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Document 81. Brandstetter H, Kuhne A, Bode W, Huber R, von der Saal W, Wirthensohn K, Engh RA. J Biol Chem 1996; 47:29988–29992. http://legacy.netlibrary.com/nlreader/nlReader.dll?bookid=12640&filename=Page_294.html (2 of 2) [4/5/2004 5:17:42 PM]
Document 12 Polypeptide Modulators of Sodium Channel Function as a Basis for the Development of Novel Cardiac Stimulants Raymond S. Norton Biomolecular Research Institute, Parkville, Victoria, Australia I. Introduction Page 295 Cardiovascular diseases remain one of the major causes of premature death in western societies. Chronic congestive heart failure (CHF) in particular is a common disease with a poor prognosis, median survival times after the onset of heart failure being 1.7 years in men and 3.2 years in women [1]. Current treatment relies on diuretics to reduce fluid volume, vasodilators to decrease the work load of the heart, and positive inotropic agents to increase cardiac contractility [2]. The most commonly prescribed of the positive inotropes is the cardiac glycoside digoxin (Figure 1) [3]. Although this drug has been in therapeutic use for over two hundred years, its efficacy in patients with a sinus rhythm has remained controversial, and evidence for its beneficial effects is quite recent [3–5]. It is also possible that these beneficial effects are not due solely to the positive inotropic activity of digoxin and that its neurohormonal effects may also be important [2, 5–7] Nevertheless, digoxin remains a widely used drug [3] and it follows that a suitable replacement or adjunct would find access to a significant market worldwide. The incentive to develop such a replacement follows from the low therapeutic index of digoxin [8,9] and the relatively common occurrence of side effects due to digitalis toxicity. In the 1960s and 1970s, 20–30% of patients receiving digitalis experienced serious toxicity and about one quarter of this group died [6, 10]. Digitalis toxicity is manifest in CNS side-effects such as http://legacy.netlibrary.com/nlreader/nlReader.dll?bookid=12640&filename=Page_295.html [4/5/2004 5:17:59 PM]
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Structure-based Drug Design 14 Stru
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Document 163. Lacey SF, Larder BA.
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Document Page 125 binding site on t
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Document We determined the structur
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Document large solvent channels and
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Document Page 166 As predicated, th
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Document References 1. Parks RE Jr.
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Document 17. Ealick SE, Rule SA, Ca
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Document 6 Structural Implications
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Document Page 176 0.43 Å) as the c
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Document IX. S2' Interactions Page
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Document Important for the validity
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Document Figure 4 Amino acids impor
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Document III. Results and Discussio
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Document Page 202 269, and valine-2
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Document Figure 6 Structure of α h
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Document Page 205 enzyme and of phe
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Document Page 207 sure and the acti
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Document 29. Baker ME. Genealogy of
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Document 2. Blundell TL, Cooper J,
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Document 17. Szelke M. Chemistry of
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Document Table 1 Approval Indicatio
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Document Page 438 proteins. One pot
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Document Page 441 sequence of the m
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Document Page 488 against most of t
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Document A. The Canyon Page 491 The
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Document Subsequent studies have sh
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Document Page 495 of the RNA and pr
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Document Figure 4 A ribbon diagram
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Document Figure 5 Some compounds wh
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Document Figure 7 HRV14 VP1 hydroph
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Document D ddI, 152 tumour necrosis
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Document Phosphoglycerate kinase (P
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Document [Protease targets] serinyl
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