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With cholestyramine was added after week 12 to all patients in the study with baseline LDL-C values 4.1 mmol L. These baseline levels were present in 25% of the study population. The primary endpoint, assessed by QCA, was within-patient per-lesion change in minimum lumen diameter MLD ; of qualifying lesions. QCA were evaluated at baseline and 2.5 years. LESCOL * significantly slowed the progression of coronary atherosclerosis. Primary endpoint analysis showed significantly less progression in the all LESCOL * cholesterolamine ; versus all placebo patients change in MLD -0.028 mm versus -0.100 mm, p 0.01 ; and for fluvastatin alone versus placebo alone change in MLD -0.024 versus -0.094 mm, p 0.02 ; . Beneficial trends with treatment were consistently seen in clinical event rates new occurrence or worsening of angina, coronary revascularization procedures [PTCA] or CABG surgery, myocardial infarction [MI] and total mortality ; within the 2.5 years treatment, but were not statistically significant. This trial was however not designed to demonstrate a reduction in the risk of coronary morbidity and mortality.
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Goal LDL level and dosage, cost * and efficacy of different statins Baseline LDL level 130 to 159 mg per dL 3.35 to 4.10 mmol per L ; 130 mg per dL patients without CHD or diabetes ; Cerivastatin Baycol ; , one 0.3-mg tablet daily; $40 per month; lowers LDL 30% or Pravastatin Pravachol ; , one half of a 20-mg tablet daily; $34 per month; lowers LDL 19% or Atorvastatin, one half of a 20-mg tablet daily; $45 per month; lowers LDL 38% or Fluvastatin Lescoll ; , 20-mg or 40-mg tablet daily; $40 per month; lowers LDL 17% to 23% 160 to 189 mg per dL 4.15 to 4.90 mmol per L ; Cerivastatin, 0.4-mg tablet daily; $40 per month; lowers LDL 36% or Atorvastatin, one half of a 20-mg tablet daily; $45 per month; lowers LDL 38% or Atorvastatin, 10-mg tablet daily; $55 per month; lowers LDL 38% or Simvastatin, one half of a 40-mg tablet daily; $57 per month; lowers LDL 35% or Simvastatin, 20-mg tablet daily; $114 per month; lowers LDL 35% 190 mg per dL 4.90 mmol per L ; Atorvastatin, one half or one 40-mg tablet daily; $53 to $105 per month; lowers LDL 46% to 51% or Simvastatin, one half to one 80-mg tablet daily; $57 to $114 per month; lowers LDL 40% to 48% LDL low-density lipoprotein cholesterol; CHD coronary heart disease. * --Estimated cost to the pharmacist based on average wholesale prices rounded to the nearest dollar ; in Red Book. Montvale, N.J.: Medical Economics Data, 1999. Cost to the patient may be greater, depending on prescription filling fee. Information from Jones P, Kafonek S, Laurora I, Hunninghake D. Comparative dose efficacy study of atorvastatin versus simvastatin, pravastatin, lovastatin, and fluvastatin in patients with hypercholesterolemia the CURVES study ; . J Cardiol 1998; 81: 582-7 [Published erratum appears in J Cardiol 1998; 82: 128], and Sasaki J, Arakawa K, Yamamoto K, Kobori S, Ageta M, Kono S. A long-term comparative trial of cerivastatin sodium, a new HMG-CoA reductase inhibitor, in patients with primary hypercholesterolemia. Clin Ther 1998; 20: 539-48. Atorvastatin, one or two 40-mg tablets or one 80-mg tablet daily; $105 to $210 per month; lowers LDL 51% to 54% or Simvastatin, 80-mg tablet daily; $114 per month; lowers LDL 48% 100 mg per dL patients with CHD or diabetes ; Cerivastatin, 0.4-mg tablet daily; $40 per month; lowers LDL 36% or Atorvastatin Lipitor ; , one half of a 20-mg tablet daily; $45 per month; lowers LDL 38% or Atorvastatin, 10-mg tablet daily; $55 per month; lowers LDL 38% or Simvastatin Zocor ; , one half of a 40-mg tablet daily; $57 per month; lowers LDL 35% Atorvastatin, one half of a 40-mg tablet daily; $53 per month; lowers LDL 46% or Simvastatin, one half of an 80-mg tablet daily; $57 per month; lowers LDL 40% or Atorvastatin, 20-mg tablet daily; $90 per month; lowers LDL 46% or Pravastatin, two 40-mg tablets daily; $224 per month; lowers LDL 40.
Sunday May 21, 2006 Continued 1: 00 1: Medical Office Time Management Dr. Benjamin Burko In his first session, Dr. Burko will discuss how to create time where there seems to be none ; and use this time to either see more patients, or enhance the quality of each patient visit or create more free-time as well as practical techniques to achieve these objectives. In addition, innovative sources of practice revenue shall be explored 1: 50 Question & Answer Session Break break 2: 00 2: Doctoring dangerous to your health? Dr. Olaf Aasland In his second session, Dr. Aasland will discuss stress, coping and social support along with the modern patient-doctor relationship. He will also discuss physician health with emphasis on status and gender differences and how medical errors affect the doctors' work and lives. 2: 50 3: Question & Answer Session.
THE Joui .r' OF NUCLEARMEDICINE ol. 41 o. 6 une 2000 V N J and levaquin.
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Treatment Of Dysthymia Few studies have examined the pharmacotherapy of dysthymia, possible because of long-held beliefs that nonmajor depressions were less responsive to pharmacotherapy. What data do exist, however, do not support this belief. Most studies are of a relatively short duration of treatment, ranging from 4 to 12 weeks. For this time period there are data to support the use of most classes of antidepressants. These studies are summarized in Table 69.3. Thus, the weight of evidence suggests that most agents that are effective for major depression are also effective for dysthymia, at least in the acute phase of treatment. ACKNOWLEDGMENTS Dr. Keller has received research support and or served as a consultant or on an advisory board for a number of different pharmaceutical companies including Pfizer, Bristol-Myers Squibb, Forrest Laboratories, Wyeth-Ayerst Laboratories, Merck, Janssen, Eli Lilly, Organon, Pharmacia Upjohn, SmithKline Beecham, Zeneca, Mitsubishi Pharmaceuticals, Scirex, Janus Pharmaceuticals, Sepracor Pharmaceuticals, Somerset Pharmaceuticals, and Sanofi-Synthelabo. REFERENCES and levothroid, for example, prednisone.
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Emergency Medicine & Acute Care: A Critical Appraisal Series 24 March 13-17, Cozumel, Mexico March 21-25, Lake Tahoe, NV March 24-27, Orlando, FL March 31-April 3, Los Angeles, CA April 21-24, New Orleans, LA April 29-May 2, Myrtle Beach, SC May 12-15, Chicago, IL May 16-19, Las Vegas, NV June 9-12, San Francisco, CA June 16-19, New York, NY Information: 800-458-4779 16th Annual High Risk Emergency Medicine April 11-12, Las Vegas, NV May 19-20, Las Vegas, NV Information: 800-651-CEME 25th Annual Mammoth Mountain Emergency Medicine Conference March 6-11, Mammoth Lakes, CA Information: 949-650-4156 Wilderness Medicine June 11-17, 2005, Klamath River, CA August 3-7, 2005, Big Sky Resort, MT March 8-12, 2006, Whistler, B.C. May 17-21, 2006, Santa Fe, NM Information: 800-522-8747.
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LANTUS .15 LAPASE .34 LASIX .34 LAXATIVES .38 leflunamide.9 LESCOL .17 leucovorin.22 LEUKERAN.22 leuprolide acetate .22 LEVAQUIN .36 LEVLEN .28, 29 LEVLITE.28 levobunolol hcl .42 levocarnitine .35 levora .28 levothroid.45 levothyroxine sodium.45 levoxyl .45 LEVSIN .45 LEXAPRO .14 LEXIVA.24 LEXXEL.19 LIALDA.36 LIDODERM .32 lindane 1% shampoo.32 LIPITOR .18 LIPRAM.34 lisinopril .19 lisinopril hydrochlorothiazide .19 lithium carbonate .23 LO OVRAL .28 LOCOID .32 LODINE.9 LODINE XL .9 LOESTRIN .28 LOESTRIN FE.28 LOFIBRA.18 LOMOTIL .16 loperamide hcl.16 LOPRESSOR.19, 26 LOPRESSOR HCT.19 LOPROX .32 LORABID .20 loratadine over-the-counter ; .17 loratadine pseudoephedrine.30 LOTEMAX .42.
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| Mevacor vs lescolTable 1: Abnormal scars: etiologic categories Adapted from Choi JM, Rohrer T, Kaminer M, Batra RS. Surgical approaches to patients with scarring. In: Arndt, KA, ed. Scar Revision--Procedures in Cosmetic Dermatology. East Sussex: Elsevier Science. In press.
June 2005. On 28 June 2006, the Board appointed Huw Jones as an independent Nonexecutive Director. He has relevant pharmaceutical commercial experience and the Directors believe his appointment ensures that the composition and breadth of experience of the Board is appropriate for the Company. Simon Best, who has been Nonexecutive Chairman since and loestrin.
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They include pravastatin pravachol ; , simvastatin zocor ; , fluvastatin lescop ; , atorvastatin lipitor ; , and rosuvastatin crestor ; and many others.
| 1. Istvan ES, Deisenhofer J. Structural mechanism for statin inhibition of HMG-CoA reductase. Science. 2001; 292: 11601164. Ballantyne CM, Andrews TC, Hsia JA, et al. Correlation of nonhigh-density lipoprotein cholesterol with apolipoprotein B: effect of 5 hydroxymethylglutaryl coenzyme A reductase inhibitors on nonhigh-density lipoprotein cholesterol levels. J Cardiol. 2001; 88: 265269. Davidson M, Ma P, Stein EA, et al. Comparison of effects on low-density lipoprotein cholesterol and high-density lipoprotein cholesterol with rosuvastatin versus atorvastatin in patients with type IIa or IIb hypercholesterolemia. J Cardiol. 2002; 89: 268275. Schaefer JR, Schweer H, Ikewaki K, et al. Metabolic basis of high density lipoproteins and apolipoprotein A-I increase by HMG-CoA reductase inhibition in healthy subjects and a patient with coronary artery disease. Atherosclerosis. 1999; 144: 177184. Larsen ML, Illingworth DR. Drug treatment of dyslipoproteinemia. Med Clin North Am. 1994; 78: 225245. McTaggart F, Buckett L, Davidson R, et al. Preclinical and clinical pharmacology of rosuvastatin, a new 3-hydroxy-3methylglutaryl coenzyme A reductase inhibitor. J Cardiol. 2001; 87 suppl ; : 28B32B. 7. Martin PD, Dane AL, Schneck DW, et al. Disposition of new HMG-CoA reductase inhibitor ZD4522 following dosing in healthy subjects [abstract]. J Clin Pharmacol. 2000; 40: 1056. Abstract 48. 8. Simonson SG, Martin PD, Mitchell PD, et al. Pharmacokinetics and pharmacodynamics of rosuvastatin in hepatically impaired subjects [abstract]. Clin Pharmacol Ther. 2001; 69: P86. Abstract PIII88. 9. Prescribing information for Lipitor, Zocor, Mevacor, Pravachol, Lescol. Physician's Desk Reference PDR ; . 56th ed. Montvale, NJ: Medical Economics Co Inc; 2002. 10. Lennernas H, Fager F. Pharmacodynamics and pharmacokinetics of the HMG-CoA reductase inhibitors. Clin Pharmacokinet. 1997; 32: 403425. Blum CB. Comparison of properties of four inhibitors of A reductase. J Cardiol. 1994; 73 suppl ; : 3D11D. 12. Knopp RH. Drug treatment of lipid disorders. N Engl J Med. 1999; 341: 498511. Buckett L, Ballard P, Davidson R, et al. Selectivity of ZD4522 for inhibition of cholesterol synthesis in hepatic versus nonhepatic cells [abstract]. Atherosclerosis. 2000; 151: 41. Abstract MoP29: W6 and lorazepam.
317 EXPRESSION OF A FOREIGN ANTIPARASITIC GENE IN TRANSGENIC ANOPHELINE MOSQUITOES. Moreira LA, Daffre S, Jacobs-Lorena M. Centro de Pesquisas Rene RachouFIOCRUZ, Belo Horizonte-MG, Brazil; Departamento de Parasitologia, Universidade de So Paulo, So Paulo-SP, Brazil; Department of Genetics, School of Medicine, Case Western Reserve University, Cleveland, OH. Interference with the mosquito vectorial capacity is an important strategy for malaria control that needs further exploitation. One approach would be to introduce into the mosquito a gene whose product is harmful to the parasite but innocuous to the mosquito. Previously we demonstrated that the Anopheles gambiae carboxypeptidase AgCP ; promoter is strongly and rapidly induced in the midgut of transgenic mosquitoes upon blood ingestion. The transformation of vector species is now routine and recently, it has been demonstrated that transgenic mosquitoes able to block parasite development can be obtained. However, it is important that different antiparasitic genes be available as alternative candidates, because of the likely possibility that parasite strains resistant to the blockage imposed by the transgene will develop. This is a project to construct a hybrid gene using a midgut-specific promoter linked to the antiparasitic gomesin gene. Gomesin is known to kill bacteria, fungi and Leishmania, and preliminary experiments suggest that it also kills Plasmodium while being innocuous to the mosquito. This construct will be inserted into the germ line of Anopheles stephensi and the transgenic mosquitoes will be tested for refractoriness to the parasite. Furthermore, the microinjection technique will be adapted to Brazilian anophelines, such as An. albitarsis and An. aquasalis. The transgenic mosquitoes will then be tested for transmission blockage with human Plasmodium spp. in membrane feeding experiments. The present proposal intends to broaden the study of transgenic mosquitoes in South America, as an alternative strategy for malaria control, for example, lfscol medication.
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Additionally, we gain new sustained-release drug delivery technologies that complement our own capabilities. Andrx technology has resulted in at least one potentially significant partnership, namely our alliance with Takeda Pharmaceutical Company Limited Takeda ; on ACTOplus metTM XR, a promising product for treating diabetes. Longer term, we expect this alliance will provide a significant contribution to our business and a solid return to shareholders. Another benefit of the acquisition is Anda, a stand-alone distribution business which offers over 7, 000 quality pharmaceutical products from manufacturers around the world, directly serving retailers, hospitals and physicians. Anda becomes a new division within Watson, providing us with new service capabilities that will further extend our relationships into the healthcare community. It is no small task to combine two companies. Given the fact that Andrx's assets are highly complementary to our own, the overall integration process has run smoothly and we have already made significant progress on integrating our businesses. Clearly there are some compliance issues to work through with FDA relating to the operation of Andrx's facilities in Davie, Florida, but we believe we have the resources and capabilities to resolve these issues. We are delighted to welcome the 1, 700 Andrx, Anda and VIP employees to Watson and look forward to continued growth in progress, made possible by our newly enhanced operations.
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