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All patients received some type of treatment for APL-st Table 4 ; . In the whole series, 43. Table 4. Survival After High-Dose Chemotherapy With Hematopoietic Stem Cell Rescue and gemzar. Acquired IPR&D programs and technology platforms reaching technological feasibility. In addition, once research is completed, each product candidate acquired from AnorMED, Avigen, Bone Care, Verigen and ILEX Oncology will need to complete a series of clinical trials and receive FDA or other regulatory approvals prior to commercialization. Our current estimates of the time and investment required to develop these products and technologies may change depending on the different applications that we may choose to pursue. We cannot give assurances that these programs will ever reach technological feasibility or develop into products that can be marketed profitably. In addition, we cannot guarantee that we will be able to develop and commercialize products before our competitors develop and commercialize products for the same indications. If products based on our acquired IPR&D programs and technology platforms do not become commercially viable, our results of operations could be materially adversely affected. The following table sets forth IPR&D projects for companies and certain assets acquired since 2004 amounts in millions, except percent data.

VI. Effects of T on Cardiovascular Risk Factors. Consider various possible outcomes of a hypothetical extension of our study to include a 3- to 6-month follow-up assessment. Under one scenario, both the cognitive dysfunction and the alcoholic denial would resolve. That outcome would support our proposition that the denial was related to cognitive dysfunction. In the alternative scenario, the cognitive dysfunction would resolve while the alcoholic denial remained strong. That would suggest that some alcoholics are simply chronically high in denial, regardless of their current degree of cognitive dysfunction. However, that hypothetical outcome would not invalidate our actual ; finding that high-denial alcoholics were more cognitively impaired than lowdenial alcoholics during the first few weeks of abstinence. At best, such an outcome would cause us to reinterpret our initial findings as indicating that these chronically high denial alcoholics are highly susceptible to cognitive impairment in the early stages of recovery. It is unlikely that the association of high denial with cognitive dysfunction in early recovery was simply coincidental, given that low-denial alcoholics did not show similar cognitive impairments at the same point in their recovery. On a related point, it is somewhat uncommon for high-denial alcoholics to remain abstinent for as long as 3 to months, especially prior to treatment. Thus, in their usual condition these patients are likely to be cognitively compromised. If that cognitive dysfunction contributes to their denial, this is a clinically important issue that should be taken into account in treatment planning. We should point out that neither the neuropsychological assessment nor the assessment of denial occurred while the subjects were actively detoxifying or acutely con and gentamicin. In this model, estimation of the physical relationship between the key DHP binding residues and the outer surface of the calcium channel pore was based in part on data obtained with charged DHP derivatives and native L-type calcium channels Bangalore et al., 1994 ; . However, previous studies have shown that addition of a charged group to a DHP compound markedly alters the functional modulation of channel activity by these drugs Bangalore et al., 1994 ; . These functional changes in channel modulation may be a consequence of restricted access to a common receptor binding domain for charged, but not neutral, forms of the drug as predicted within the framework of the modulated receptor hypothesis Hille, 1977; Hondeghem and Katzung, 1977 ; . However, it is also possible that addition of a charged group to a DHP molecule may restrict access of the DHP moiety to some or all of the residues that have been shown to constitute the neutral drug binding domain and or underlie neutral drug-channel interactions. This restriction to a subset of key residues, could confer distinct functional consequences upon the drug-bound channel. To distinguish between these possibilities, we have systematically investigated the sensitivity of an ionized DHP compound to mutation of individual amino acids of segments IIIS5, IIIS6, and IVS6 of 1c which have previously been shown to markedly reduce channel modulation and or binding by the neutral compound isradipine. To select key residues that might affect charged DHP interactions we relied on previous site-directed and alanine scanning mutagenesis studies of both 1S and 1c subunits that have revealed important residues underlying neutral drug interactions. We mutated a tyrosine Tyr1174 ; and two isoleucine Ile1175, Ile1178 ; residues arranged in a YIXXI segment as well as a methionine Met1183 ; in IIIS6. We also tested the effects of mutation of a tyrosine Tyr1485 ; , methionine Met1486 ; , and one of two isoleucines Ile1493 ; in the YM X ; 5I sequence of IVS6 previously shown to be key to neutral DHP interactions Peterson et al., 1996; Schuster et al., 1996; Bodi et al., 1997; Peterson et al., 1997 ; . Finally, because the recent mutation of a threonine residue in IIIS5 Thr1061 ; potently reduced neutral DHP inhibition of electrophysiologically-assayed channel activity as well as radioligand binding to expressed protein Grabner et al., 1996; Mitterdorfer et al., 1996; Ito et al., 1997 ; , we tested the effects of mutating this residue on charged DHP interactions. We used custom synthesized DHP derivatives in which either a neutral or permanently charged head group was separated by a fixed length 10 ; hydrocarbon spacer chain from a common DHP moiety Bangalore et al., 1994 ; . We studied channel block by the neutral and charged forms of the test drug as a function of channel construct and membrane potential. Our results suggest that the presence of a permanently charged head group restricts the access of the attached DHP moiety to a subset of interaction residues on the 1c subunit in a voltage-dependent manner. Furthermore, these restricted interactions confer distinct functional properties upon the charged DHP molecules.

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