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Chobanian AV, Bakris GL, Black HR, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003; 289 19 ; : 2560-2572. SHEP Cooperative Research Group. Prevention of stroke by antihypertensive drug treatment in older persons with isolated systolic hypertension. Final results of the Systolic Hypertension in the Elderly Program SHEP ; . JAMA. 1991; 265 24 ; : 3255-3264. ALLHAT Collaborative Research Group. Major cardiovascular events in hypertensive patients randomized to doxazosin vs chlorthalidone: the antihypertensive and lipid-lowering treatment to prevent heart attack trial ALLHAT ; . JAMA. 2000; 283 15 ; : 1967-1975. Arauz-Pacheco C, Parrott MA, Raskin P. The treatment of hypertension in adult patients with diabetes. Diabetes Care. 2002; 25 1 ; : 134-147. UK Prospective Diabetes Study Group. Efficacy of atenolol and captopril in reducing risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 39. BMJ. 1998; 317 7160 ; : 713-720. Yusuf S, Sleight P, Pogue J, Bosch J, Davies R, Dagenais G. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. N Engl J Med. 2000; 342 3 ; : 145-153. Heart Outcomes Prevention Evaluation Study Investigators. Effects of ramipril on cardiovascular and microvascular outcomes in people with diabetes mellitus: results of the HOPE study and MICRO-HOPE substudy. Lancet. 2000; 355 9200 ; : 253-259. Estacio RO, Jeffers BW, Hiatt WR, Biggerstaff SL, Gifford N, Schrier RW. The effect of nisoldipine as compared with enalapril on cardiovascular outcomes in patients with noninsulin-dependent diabetes and hypertension. N Engl J Med. 1998; 338 10 ; : 645-652. Hansson L, Lindholm LH, Niskanen L, et al. Effect of angiotensin-converting-enzyme inhibition compared with conventional therapy on cardiovascular morbidity and mortality in hypertension: the Captopril Prevention Project CAPPP ; randomized trial. Lancet. 1999; 353 9153 ; : 611-616. Tatti P, Pahor M, Byington RP, et al. Outcome results of the Fosinopril Versus Amlodipine Cardiovascular Events Randomized Trial FACET ; in patients with hypertension and NIDDM. Diabetes Care. 1998; 21 4 ; : 597-603. Pahor M, Psaty BM, Alderman MH, Applegate WB, Williamson JD, Furberg CD. Therapeutic benefits of ACEIs and other antihypertensive drugs in patients with type 2 diabetes. Diabetes Care. 2000; 23 7 ; : 888-892. Brenner B, Cooper ME, de Zeeuw D, et al. Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy. N Engl J Med. 2001; 345 12 ; : 861-869. Parving HH, Lehnert H, Crochner-Mortensen J, et al. The effect of irbesartan on the development of diabetic nephropathy in patients with type 2 diabetes. N Engl J Med. 2001; 345 12 ; : 870-878.
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Additional equity or debt financing may not be available to us on acceptable terms, or at all. If we raise additional capital by issuing equity securities, substantial dilution to our existing stockholders may result which could decrease the market price of our common stock due to the sale of a large number of shares of our common stock in the market, or the perception that these sales could occur. These sales, or the perception of possible sales, could also impair our ability to raise capital in the future. In addition, the terms of any equity financing may adversely affect the rights of our existing stockholders. If we raise additional funds through strategic alliance or licensing arrangements, we may be required to relinquish rights to certain of our technologies or product candidates, or to grant licenses on terms that are unfavorable to us, which could substantially reduce the value of our business. If we are unable to obtain sufficient additional financing, we would be unable to meet our obligations and we would be required to delay, reduce or eliminate some or all of our business operations, including the pursuit of licensing, strategic alliances and development of drug delivery programs. If our clinical trials are not successful or take longer to complete than we expect, we may not be able to develop and commercialize our products. In order to obtain regulatory approvals for the commercial sale of potential products utilizing our CDT platform, we or our collaborators will be required to complete clinical trials in humans to demonstrate the safety and efficacy, or in certain cases, the bioequivalence, of the products. However, we or our collaborators may not be able to commence or complete these clinical trials in any specified time period, or at all, either because the appropriate regulatory agency objects or for other reasons, including: unexpected delays in the initiation of clinical sites; slower than projected enrollment of eligible patients; competition with other ongoing clinical trials for clinical investigators or eligible patients; scheduling conflicts with participating clinicians; limits on manufacturing capacity, including delays of clinical supplies; and, the failure of our products to meet required standards!
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Tension, the evidence base is variegated, ever-increasing, and controversial. "Targeting Improved Tolerability and Novel Mechanisms in the Management of Cardiovascular Risk, " an educational symposium, was held November 12-16, 2006, during the 79th annual Scientific Sessions of the American Heart Association in Chicago. The symposium was jointly sponsored by the Postgraduate Institute for Medicine and Advantage Communications and supported by an unrestricted grant from Forest Laboratories, Inc. Peter Libby, MD, chaired the symposium, which focused on addressing the available evidence for the use of various classes of agents and various individual agents in managing cardiovascular risk in late.
Borrowed under the line of credit in the case of other equipment are repayable over 36 months and bear interest at the rate of 10.45% per annum. On March 9, 2006, we entered into an amendment to the lease for our new Cambridge, Massachusetts office and laboratory facility in order to secure additional space. Because the amendment increases the total space we rent at the Cambridge location, we were obligated to increase the amount of the standby letter of credit required under the lease from $2.5 to $4.0 million. In addition, under the lease agreement as amended, we expect to receive approximately $6.9 million in total tenant improvement funds from our landlord. We submitted approximately $4.0 million in tenant improvement reimbursements to the landlord for which we received payment in July 2006. We expect to invest approximately $4.3 million in additional leasehold improvements, equipment, furniture and fixtures associated with the construction of our expansion space, which will be offset by the remaining $2.9 million in additional tenant improvement allowances from our landlord. Contractual Obligations and Commitments The following table summarizes our contractual obligations at December 31, 2006 and the effects such obligations are expected to have on our liquidity and cash flows in future periods and
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Results Addition of HCTZ 6.25 mg contributed significantly to the blood pressure lowering effects of bisoprolol 5 mg no p value reported ; . Combination of bisoprolol 5 mg and HCTZ 6.25 mg produced a significant reduction in mean sitting SBP and DBP from baseline -15.8 mmg -12.6 mm Hg ; than bisoprolol 5 mg alone -10 mm Hg -10.5 mm Hg ; and HCTZ 25 mg alone -10.2 mm Hg -8.5 mm Hg ; no p values reported ; . Bisoprolol 5 mg and HCTZ 6.25 mg in combination had a 73% response rate compared to 61% for the bisoprolol group and 47% for the HCTZ group no p values reported ; . Bisoprolol 5 mg and HCTZ 6.25 mg in combination was found to be significantly more effective than bisoprolol 5 mg or HCTZ 25 mg in all subgroups of patients regardless of age, race, gender, or smoking history no p values reported ; . Bisoprolol 5 mg and HCTZ 6.25 mg in combination did not have an increase in frequency or severity of adverse events. The adverse events were comparable to that in the placebo group no p value reported ; . Bisoprolol 5 mg and HCTZ 6.25 mg in combination group had less hypokalemia 1% ; , than the HCTZ 25mg group 6.5% ; no p value reported ; . Atenolol and chlorthalidone combination product resulted in a further significant reduction in blood pressure no p value reported ; . Mean blood pressure reduction obtained by the atenolol and chlorthalidone combination product was 30 15 mm the standing position no p value reported ; . Serum potassium rose significantly with the combination atenolol and chlorthalidone combination product compared with the chlorthalidone alone no p value reported.
Everyone should be able to sit on their front porch or open a window, " says Elsie Herring. "You can't do that here in southeastern North Carolina, where the hog industry is concentrated." Herring is referring to the sickening odor of hog waste that wafts over her home from a nearby hog factory in Duplin County. She is one of 13 "community voices" we recorded to publicize the plight of the mostly low-income people who live around these huge operations. The hog factories use primitive waste lagoons that pollute ground water and can cause health problems for residents. Evelyn Powell of Edgecombe County says, "You can't go outside and have cookouts. They're out. Your whole lifestyle is a disaster." The video interviews are available on our Hog Watch web site at hogwatch . "We hope these real stories of real people challenge every lawmaker in the state to listen, " says Kris Thornburg, our project coordinator. "We're pushing for a mandate to replace the outdated waste lagoons with systems that protect health and the environment." Those interviewed say their pleas have gone unanswered so far. Our scientist Dr. Joe Rudek is involved in a major study of alternatives to waste lagoons and hopes to be able to point the way to a solution soon and
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Acting to block monoamine uptake into the HT-22 cells, the effects of the inhibitors on MAO activity in whole cells was compared with the effects on enzyme activity in cell homogenates by using treatment conditions similar to those used to assay the effects of these agents on glutamate toxicity. The uptake inhibitors would be expected to block MAO activity in whole cells through inhibition of substrate uptake but have little or no effect on MAO activity in cell homogenates. We used this indirect assay to monitor monoamine uptake by the HT-22 cells because direct assays generally require pretreatment of the cells with MAO inhibitors Michel and Hefti, 1990 ; , which could complicate the interpretation of the results. For each of the uptake inhibitors tested, two concentrations were used: one at which little or no protection from glutamate toxicity was seen and one at which maximal protection from glutamate toxicity was seen. As shown in Table 3, none of the uptake inhibitors had a large effect on MAO activity in cell homogenates. In contrast, at the concentrations that protected the HT-22 cells from glutamate toxicity, the uptake inhibitors significantly reduced MAO activity in whole cells, whereas lower concentrations of the uptake inhibitors had little or no effect. These results, as well as those shown in Table 2 and Figure 4, also demonstrate that the HT-22 cells are capable of monoamine uptake. Although the concentrations of the uptake inhibitors that inhibited glutamate toxicity did not block monoamine uptake completely, the data are consistent with the possibility that these inhibitors decreased intracellular monoamine levels, and thereby oxidase activity, enough to reduce the amount of H2O2 production to a level that did not overwhelm the capacity of the cells for eliminating it. The results with the monoamine uptake inhibitors suggested that the culture medium was a source of monoamines that could potentiate cell damage in the presence of glutamate. Because the medium itself DMEM ; does not contain monoamines, the most likely source is the serum. To test this possibility, HT-22 cells were treated with glutamate in either a defined medium without serum N2 medium; Bottenstein and Sato, 1979 ; or medium with serum that was pretreated with charcoal to remove monoamines and.
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Non-prescription medications known as adrenergics because they mimic the effects of adrenaline also called epinephrine ; . This is the "fight-or-flight" hormone that evolved in mammals to speed up the body for coping with such emergencies as outrunning a lion or avoiding an oncoming car. Many decongestants contain a synthetic version of adrenaline, called pseudoephedrine, which relaxes the lung's bronchial passages, stimulates the heart rate, and constricts blood vessels. Another problem with adrenergics is that they constrict muscles in the prostate and bladder making it harder to urinate. Antihistamines, such as diphenhydramine Benadryl ; , can also slow urine flow in some men. Anyone who has BPH and hypertension high blood pressure ; or congestive heart disease, and is taking diuretics, such as chlorthalidone or hydrochlorothiazide, should discuss the risks and.
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7 Antoni FA. Hypothalamic control of adrenocorticotropin secretion: advances since the discovery of 41-residue corticotropinreleasing factor. Endocrine Reviews 1986 7 351378. Jones MT & Gillham B. Factors involved in the regulation of adrenocorticotropic hormone beta-lipotropic hormone. Physiological Reviews 1988 68 743818. Ben-Jonathan N, Laudon M & Garris PA. Novel aspects of posterior pituitary function: regulation of prolactin secretion. Frontiers In Neuroendocrinology 1991 12 231277. Swanson LW. The hypothalamus. In Handbook of Chemical Neuroanatomy. Vol. 5: Integrated Systems of the CNS. Part I: Hypothalamus, Hippocampus, Amygdala, Retina, pp 137. Eds A Bjorklund, T Hokfelt, LW Swanson. Amsterdam: Elsevier, 1987. 11 Inagaki N, Yamatodani A, Ando-Yamamoto M, Tohyama M, Watanabe T & Wada H. Organization of histaminergic fibers in the rat brain. Journal of Comparative Neurology 1988 273 283300. Panula P, Pirvola U, Auvinen S & Airaksinen MS. Histamineimmunoreactive nerve fibers in the rat brain. Neuroscience 1989 28 585610. Kjr A, Larsen PJ, Knigge U, Mller M & Warberg J. Histamine stimulates c-fos expression in hypothalamic vasopressin-, oxytocin-, and corticotropin-releasing hormone-containing neurons. Endocrinology 1994 134 482491. Kjr A, Larsen PJ, Knigge U & Warberg J. Histaminergic activation of the hypothalamic-pituitary-adrenal axis. Endocrinology 1994 135 11711177. Kjr A, Knigge U & Warberg J. Involvement of oxytocin in histamine- and stress-induced ACTH and prolactin secretion. Neuroendocrinology 1995 61 704713. Kjr A, Knigge U, Plotsky PM, Bach FW & Warberg J. Histamine H1- and H2-receptor activation stimulates ACTH and betaendorphin secretion by increasing corticotropin-releasing hormone in hypophysial portal blood. Neuroendocrinology 1992 56 851855. Kjr A, Knigge U, Rouleau A, Garbarg M & Warberg J. Dehydration-induced release of vasopressin involves activation of hypothalamic histaminergic neurons. Endocrinology 1994 135 675681. Schagen FHE, Knigge U, Kjr A, Larsen PJ & Warberg J. Involvement of histamine in suckling-induced release of oxytocin, prolactin and adrenocorticotropin in lactating rats. Neuroendocrinology 1996 63 550558. Ganellin CR. Chemistry and structureactivity relationship of drugs acting on histamine receptors. In Pharmacology of Histamine Receptors, pp 10102. Eds CR Ganellin, ME Parsons. Bristol: Wright, 1982. 20 Knigge U, Matzen S & Warberg J. Histaminergic mediation of the stress-induced release of prolactin in male rats. Neuroendocrinology 1988 47 6874. Kjr A, Knigge U, Bach FW & Warberg J. Histamine- and stressinduced secretion of ACTH and beta-endorphin: involvement of corticotropin-releasing hormone and vasopressin. Neuroendocrinology 1992 56 419428.
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305. CRYSTAL STRUCTURE OF HUMAN HDAC8 PROVIDES INSIGHTS INTO THE CLASS I HISTONE DEACETYLASES. John R. Somoza 1, Robert J. Skene 2, Bradley A. Katz 1, Clifford Mol 2, Joseph Ho 1, Andy J. Jennings 2, Christine Luong 1, Andrew Arvai 2, Joseph J. Buggy 1, Ellen Chi 2, Jie Tang 1, Bi-Ching Sang 2, Erik Verner 1, Robert Wynands 2, Ellen M. Leahy 1, Douglas R. Dougan 2, Gyorgy Snell 2, Marc Navre 2, Knuth Mark W 2, Ronald V. Swanson 2, Duncan E. McRee 2, and Leslie W. Tari 2. 1 ; Department of Medicinal Chemistry, Celera, 180 Kimball Way, South San Francisco, CA 94080, john.somoza celera , 2 ; Syrrx, Inc The modulation of the histone acetylation plays an essential part in regulating gene transcription. Two groups of enzymes affect histone acetylation: histone acetyl transferases HATs ; and histone deacetylases HDACs ; , which catalyze the addition and removal, respectively, of the acetyl groups from the -amino groups of lysines in histones. The removal of acetyl groups by the HDACs promotes the condensation of chromatin and leads to a repression of transcription. The deregulation of the HDACs has been linked to several types of cancer, suggesting a potential use for HDAC inhibitors in oncology. In this presentation we describe the first crystal structures of a human HDAC: the structures of human HDAC8 complexed with four structurally diverse hydroxamate inhibitors. This work sheds light on the catalytic mechanism of the HDACs and suggests how phosphorylation of Ser39 affects HDAC8 activity. These structures also provide a framework for the identification of novel HDAC inhibitors. 308. DISCOVERY OF BMS-536924, A SMALL MOLECULE INHIBITOR OF IGF-1R WITH BROAD SPECTRUM IN VIVO ACTIVITY. Mark D. Wittman 1, Joan Carboni 2, Francis Y. Lee 3, Balu Balasubramanian 4, Francis Beaulieu 5, Frennesson David 5, Subramaniam Krishnanathan 4, Liu Peiying 5, Carl Ouellet 3, Xiaopeng Sang 5, Mark G. Saulnier 1, Karen Stoffan 5, Upender Velaparthi 1, Dolatrai M. Vyas 1, Henry S. Wong 4, and Kurt Zimmermann 1. ; Discovery Chemistry, Bristol Myers Squibb Co, Pharmaceutical Research Institute, 5 Research Parkway, Wallingford, CT 06492-7660, mark.wittman bms , 2 ; Oncology Drug Discovery, Bristol Myers Squibb Co, Pharmaceutical Research Institute, 3 ; Oncology Drug Discovery, Bristol-Myers Squibb Co Pharmaceutical Research Institute, 4 ; Synthesis Group, Bristol-Myers Squibb Co Pharmaceutical Research Institute, 5 ; Discovery Chemistry, Bristol-Myers Squibb Co Pharmaceutical Research Institute Considerable attention has been focused on understanding the role of insulinlike growth factor I receptor IGF-1R ; signaling in stimulating mitogenesis, transformation to the oncogenic phenotype, and the anti-apoptotic effects observed in malignant cells. Signaling through IGF-1R results in activation two important signaling pathways for tumor growth; the RAS Raf MAP Kinase pathway primarily responsible for mitogensis as well as the PI-3 kinase pathway which has an anti-apototic role. Epidemiological studies have also highlighted the importance of IGF-1R in key tumor types by correlating elevated IGF-I levels with increased risk of developing colon, breast, prostate, and lung tumors. The emerging importance of this target has provided the driving force behind the search for antagonists of IGF-1R, including both biologics that target the ligand binding domain as well as small molecule kinase inhibitors. Recently, pyrroloprimidines, selected tryphostin analogs, and picropodophylin have been reported to inhibit the kinase activity of IGF-1R. This presentation will describe the SAR studies leading to the identification of BMS-536924, a new small molecule kinase inhibitor of IGF-1R, and the broad spectrum of anti tumor efficacy that has been observed with this compound.
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