation would be arrived at, one in which the speaker was not taken to have asserted the propositional content of the sentence uttered, as in cases of irony or reported speech. Notice two things here: firstly the hearer is not entertaining assumptions about what is encoded by the choice of mood; secondly he is not entertaining thoughts about the type of world the proposition expressed is presented as representing. A `real' semantics analysis of the communicated message, couched in possible worlds terminology, is of course possible, but it plays no role in the mental life of the hearer and forteo.
Allergies: Tell your doctor if you have ever had any unusual or allergic reactions with the previous use of Vytorin or drugs such as Zocor simvastatin ; , Zetia ezetimibe ; , Lipitor atorvastatin ; , Lescol fluvastatin ; or Pravachol pravastatin ; . Other medicines: Before starting Vytorin, tell your doctor about ALL drugs you take. This includes prescription and nonprescription medicines, vitamins, and herbal products. Alcohol: Tell your doctor if you have ever had a history of alcohol problems. Other health problems: Tell your doctor if you have ever had any other medical problems such as liver or kidney disease. For women: Vytorin should not be taken by a woman of childbearing age unless she is using a reliable method of birth control. The effect of Vytorin on a fetus is unknown.
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Oleoyl-Estrone for the Treatment of Overweight and Obesity Obesity is a public health issue of epidemic proportions. Diet and exercise are the safest and most effective methods of losing weight, but their effects are generally slow, and many people find the regimens difficult to maintain. Consequently, most overweight obese patients lose only moderate amounts of weight and are unable to keep the weight off. Most current medications for obesity must be used in conjunction with diet and exercise but provide only small increases in weight loss; more importantly, they have substantial side effects that limit their use. Oleoyl-estrone, Manhattan's lead compound, is a small molecule that was developed by researchers at the University of Barcelona, Spain. Unlike many weight-loss drugs, oleoyl-estrone is effective with oral administration. In preclinical animal studies, oleoyl-estrone achieved weight loss and body-fat reduction even with unrestricted food intake. Manhattan's weight-control agent also acts on some of the diseases associated with obesity: Lowers arterial tension, thus reducing hypertension and fortovase.
Several mechanisms could account for the plaque-stabilizing effect of statins that was elegantly demonstrated in animal models.41 Reduction of LDL-cholesterol may contribute to the downsizing of the lipid core.42 Statins inhibit uptake of oxidized LDL by CD36, 43 scavenger receptor A, 44 and lectin-like oxidized LDL LOX-1 ; receptor45 and inhibit macrophage oxidative properties.24 These effects of statins could theoretically contribute to reduced foam cell formation. Elevated plasma levels of several markers of the inflammatory cascade have been shown to predict future risk of plaque rupture. These markers include P-selectin, interleukin-6, tumor necrosis factor- , soluble ICAM-1, and CRP.36 The beneficial effect of statins on the inflammatory process has been discussed above. Weakening of the fibrous cap in unstable plaques is associated with increased production of matrix metalloproteinases MMPs ; by macrophages. In cultured macrophage, fluvastatin decreased the activity of MMP-9 by 20% to 40%.46 In a study in humans, 47 pravastatin treatment changed the composition of carotid artery plaques in a manner that favored stabilization. Patients with carotid artery stenosis received either pravastatin 40 mg d or no therapy for 3 months before carotid endarterectomy. Plaques removed from the statin-treated group were composed of significantly less lipid and oxidized LDL, fewer macrophages, and fewer T cells. They had higher collagen content and demonstrated less MMP-2 immunoreactivity than control plaques. In addition, apoptosis was significantly reduced and immunoreactivity to tissue inhibitor of metalloproteinase-1 a potent inhibitor of MMP-1 and MMP-9 ; was significantly increased in the pravastatin group compared with controls.47.
Is decreased LDL levels by 10 to percent. HDL levels increase about 5 percent. Triglycerides may also rise initially, but they return to baseline within a few weeks. Reductase inhibitors atorvastatin [Lipitor], fluvastatin [Lescol], lovastatin [Mevacor], pravastatin [Pravachol], rosuvastatin [Crestor], and simvastatin [Zocor] ; block synthesis of cholesterol in the liver by competitively inhibiting HMG-CoA reductase activity. They induce an increase in high-affinity LDL receptors, resulting in an increased catabolism of LDL and an increase in the liver's extraction of LDL precursors. The net result is decreased LDL levels by 25 to percent. Modest decreases in triglycerides of 12 to percent and increases in HDL of 8 to percent also occur and fosamprenavir.
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Hydroxy-3-methylglutaryl coenzyme a reductase inhibitor. Am] Cardiol1995; 76: 37A-40A. 15. Greten H, Beil FU, 5chneider], et al. Treatment of primary hypercholesterolemia: fluvastatin vs bezafibrate. Am] Med 1994; 96 sup 4A ; : 395-425 and fluvastatin.
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