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• Therapeutic Expertise
• Cardi* (9)
• CNS/Neuro* (2)
• Diagnostic*
• Musculoskeletal
• Oncology/Cancer (8)
• Other (as listed on www.bioimaging.com/product/therap.html) (7)

Prokineticin receptor-1 induces neovascularization and epicardial-derived progenitor cell differentiation.

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Lead Author: Urayama K

Additional Authors: Guilini C, Turkeri G, Takir S, Kurose H, Messaddeq N, Dierich A, Nebigil CG.

Arterioscler Thromb Vasc Biol., 2008-05-01, 28(5):841-9.

Centre National de la Recherche Scientifique (CNRS), Université Louis Pasteur-Strasbourg I, Ecole Supérieure de Biotechnologie de Strasbourg, Illkirch, France.

MIB Abstract ID Number: 15256

PreMedline Identifier: 18421008

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Copper deficiency increases the virulence of amyocarditic and myocarditic strains of coxsackievirus B3 in mice.

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Lead Author: Smith AD

Additional Authors: Botero S, Levander OA.

J Nutr., 2008-05-01, 138(5):849-55.

Diet, Genomics, and Immunology Laboratory, Beltsville Human Nutrition Research Center, Agricultural Research Service, USDA, Beltsville, MD 20705, USA. allen.smith@ars.usda.gov

Deficiency in several trace elements, including copper and selenium, is associated with increased levels of oxidative stress. Copper deficiency also has been shown to impair immune function. Previous work by others demonstrated that passage of an amyocarditic or myocarditic strain of coxsackievirus B3 (CVB3) through selenium- or vitamin E-deficient mice led to increased cardiac pathology. To determine whether a copper deficiency would similarly alter the pathogenesis of CVB3 infections, Swiss outbred dams and their litters were fed copper-deficient diets from birth and received either deionized water or water with 0.315 mmol/L copper as copper sulfate. At 4 wk of age, copper-adequate or -deficient male and female offspring were infected with an amyocarditic or myocarditic strain of CVB3. Heart titers were elevated at d 3 and 7 postinfection in copper-deficient mice infected with the myocarditic CVB3 strain (CVB3/20) but only at d 7 in deficient mice infected with the amyocarditic CVB3 strain (CVB3/0) compared with copper-adequate controls. Copper-deficient mice infected with either strain of CVB3 had increased cardiac pathology compared with copper-adequate controls. Genomic sequences of viruses isolated from copper-adequate and -deficient mice were identical. Heart cytokine expression was elevated in copper-deficient CVB3-infected mice compared with infected controls. Circulating CVB3-specific IgG2a but not IgM levels were decreased in copper-deficient mice. Thus, copper deficiency is associated with an increased inflammatory response but decreased acquired immune response to CVB3 infection that results in increased cardiac pathology, presumably due to increased viral load.

MIB Abstract ID Number: 15257

PreMedline Identifier: 18424590

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The effects of general anesthesia on the central nervous and cardiovascular system toxicity of local anesthetics.

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Lead Author: Copeland SE

Additional Authors: Ladd LA, Gu XQ, Mather LE.

Anesth Analg., 2008-05-01, 106(5):1429-39, table of contents.

Department of Anaesthesia and Pain Management, University of Sydney at Royal North Shore Hospital, Sydney NSW 2065, Australia.

BACKGROUND: Local anesthetic toxicity is often studied experimentally in acutely prepared, anesthetized laboratory animals. We determined the influence of halothane/O(2) anesthesia on cardiovascular and central nervous system (CNS) toxic responses to six amide-type local anesthetics administered i.v.. METHODS: Behavioral, cardiovascular, and pharmacokinetic responses were determined in previously instrumented ewes (approximately 45-50 kg, n = 18), on separate occasions when conscious and anesthetized, to bupivacaine (100 mg), levobupivacaine (125 mg), ropivacaine (150 mg), lidocaine (350 mg), mepivacaine (350 mg), prilocaine (350 mg), and saline (control) infused i.v. over 3 min. RESULTS: The local anesthetics caused convulsions in conscious sheep, but no overt CNS effects in anesthetized sheep. Negative inotropy and slight bradycardia without changes in arterial blood pressure occurred initially in conscious sheep, followed by positive inotropy, tachycardia, and hypertension at the abrupt onset of CNS excitotoxicity, along with widening of QRS complexes. Fatal cardiac arrhythmias occurred in, respectively, 3 of 11, 2 of 12, and 2 of 13 conscious sheep infused with bupivacaine, levobupivacaine, and ropivacaine; in 1 of 9 with prilocaine, electromechanical dissociation (followed by polymorphic ventricular tachycardia) caused death. In anesthetized sheep, cardiovascular depression, preexisting from the general anesthesia, was exacerbated by all local anesthetics, and increased QRS width was prolonged; concurrent blood local anesthetic concentrations were doubled. Nevertheless, all anesthetized animals survived. CONCLUSIONS: General anesthesia produced physiological perturbations, exacerbated local anesthetic-induced cardiovascular depression, and changed the pharmacokinetics of toxic doses of local anesthetics. However, cardiovascular fatalities from local anesthetics occurred only in conscious animals.

MIB Abstract ID Number: 15259

PreMedline Identifier: 18420857

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Involvement of tumor necrosis factor-alpha in angiotensin II-mediated effects on salt appetite, hypertension, and cardiac hypertrophy.

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Lead Author: Sriramula S

Additional Authors: Haque M, Majid DS, Francis J.

Hypertension. , 2008-05-01, 51(5):1345-51. Epub 2008 Apr 7.

Comparative Biomedical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803, USA.

Hypertension is considered a low-grade inflammatory condition induced by various proinflammatory cytokines, including tumor necrosis factor (TNF)-alpha. Recent studies have implicated an involvement of TNF-alpha in the development of salt-sensitive hypertension induced by angiotensin II (Ang II). To understand further the relationship between TNF-alpha and Ang II, we examined the responses to Ang II in TNF-alpha knockout (TNF-alpha(-/-)) mice in the present study. A continuous infusion of Ang II (1 microg/kg per minute) for 2 weeks was given to both TNF-alpha(-/-) and wild-type (WT) mice with implanted osmotic minipumps. Daily measurement of water intake, salt intake, and urine output were performed using metabolic cages. Blood pressure was monitored continuously with implanted radiotelemetry. Ang II administration for 2 weeks caused increases in salt (0.2+/-0.07 to 5.6+/-0.95 mL/d) and water (5.4+/-0.34 to 11.5+/-1.2 mL/d) intake and in mean arterial pressure (115+/-1 to 151+/-3 mm Hg) in wild-type mice, but these responses were absent in TNF-alpha(-/-) mice (0.2+/-0.04 to 0.3+/-0.09 mL/d, 5.5+/-0.2 to 6.1+/-0.07 mL/d, and 113+/-2 to 123+/-3 mm Hg, respectively). Cardiac hypertrophy induced by Ang II was significantly attenuated in TNF-alpha(-/-) mice compared with wild-type mice. In a group of TNF-alpha(-/-) mice, when replacement therapy was made with recombinant TNF-alpha, Ang II induced similar responses in salt appetite, mean arterial pressure, and cardiac hypertrophy, as observed in wild-type mice. These results suggest that TNF-alpha plays a mechanistic role in mediating chronic Ang II-induced effects on salt appetite and blood pressure, as well as on cardiac hypertrophy.

MIB Abstract ID Number: 15262

PreMedline Identifier: 18391105

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Structure-based identification of small-molecule angiotensin-converting enzyme 2 activators as novel antihypertensive agents.

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Lead Author: Hernández Prada JA

Additional Authors: Ferreira AJ, Katovich MJ, Shenoy V, Qi Y, Santos RA, Castellano RK, Lampkins AJ, Gubala V, Ostrov DA, Raizada MK.

Hypertension. , 2008-05-01, 51(5):1312-7. Epub 2008 Apr 7.

McKnight Brain Institute and Department of Physiology, College of Medicine, University of Florida, Gainesville, USA.

Angiotensin-converting enzyme 2 (ACE2) is a key renin-angiotensin system enzyme involved in balancing the adverse effects of angiotensin II on the cardiovascular system, and its overexpression by gene transfer is beneficial in cardiovascular disease. Therefore, our objectives were 2-fold: to identify compounds that enhance ACE2 activity using a novel conformation-based rational drug discovery strategy and to evaluate whether such compounds reverse hypertension-induced pathophysiologies. We used a unique virtual screening approach. In vitro assays revealed 2 compounds (a xanthenone and resorcinolnaphthalein) that enhanced ACE2 activity in a dose-dependent manner. Acute in vivo administration of the xanthenone resulted in a dose-dependent transient and robust decrease in blood pressure (at 10 mg/kg, spontaneously hypertensive rats decreased 71+/-9 mm Hg and Wistar-Kyoto rats decreased 21+/-8 mm Hg; P<0.05). Chronic infusion of the xanthenone (120 microg/day) resulted in a modest decrease in the spontaneously hypertensive rat blood pressure (17 mm Hg; 2-way ANOVA; P<0.05), whereas it had no effect in Wistar-Kyoto rats. Strikingly, the decrease in blood pressure was also associated with improvements in cardiac function and reversal of myocardial, perivascular, and renal fibrosis in the spontaneously hypertensive rats. We conclude that structure-based screening can help identify compounds that activate ACE2, decrease blood pressure, and reverse tissue remodeling. Administration of ACE2 activators may be a valid strategy for antihypertensive therapy.

MIB Abstract ID Number: 15263

PreMedline Identifier: 18391097

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Downregulation of VEGF-D expression by interleukin-1beta in cardiac microvascular endothelial cells is mediated by MAPKs and PKCalpha/beta1.

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Lead Author: Mountain DJ

Additional Authors: Singh M, Singh K.

J Cell Physiol. , 2008-05-01, 215(2):337-43.

Department of Physiology, James H. Quillen College of Medicine, James H. Quillen Veterans Affairs Medical Center, East Tennessee State University, Johnson City, Tennessee 37614, USA.

Interleukin-1beta (IL-1beta) is a proinflammatory cytokine increased in the heart following myocardial infarction. Vascular endothelial growth factors (VEGFs) are implicated in angiogenesis due to their involvement in the recruitment and proliferation of endothelial cells. Here we studied expression of VEGFs in response to IL-1beta in rat cardiac microvascular endothelial cells (CMECs) and investigated the signaling pathways involved in the regulation of VEGF-D. cDNA array analysis indicated that IL-1beta modulates the expression of numerous angiogenesis-related genes, notably decreasing the expression of VEGF-D. RT-PCR and Western blot analyses confirmed decreased expression of VEGF-D in response to IL-1beta. IL-1beta decreased the expression of VEGF-C to a lesser extent with no effects on VEGF-A or -B. Inhibition of ERK1/2, JNKs, or PKCalpha/beta1 alone partially inhibited IL-1beta-induced VEGF-D downregulation. Concurrent inhibition of ERK1/2 or JNKs and PKCalpha/beta1 resulted in a synergistic inhibition of IL-1beta-induced decreases in VEGF-D. Inhibition of ERK1/2 partially inhibited IL-1beta-stimulated inactivation of GSK-3beta with no effect on beta-catenin levels. Inhibition of GSK-3beta using SB216763 inhibited basal VEGF-D expression. We conclude that IL-1beta downregulates VEGF-D expression in CMECs via the involvement of ERK1/2, JNKs, and PKCalpha/beta(1). This is the first report to indicate inhibition of VEGF-D gene expression in response to IL-1beta in cardiac microvascular endothelial cells, a cell type of central interest in angiogenesis. (c) 2007 Wiley-Liss, Inc. 

MIB Abstract ID Number: 15264

PreMedline Identifier: 17929249

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Intramural delivery of rapamycin with alphavbeta3-targeted paramagnetic nanoparticles inhibits stenosis after balloon injury.

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Lead Author: Cyrus T

Additional Authors: Zhang H, Allen JS, Williams TA, Hu G, Caruthers SD, Wickline SA, Lanza GM.

Arterioscler Thromb Vasc Biol., 2008-05-01, 28(5):820-6. Epub 2008 Feb 21.

Division of Cardiology, Washington University School of Medicine, Saint Louis, Mo. 63108, USA. tcyrus@im.wustl.edu

Comment in:

BACKGROUND: Drug eluting stents prevent vascular restenosis but can delay endothelial healing. A rabbit femoral artery model of stenosis formation after vascular injury was used to study the effect of intramural delivery of alpha(v)beta(3)-integrin-targeted rapamycin nanoparticles on vascular stenosis and endothelial healing responses. METHODS AND RESULTS: Femoral arteries of 48 atherosclerotic rabbits underwent balloon stretch injury and were locally treated with either (1) alpha(v)beta(3)-targeted rapamycin nanoparticles, (2) alpha(v)beta(3)-targeted nanoparticles without rapamycin, (3) nontargeted rapamycin nanoparticles, or (4) saline. Intramural binding of integrin-targeted paramagnetic nanoparticles was confirmed with MR molecular imaging (1.5 T). MR angiograms were indistinguishable between targeted and control arteries at baseline, but 2 weeks later they showed qualitatively less luminal plaque in the targeted rapamycin treated segments compared with contralateral control vessels. In a first cohort of 19 animals (38 vessel segments), microscopic morphometric analysis of the rapamycin-treated segments revealed a 52% decrease in the neointima/media ratio (P<0.05) compared to control. No differences (P>0.05) were observed among balloon injured vessel segments treated with alpha(v)beta(3)-targeted nanoparticles without rapamycin, nontargeted nanoparticles with rapamycin, or saline. In a second cohort of 29 animals, endothelial healing followed a parallel pattern over 4 weeks in the vessels treated with alpha(v)beta(3)-targeted rapamycin nanoparticles and the 3 control groups. CONCLUSIONS: Local intramural delivery of alpha(v)beta(3)-targeted rapamycin nanoparticles inhibited stenosis without delaying endothelial healing after balloon injury.

MIB Abstract ID Number: 15269

PreMedline Identifier: 18292395

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Pulmo Biotech Inc - Appointment of Chief Financial Officer

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Lead Author: [none given]

Market News Publishing, 2008-05-02

Pulmo BioTech Chief Executive Officer Garry McCann said that he was very pleased that Rajiv had agreed to join the company and that Rajiv's experience and financial acumen would be of great benefit to the company as it moved towards completion of its Phase I Human Trials and then into Phase II.

Rajiv has twenty one years of extensive experience in the investment banking and finance industry covering financial control, evaluation of businesses, regulatory liaison and development of macro/micro risk management systems.

Rajiv was educated at Westminster College in London, UK and the University of Delhi in India. He has an Honours Degree in Commerce and is a Member of the Institute of Chartered Accountants, a Member of the Securities and Futures Authority and a Member of the Global Association of Risk Professionals.

About Pulmo BioTech Inc.

Pulmo BioTech Inc. specializes in the development and marketing of medical technology and research. Our proven strengths combine extensive commercial experience and academic credentials. The principal staff members are acknowledged experts in their specialized fields, and work with a broad range of investment institutions. Pulmo BioTech's mission is to utilize scientific imagination and drive, together with managerial and financial acumen, to bring innovative and profitable products to the marketplace to the benefit of all stock holders.

About PulmoScience Inc.

PulmoScience Inc. was established in 2006, and is currently developing a non-invasive Molecular Imaging technique for the diagnosis of Pulmonary Embolism, Pulmonary Hypertension and Lung Inflammatory diseases under the trade name PulmoBind

The company was conceived within the Montreal Heart Institute "MHI" (a world renowned hospital and educational facility). Jointly owned by MHI subsidiary Innovacor as the technical and operational partner, Dr Jocelyn Dupuis (the scientific director and originator of the PulmoBind Molecular Imaging technology), and by Pulmo BioTech Inc as the funding partner, PulmoScience Inc aims to develop this unique and exciting technology, to fund necessary trials, and to bring the products to market.

PulmoScience believes that the market for its product candidates is worth in excess of $500 million per annum and that, provided Regulatory Approval is achieved, the safety and efficacy of its products could allow it to dominate that market.

About PulmoBind

PulmoBind uses an intravenously delivered radionuclide tagged molecule which specifically bonds to the inner walls of the circulatory system in the lungs, and by the use of an external Gamma Camera allows an image of the integrity of the blood vessels throughout the lungs to be seen by a diagnostic clinician. PulmoScience is currently undertaking Regulatory Approval for Phase I Human Trials, and while subsequent results from additional tests might not corroborate the current results, PulmoScience believes that PulmoBind has the potential to dominate the market for the diagnosis of Pulmonary Embolism. In particular, this belief is driven by PulmoScience's expectations of the improved safety and efficacy that PulmoBind will offer when compared to the current incumbent nuclear medicine based technology for the diagnosis of Pulmonary Embolism. In addition, early indications are that PulmoBind could be highly effective in the early stage diagnosis of Pulmonary Hypertension, a condition for which there is no current front line diagnostic test. The addressable market for the product candidates being developed by PulmoScience is believed by the company to be worth in excess of $500 million per annum.

Forward-Looking Statements

Forward-looking statements contained in this and other written and oral reports are made based on known events and circumstances at the time of release, and as such, are subject in the future to unforeseen uncertainties and risks. All statements regarding future performance, earnings projections, regulatory approval, events or developments are forward-looking statements. It is possible that the future performance and of the company may differ materially from current expectations, depending on economic conditions and the uncertainty of regulatory approval. A change in economic conditions may have a particularly volatile effect on results. Among the other factors which may affect future performance are: competitive market conditions and resulting effects on sales and pricing; increases in raw-material costs that cannot be recovered in product pricing; and global economic factors, including difficulties entering new markets and general economic conditions such as inflation, interest rates and credit availability. The company makes these statements as of the date of this disclosure, and undertakes no obligation to update them.

MIB Abstract ID Number: 15294

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IDev Technologies, Inc.IDev Technologies, Inc. Closes $25 Million Financing

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Lead Author: [none given]

Biotech Week, 2008-05-07

MIB Abstract ID Number: 15296

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STEMCELLS INC, 10K, May 6, 2008

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Lead Author: [none given]

2008-05-06

STEMCELLS INC, 10K, May 6, 2008   

The Company- STEMCELLS INC

Our research and development (R&D) programs are focused on identifying and developing potential cell-based therapeutics which can either restore or support organ function. Since we relocated our corporate headquarters and research laboratories to California in 1999 our R&D efforts have primarily been directed at refining our methods for identifying, isolating, culturing, and purifying the human neural stem cell and human liver engrafting cells (hLEC) and developing these as potential cell-based therapeutics for the central nervous system (CNS) and the liver, respectively. We are currently conducting a Phase I clinical trial of our HuCNS-SC ® product candidate (purified human neural stem cells) as a treatment for infantile and late infantile neuronal ceroid lipofuscinosis (NCL), a fatal neurodegenerative disease often referred to as Batten disease. We have completed enrollment and dosing for this six-patient trial and expect it to be completed in early 2009. Our CNS Program is continuing research and preclinical development for additional potential indications in the CNS field. We are targeting to initiate clinical trials to test our HuCNS-SC product candidate for a spinal cord indication in 2008 and for a myelin disorder in the brain by the end of 2008. In our Liver Program, we are in

For a brief description of our significant research and development programs see Overview "Research and Development Programs" in the Business Section of Part I, Item 1 included in our Annual Report on Form 10-K for the fiscal year ended December 31, 2007. We have also conducted research on several other cell types and in other areas, which could lead to other possible product candidates, process improvements or further research activities. We have not derived any revenue or cash flows from the sale or commercialization of any products except for license revenue for certain of our patented cells and media for use in research. As a result, we have incurred annual operating losses since inception and expect to incur substantial operating losses in the future. Therefore, we are dependent upon external financing from equity and debt offerings and revenue from collaborative research arrangements with corporate sponsors to finance our operations. We have no such collaborative research arrangements at this time and there can be no assurance that such financing or partnering revenue will be available when needed or on terms acceptable to us. Before we can derive revenue or cash inflows from the commercialization of any of our product candidates, we will need to: (i) conduct substantial in vitro testing and characterization of our proprietary cell types, (ii) undertake preclinical and clinical testing for specific disease indications; (iii) develop, validate and scale-up manufacturing processes to produce these cell-based therapeutics, and (iv) pursue required regulatory approvals. These steps are risky, expensive and time consuming. Overall, we expect our R&D expenses to be substantial and to increase for the foreseeable future as we continue the development and clinical investigation of our current and future product candidates. However, expenditures on R&D programs are subject to many uncertainties, including whether we develop our product candidates with a partner or independently. We cannot forecast with any degree of certainty which of our current product candidates will be subject to future collaboration, when such collaboration agreements will be secured, if at all, and to what degree such arrangements would affect our development plans and capital requirements. In addition, there are numerous factors associated with the successful commercialization of any of our cell-based therapeutics, including future trial design and regulatory requirements, many of which cannot be determined with accuracy at this time given the stage of our development and the novel nature of stem cell technologies. The regulatory pathways, both in the United States and internationally, are complex and fluid given the novel and, in general, clinically unproven nature of stem cell technologies. At this time, due to such uncertainties and inherent risks, we cannot estimate in a meaningful way the duration of, or the costs to complete, our R&D programs or whether, when or to what extent we will generate revenues or cash inflows from the commercialization and sale of any of our product candidates. While we are currently focused on advancing each of our product development programs, our future R&D expenses will depend on the determinations we make as to the scientific and clinical prospects of each product candidate, as well as our ongoing assessment of the regulatory requirements and each product candidate's commercial potential. Given the early stage of development of our product candidates, any estimates of when we may be able to commercialize one or more of these products would not be meaningful. Moreover, any estimate of the time and investment required to develop potential products based upon our proprietary HuCNS-SC and hLEC technologies will change depending on the ultimate approach or approaches we take to pursue them, the results of preclinical and clinical studies, and the content and timing of decisions made by the FDA and other regulatory authorities. There can be no assurance that we will be able to develop any product successfully, or that we will be able to recover our development costs, whether upon commercialization of a developed product or otherwise. We cannot provide assurance that any of these programs will result in products that can be marketed or marketed profitably. If certain of our development-stage programs do not result in commercially viable products, our results of operations could be materially adversely affected.

MIB Abstract ID Number: 15289

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Recommendations and treatment strategies for the management of acute ischemic stroke.

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Lead Author: Segura T

Additional Authors: Calleja S, Jordan J.

Expert Opin Pharmacother., 2008-05-07, 9(7):1071-85.

Hospital General Universitario de Albacete, Department of Neurology, Albacete-02006, Spain. tseguram@meditex.es

BACKGROUND: Stroke is one of the leading causes of mortality and disability worldwide. From the establishment of the penumbra concept, ischemic stroke has been recognized as a dynamic process and two main therapeutic strategies have been designed: one that tries to reopen the occluded artery and the second aims to protect the penumbra brain tissue until the physiologic mechanisms-or the treatment-stop the ischemia. OBJECTIVE: To review the most recent, high-quality evidence for acute stroke treatment. METHODS: Systematic review of relevant published studies focused in several aspects of acute ischemic stroke management, from neuroprotection to thrombolysis. CONCLUSIONS: After the publication of NINDS rt-PA study, the classical nihilistic approach to ischemic stroke started to change and thrombolytic treatment was approved in the treatment of patients with acute ischemic stroke presenting within 3 h from onset of symptoms. Advances in this field are proceeding on several fronts, including the use of next-generation plasminogen activators and glycoprotein IIb/IIIa inhibitors, refined patient selection with advanced magnetic resonance imaging sequences, endovascular approaches to thrombolysis and thrombectomy, and adjuvant use of ultrasound. Abrupt deprivation of oxygen and glucose to neuronal tissues elicits a series of pathologic cascades, leading to the spread of neuronal death. Of the numerous pathways identified, excessive activation of glutamate receptors, accumulation of intracellular Ca(2+) cations, abnormal recruitment of inflammatory cells, excessive production of free radicals and initiation of pathologic apoptosis are believed to play critical roles in ischemic damage, especially in the penumbral zone. Several neuroprotective agents designed to block these cascades have been investigated in animal models of cerebral ischemia and numerous agents have been found to reduce infarct size. However, translation of neuroprotective benefits from the laboratory bench to the emergency room has not been successful. Other measures, such as the relevance of body position in the acute phase of stroke, anticoagulant and antiplatelet agents or the effects of statins and antihypertensive therapy, are discussed in this paper, with an overview of the relevance of stroke units.

MIB Abstract ID Number: 15303

PreMedline Identifier: 18422467

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Characterization of gene expression profiles of 3 different human oral squamous cell carcinoma cell lines with different invasion and metastatic capacities.

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Lead Author: Erdem NF

Additional Authors: Carlson ER, Gerard DA.

J Oral Maxillofac Surg., 2008-05-01, 66(5):918-27.

Department of Oral and Maxillofacial Surgery, University of Tennessee Graduate School of Medicine, University of Tennessee Cancer Institute, Knoxville, TN, USA.

MIB Abstract ID Number: 15270

PreMedline Identifier: 18423281

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Precancerous carcinogenesis of human breast epithelial cells by chronic exposure to benzo[a]pyrene.

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Lead Author: Siriwardhana N

Additional Authors: Wang HC.

Mol Carcinog., 2008-05-01, 47(5):338-48.

Anticancer Molecular Oncology Laboratory, Department of Pathobiology, College of Veterinary Medicine, The University of Tennessee, , Knoxville, TN 37996, USA.

Precancerous carcinogenesis of human breast epithelial cells by chronic exposure to benzo[a]pyrene.

To understand carcinogenesis of human breast epithelial cells induced by chronic exposure to environmental pollutants, we studied biological and molecular changes in progression of cellular carcinogenesis induced by accumulated exposures to the potent environmental carcinogen benzo[a]pyrene (B[a]P). Increasing exposures of human breast epithelial MCF10A cells to B[a]P at picomolar concentrations resulted in cellular transformation from a noncancerous stage to precancerous substages, in which cells acquired the cancerous abilities of a reduced dependence on growth factors, anchorage-independent growth, and disruption in acini formation on reconstituted basement membranes. Using cDNA microarrays, we detected seven upregulated genes related to human cancers in B[a]P-transformed MCF10A cells. Using this model, we verified that green tea catechin significantly (P < 0.05) suppressed B[a]P-induced carcinogenesis. Our studies indicate that this cellular model may serve as a cost-efficient, in vitro system, mimicking the chronic carcinogenesis of breast cells that likely occurs in early stages of carcinogenesis in vivo, to identify agents that inhibit cellular carcinogenesis. (c) 2007 Wiley-Liss, Inc.

MIB Abstract ID Number: 15271

PreMedline Identifier: 17932946

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LA JOLLA PHARMACEUTICAL CO, EXHIBIT TYPE: EXHIBIT 1, May 7, 2008

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Lead Author: [none given]

2008-05-07

SAN DIEGO, California, 92121

Table of Contents

About this prospectus This prospectus is part of a Registration Statement that we filed with the Securities and Exchange Commission, or the SEC, using a "shelf" registration process. Under this shelf process, we may sell any combination of the securities described in this prospectus in one or more offerings up to a total public offering price of $77,000,000 (or its equivalent in foreign or composite currencies). This prospectus provides you with a general description of the securities we may offer. Each time we sell securities, we will provide a prospectus supplement that will contain specific information about the securities being offered and the terms of that offering. The prospectus supplement may also add to, update or change information contained in this prospectus. You should read both this prospectus and any prospectus supplement together with the additional information described under the heading "Where You Can Find More Information" carefully before making an investment decision. Unless the context otherwise requires, in this prospectus, "LJPC," "the Company," "we," "us," "our" and similar names refer to La Jolla Pharmaceutical Company and its subsidiary. About La Jolla Pharmaceutical Company We are a biopharmaceutical company focused on developing innovative pharmaceutical products to improve human health by addressing unmet medical needs. Our lead product candidate, Riquent, is designed to treat lupus renal disease by preventing or delaying renal flares. Riquent is currently in a Phase 3 clinical trial under a Special Protocol Assessment and has been granted Fast Track designation by the FDA. Lupus renal disease is a chronic illness that can lead to irreversible renal damage, renal failure and the need for dialysis, and is a leading cause of death in lupus patients. Lupus is an antibody-mediated disease caused by autoantibodies, of which antibodies to double-stranded DNA, or dsDNA, are an important subgroup. Riquent is designed to prevent or delay renal flares by lowering the levels of circulating antibodies to dsDNA, which are believed to cause lupus renal disease. Current treatments for this autoimmune disorder often address only symptoms of the disease, or nonspecifically suppress the normal operation of the immune system, which can result in severe, negative side effects and hospitalization. We believe that Riquent has the potential to treat lupus renal disease without these severe, negative side effects. The Lupus Foundation estimates that there are approximately one million lupus patients in the United States. We believe that 30% to 50% of these lupus patients have renal disease. We have also developed novel, orally-active, small-molecule SSAO inhibitors for the treatment of autoimmune diseases and acute and chronic inflammatory disorders. Preclinical studies have shown that these inhibitors reduce disease activity in animal models of multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, stroke, systemic inflammation and acute inflammation. Corporate information We were incorporated in the State of Delaware in 1989. Our principal executive offices are located at 6455 Nancy Ridge Drive, San Diego, California 92121 and our telephone number is (858) 452-6600. Our website is located at www.ljpc.com. We make available on our website, free of charge, a link to our Annual Report on Form 10-K, Quarterly Reports on Form 10-Q, Current Reports on Form 8-K and amendments to those reports as soon as practicable after we electronically file such material with the Securities and Exchange Commission, or SEC. The information contained on our website is not part of this prospectus. Risk factors Investing in our securities involves risk. The prospectus supplement applicable to each type or series of securities we offer will contain a discussion of the risks applicable to an investment in La Jolla

MIB Abstract ID Number: 15287

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Cellectar, state in new territory; Wisconsin sprouting companies at leading edge of drug industry

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Lead Author: KATHLEEN GALLAGHER

The Milwaukee Journal Sentinel, 2008-05-04

Inside is a manufacturing plant that is one of only four in the country with the ability to make pharmaceuticals using radioactive ingredients.

Cellectar's $3.3 million custom-designed building has 1-foot thick concrete walls and a sophisticated control system for monitoring pressure and air flow that sends e-mails, then phone calls, if so much as one fan goes awry. It's the first completely new, radiopharmaceutical drug manufacturing facility built in the United States in 20 years, said Bill Clarke, Cellectar's president and chief executive officer.

It isn't by any means as large as radiopharmaceutical manufacturing facilities owned by GE Healthcare, Covidien or Bristol- Myers Squibb, but it represents a giant step forward into an important area for Wisconsin's biotech industry: drug development.

"The ante is bigger, the risk is bigger, but if you have a success story, the markets are enormous -- in some cases, in the billions of dollars," said John Neis, senior partner at Venture Investors, a Madison venture capital firm that helped raise $13 million for Cellectar in January.

Led by veteran companies such as Promega Corp. and Gilson Inc., Madison is home to a research tools industry that sells everything from test tubes to genetic testing technologies to researchers around the world.

A breeding ground

Driven by the pharmaceutical industry's hunger for new drug candidates and aversion to the risk of developing them in the early stages, new companies have formed around the country to get promising compounds through the first two phases of the four-phase clinical trials required by the Food and Drug Administration.

In Wisconsin, the availability of larger pools of private equity money and experienced executives have combined with the wealth of life sciences research at the University of Wisconsin-Madison to create a breeding ground for drug development companies.

"We've long had the technology to have therapeutic companies here, but it's only recently that the combination of leadership and financing has come into play as well," said Tom Still, president of the Wisconsin Technology Council.

Take Cellectar. The company has raised $22 million from investors and is being run by Clarke, who was previously GE Healthcare's chief technology officer and chief medical officer.

Clarke said Cellectar is almost ready to start clinical trials for a drug based on its technology, which uses fat-like molecules to deliver radioisotopes that can either destroy malignant cells or help imaging equipment locate them.

"When you start looking at therapeutics, the cost to get regulatory approval is enormous," Neis said. "Two decades ago it just wasn't finance-able in this state."

You don't have to tell that to Hector DeLuca.

The UW biochemistry professor and top executive at Madison-based Deltanoid Pharmaceuticals LLC was one of the first drug inventors in the country to wrangle the patent rights to his federally funded drug discoveries out of the government's hands in the late 1960s so they could be commercialized.

DeLuca says his lab has produced eight pharmaceuticals, including Zemplar for Abbott Labs, that are marketed around the world. DeLuca and his wife, who is also a scientist, started Deltanoid in 2001 to get drugs from their labs and others on the Madison campus through Phase II trials so they'll be more attractive to big drug companies.

"Eighty percent of drugs that make it through Phase II trials end up as pharmaceuticals," DeLuca said.

Creating jobs in state

Getting a compound through Phase II is a complex, highly regulated process, said Trevor Twose, CEO of Madison's Mithridion Inc. and head of Biopons Inc., a Fitchburg biotech consulting firm.

The Madison area has good technology and funding, along with a base of skilled research employees and several contract research organizations that can sponsor clinical trials, Twose said. But companies still have to go out of state for advisers with drug development experience.

It's important to breed drug development companies here to "exploit the real value" of technologies developed at Wisconsin research institutions, Twose said.

"That's what creates the jobs and the thriving economy," he said.

Cellectar is capturing even more value by doing its own manufacturing.

Much of Cellectar's world-class manufacturing facility and equipment was built and designed by people and firms in Wisconsin, like Ruedebusch Development and Construction in Madison and Vulcan Global Manufacturing Solutions in Milwaukee, Clarke said.

And the state's congressional delegation has been instrumental in helping Cellectar ensure that patients will get Medicare reimbursement for its drugs, he said.

That developing infrastructure should help to create even more drug development companies for the state.

"I want to get other small pharmaceutical companies around here," Clarke said. "The more synergistic people and infrastructure you get, the better for all of us."

DRUG DEVELOPERS

Along with Cellectar, a number of Wisconsin companies are trying to develop pharmaceuticals.

Centrose LLC, Madison

ConjuGon, Madison

Deltanoid Pharmaceuticals LLC, Madison

FluGen Inc., Madison

Mithridion Inc., Madison

ProCertus BioPharm, Madison.

Quintessence Biosciences Inc., Madison

Zystor Therapeutics Inc., Wauwatosa

MIB Abstract ID Number: 15291

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Cancer; Neoprobe Receives Regulatory Clearance for Lymphoseek Clinical Study

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Lead Author: [none given]

Medical Devices & Surgical Technology Week, 2008-05-04

Neoprobe Corporation; Neoprobe Receives $3 Million in Clinical Funding

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Lead Author: [none given]

Obesity, Fitness & Wellness Week, 2008-05-03

ACT Biotech Acquires Clinical and Early Stage Oncology Portfolio Licenses From Bayer Healthcare

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Lead Author: [none given]

PR Newswire Europe, 2008-05-07

NGN Capital announced today the formation of ACT Biotech Inc., a new company dedicated to developing and commercializing targeted oral cancer drugs. ACT Biotech has entered into a license agreement with Bayer HealthCare LLC for a portfolio of clinical and early stage oncology assets. In conjunction with the agreement, ACT has raised US$12 million in the first tranche of a Series A financing led by NGN Capital, New York. The company has also now initiated the syndication process to raise a total of US$20 million, expected to be completed in the second quarter of 2008.

Under the terms of the license agreement with Bayer, ACT Biotech has acquired an anti-angiogenic receptor tyrosine kinase inhibitor entering Phase II clinical studies for colorectal cancer, amongst other indications. An additional program in-licensed in this agreement is a first-in-class multi-mode kinase inhibitor in late preclinical stage with application in a variety of cancer types. The company also acquired several additional preclinical stage programs in oncology. As part of the agreement, Bayer will maintain a minority equity stake in ACT Biotech.

Wolf-Dieter Busse, Ph.D., co-founder of Aerovance, who will serve as Chief Executive Officer of ACT Biotech stated, "We are delighted about our strong portfolio and are eager to advance these exciting cancer drug candidates with our seasoned management team of leading experts in cancer drug discovery and clinical development." In addition, the company will continue to cooperate with the Melanoma Therapeutics Foundation, which is a co-founder in ACT Biotech. The new company will be based in San Francisco, California.

"This license agreement allows Bayer to concentrate on its development program for Nexavar and other primary Oncology assets, while ACT will continue the development of promising, earlier clinical and pre-clinical assets," said Gunnar Riemann, Member of the Executive Committee of Bayer HealthCare.

"With this agreement ACT has obtained a collection of novel small molecule kinase inhibitors, which have the potential to become an integral part of a safer and more effective choice in modern cancer combination therapy," said Dr. Georg Nebgen, Managing General Partner of NGN Capital. "ACT Biotech highlights NGN's continued commitment to attract late stage innovation in drug development," said John Costantino Managing General Partner of NGN Capital.

Dr. Georg Nebgen and John Costantino of NGN Capital, Dr. Nils Behnke of Bain &Co. and Dr. Busse will constitute the Board of Directors of ACT Biotech. In addition, the management team will include Dr. Ali Fattaey, Chief Operating Officer, former Onyx VP of R&D.

About NGN Capital

NGN Capital is a global healthcare venture capital investment firm. NGN has investment capabilities across a broad spectrum of healthcare segments, including drug products, medical devices, and healthcare services, with an emphasis on later-stage opportunities. NGN has offices in New York, NY, Heidelberg, Germany, and Greenwich, CT. More information on NGN can be found at www.ngncapital.com.

About ACT Biotech, Inc.

ACT Biotech is a San Francisco-based privately-held pharmaceutical company focused exclusively on the development and commercialization of targeted cancer drugs.

Web site: http://www.ngncapital.com

NGN Capital

Georg Nebgen, Ph.D., Managing General Partner, or John Costantino, Managing General Partner, +1-212-972-0077, both of NGN Capital; or Wolf-Dieter Busse, Ph.D., Chief Executive Officer, +1-510-812-5782, for ACT Biotech

MIB Abstract ID Number: 15298

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Magnetic resonance imaging-based detection of glial brain tumors in mice after antiangiogenic treatment.

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Lead Author: Claes A

Additional Authors: Gambarota G, Hamans B, van Tellingen O, Wesseling P, Maass C, Heerschap A, Leenders W.

Int J Cancer. , 2008-05-01, 122(9):1981-6.

Department of Pathology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.

Proper delineation of gliomas using contrast-enhanced magnetic resonance imaging (CE-MRI) poses a problem in neuro-oncology. The blood brain barrier (BBB) in areas of diffuse-infiltrative growth may be intact, precluding extravasation and subsequent MR-based detection of the contrast agent gadolinium diethylenetriaminepenta-acetic acid (Gd-DTPA). Treatment with antiangiogenic compounds may further complicate tumor detection as such compounds can restore the BBB in angiogenic regions. The increasing number of clinical trials with antiangiogenic compounds for treatment of gliomas calls for the development of alternative imaging modalities. Here we investigated whether CE-MRI using ultrasmall particles of iron oxide (USPIO, Sinerem) as blood pool contrast agent has additional value for detection of glioma in the brain of nude mice. We compared conventional T1-weighted Gd-DTPA-enhanced MRI to T2*-weighted USPIO-enhanced MRI in mice carrying orthotopic U87 glioma, which were either or not treated with the antiangiogenic compound vandetanib (ZD6474, ZACTIMA). In untreated animals, vessel leakage within the tumor and a relatively high tumor blood volume resulted in good MRI visibility with Gd-DTPA- and USPIO-enhanced MRI, respectively. Consistent with previous findings, vandetanib treatment restored the BBB in the tumor vasculature, resulting in loss of tumor detectability in Gd-DTPA MRI. However, due to decreased blood volume, treated tumors could be readily detected in USPIO-enhanced MRI scans. Our findings suggest that Gd-DTPA MRI results in overestimation of the effect of antiangiogenic therapy of glioma and that USPIO-MRI provides an important complementary diagnostic tool to evaluate response to antiangiogenic therapy of these tumors. (c) 2007 Wiley-Liss, Inc.

MIB Abstract ID Number: 15302

PreMedline Identifier: 18081012

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Dietary energy source affects glucose kinetics in trained Arabian geldings at rest and during endurance exercise.

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Lead Author: Treiber KH

Additional Authors: Geor RJ, Boston RC, Hess TM, Harris PA, Kronfeld DS.

J Nutr., 2008-05-01, 138(5):964-70.

Department of Animal and Poultry Sciences, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061, USA. lyradorn@hotmail.com

Advances in modeling and tracer techniques provide new perspective into glucose utilization and potential consequences to health or exercise performance. This study used stable isotope and compartmental modeling to evaluate how adaptation to a feed high in sugar and starch (SS) compared with a feed high in fat and fiber (FF) affects glucose kinetics at rest and during exercise in horses. Six trained Arabians adapted to each feed underwent similar tests at rest and while running approximately 4 m/s on a treadmill. For both tests, horses received 100 micromol/kg body weight [6,6-(2)H]glucose through a venous catheter. Circulating tracer glucose was described for 150 min by exponential decay curves and compartmental analysis. All parameters of glucose transfer increased with exercise (P < or = 0.004). Compared with FF horses, SS horses had higher circulating glucose (P = 0.022) and fractional glucose transfer rates (min(-1)) at rest (P = 0.055). Exercise increased glucose irreversible loss (mmol/min) more in SS horses (P = 0.037). Total glucose transfer during exercise tended to be greater in SS horses (0.027 +/- 0.002 mmol/min) compared with FF horses (0.023 +/- 0.002 mmol/min) (P = 0.109). This study characterized the effect of diet on glucose kinetics in resting and exercising horses using new modeling methods. Horses adapted to a fat-supplemented feed utilized less glucose during low-intensity exercise. Fat supplementation in horses may therefore promote greater flexibility in the selection of substrate to meet energy demands for optimal health and performance.

MIB Abstract ID Number: 15267

PreMedline Identifier: 18424608

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ALTUS PHARMACEUTICALS INC., FORM TYPE: 10-Q, May 07, 2008

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Lead Author: [none given]

2008-05-07, CAMBRIDGE, Massachusetts, 02139

Overview

We are a biopharmaceutical company focused on the development and commercialization of oral and injectable protein therapeutics for gastrointestinal and metabolic disorders, with three product candidates in the clinical stage of development. We are using our proprietary protein crystallization technology to develop protein therapies, which we believe will have significant advantages over existing products and will address unmet medical needs. Our product candidates are designed to either increase the amount of a protein that is in short supply in the body or degrade and remove toxic metabolites from the blood stream. Our three most advanced product candidates are: Trizytek TM [porcine-free enzymes] (formerly ALTU-135), for which we are currently conducting a Phase III clinical trial in cystic fibrosis patients for the treatment of malabsorption due to exocrine pancreatic insufficiency and two long-term Phase III safety studies; ALTU-238, for which we have completed a Phase II clinical trial in adults for the treatment of growth hormone deficiency; and ALTU-237, for which we have completed a Phase I clinical trial for the treatment of primary hyperoxaluria and enteric hyperoxaluria. We also have a pipeline of other product candidates in preclinical research and development. We have generated significant losses as we have advanced our lead product candidates into clinical development and expect to continue to generate losses as Trizytek completes its clinical development and ALTU-238 and ALTU-237 move into later stages of clinical development. As of March 31, 2008, we had an accumulated deficit of $263.5 million.

MIB Abstract ID Number: 15285

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ENZON PHARMACEUTICALS INC, EXHIBIT TYPE: EXHIBIT 99, May 07, 2008

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Lead Author: [none given]

2008-05-07

BRIDGEWATER, NJ

Enzon Pharmaceuticals, Inc. (Nasdaq: ENZN) today announced strong first quarter 2008 financial results. For the three months ended March 31, 2008, Enzon reported a net income of $1.5 million or $0.03 per diluted share, as compared to a net loss of $2.8 million or $0.06 per diluted share for the first quarter of 2007. The Company's first quarter 2008 results were positively impacted by strong revenues across all business segments. "The Company continues to generate strong top-line results across all of our business segments," said Jeffrey H. Buchalter, chairman and chief executive officer of Enzon. "Earlier today, we announced a plan to spin-off our biotechnology business. The spin-off, upon completion, will allow the two independent companies to focus on their core competencies and appeal to their own unique shareholders." Recent Highlights

 *  The Company reduced a significant portion of its 2008 debt ahead of the required timeline to only $12.5 million.
 *  PEG-SN38 was featured in the March 15 th issue of Clinical Cancer Research published by the American Association for Cancer Research, Inc. (AACR).
 *  The Company presented preclinical data on the HIF-1alpha antagonist at the 2008 AACR annual meeting in San Diego, California.
 *  The Company closed its Phase I trial evaluating Oncaspar ® in combination with Gemzar ® for patients with solid tumors and lymphoma.
 *  In April, Cimzia ® , which utilizes Enzon's PEGylation technology, was approved in the U.S. for the treatment of moderate to severe Crohn's disease.

MIB Abstract ID Number: 15286

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Bioterrorism; Aethlon Medical to Pursue U.S. Government Biodefense Contract

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Lead Author: [none given]

Biotech Week, 2008-05-07

"Based on pre-clinical data and human treatment experience, I believe our Hemopurifier(R) is the most advanced broad-spectrum treatment for viral pathogens identified as bioterror threats," stated James A. Joyce, chairman and CEO of Aethlon Medical. To reinforce the broad spectrum capabilities of the Hemopurifier(R), Aethlon's contract response will include in vitro effectiveness data against Dengue hemorrhagic fever, Ebola hemorrhagic fever, Lassa hemorrhagic fever, H5N1 avian influenza (Bird Flu), the reconstructed 1918 influenza virus, West Nile virus, Human immunodeficiency virus (HIV), Hepatitis-C virus (HCV), and vaccinia and monkeypox, which both represent models associated with human smallpox infection.

The BAA solicitation also emphasizes that candidate treatment countermeasures will complete a phase I human safety study within a five-year contract period. To comply with this stipulation, Aethlon's contract response will include human safety data from clinical programs conducted at the Apollo Hospital and the Fortis Hospital, both in Delhi, India. Additionally, Aethlon will provide the investigational device exemption (IDE) already submitted to the U.S. Food and Drug Administration (FDA) that requests permission to initiate human safety studies of the Hemopurifier(R) as a broad-spectrum treatment countermeasure against select bioterror and pandemic threats. As human efficacy studies against bioterror threats are not permissible for obvious humanitarian reasons, the demonstration of safety remains the sole regulatory challenge in humans. Aethlon plans to request permission to initiate the IDE-related human study soon after its contract response to the BAA solicitation.

"Now that broad-spectrum therapies have evolved to become a focal point of U.S. biodefense programs, I am optimistic that the BAA contract solicitation will be the first of several opportunities to collaborate with our government to advance the commercialization of our Hemopurifier(R) as a treatment against some of the world's deadliest pathogens," stated Joyce. "Additionally, successful navigation of these opportunities may reduce our future dependence on financing from the financial markets," concluded Joyce.

Virtually all of the pathogens considered to be material bioterror threats are untreatable with traditional drug and vaccine therapies. Effective treatments are either non-existent, of limited usefulness, or vulnerable to both naturally emerging and intentionally engineered pathogens. Innovative therapies offering broad-spectrum activity against different classes of microbes could potentially be effective against both traditional and non-traditional threats. Broad-spectrum therapies also provide the possibility that a limited number of treatment countermeasures could replace the need for the staggering number of pathogen-specific drugs that would be required for emergency use in bioterror and pandemic threat programs. Additionally, broad-spectrum strategies that are able to overcome drug resistance could extend the clinical utility of existing therapies. For these reasons, the U.S. Department of Health and Human Services (HHS) recently mandated that therapies able to demonstrate broad-spectrum effectiveness against multiple pathogens are to be the focal point of government programs that fund the development and commercialization of countermeasures against bioterror and pandemic threats. Aethlon Medical considers the Hemopurifier(R) to be the leading broad-spectrum candidate as evidenced by its breadth of pre-clinical data and human treatment experience.

This article was prepared by Biotech Week editors from staff and other reports. Copyright 2008, Biotech Week via NewsRx.com.

MIB Abstract ID Number: 15290

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Cohera Medical, Inc. Announces Closing of Insider Round of Financing for Over $7.6 Million

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Lead Author: [none given]

PR Newswire (U.S.), 2008-05-07

Astute Medical Raises $6.2 Million in Series A Financing Round Led by De Novo Ventures

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Lead Author: [none given]

PR Newswire (U.S.), 2008-05-01

"This investment is an exciting event that lays the foundation for our research and development activities," said Christopher Hibberd, Astute Medical chief executive officer. "We believe the participation of our lead investor De Novo Ventures demonstrates confidence in our ability to develop innovative diagnostic tests for use in acute hospital settings."

"Astute Medical has enormous potential to identify and deliver novel diagnostic tests that address costly diseases and medical conditions," said Fred Dotzler, managing director at De Novo Ventures. "We're delighted to work with Astute Medical and see promise in their goal of bringing innovative solutions to hospitals where poor diagnostic technologies contribute to delays and higher costs."

Astute Medical, founded in 2007, is led by Christopher Hibberd and Paul McPherson Ph.D., former members of the management at Biosite Incorporated, a leading diagnostics company acquired by Inverness Medical Innovations in 2007 for $1.7 billion. Hibberd served at

Biosite for 10 years, most recently as senior vice president corporate development. Dr. McPherson was at Biosite for fourteen years, most recently as vice president research and development.

About Astute Medical, Inc.

Astute Medical is dedicated to improving diagnosis of high-risk medical conditions and diseases through the identification and validation of protein biomarkers that can serve as the basis for novel diagnostic tests. The Company's focus is community and hospital acquired acute conditions that require rapid diagnosis and risk assessment. Astute Medical will develop tests for patients who present to emergency departments with acute symptoms and for hospitalized patients who are at risk for an acute event. The Company's current areas of interest include abdominal pain, acute coronary syndrome, acute kidney injury, congestive heart failure, sepsis, and cerebrovascular disease.

SOURCE Astute Medical, Inc.

Christopher Hibberd, Chief Executive Officer of Astute Medical, Inc., +1-858-792-3544

MIB Abstract ID Number: 15300

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Hepatosplenomegaly is associated with low regulatory and Th2 responses to schistosome antigens in childhood schistosomiasis and malaria coinfection.

Direct Link to Abstract

Lead Author: Wilson S

Additional Authors: Jones FM, Mwatha JK, Kimani G, Booth M, Kariuki HC, Vennervald BJ, Ouma JH, Muchiri E, Dunne DW.

Infect Immun. , 2008-05-01, 76(5):2212-8. Epub 2008 Feb 19.

Department of Pathology, University of Cambridge, , Tennis Court Road, Cambridge, CB2 1QP, United Kingdom. sw320@cam.ac.uk

Hepatosplenomegaly among Kenyan schoolchildren has been shown to be exacerbated where there is transmission of both Schistosoma mansoni and Plasmodium falciparum. This highly prevalent and chronic morbidity often occurs in the absence of ultrasound-detectable periportal fibrosis and may be due to immunological inflammation. For a cohort of school-age children, whole-blood cultures were stimulated with S. mansoni soluble egg antigen (SEA) or soluble worm antigen (SWA). Responses to SWA were found to be predominantly Th2 cytokines; however, they were not significantly associated with either hepatosplenomegaly or infection with S. mansoni or P. falciparum. In comparison, SEA-specific Th2 cytokine responses were low, and the levels were negatively correlated with S. mansoni infection intensities and were lower among children who were coinfected with P. falciparum. Tumor necrosis factor alpha levels in response to stimulation with SEA were high, and a negative association between presentation with hepatomegaly and the levels of the regulatory cytokines interleukin-6 and transforming growth factor beta(1) suggests that a possible mechanism for childhood hepatomegaly in areas where both malaria and schistosomiasis are endemic is poor regulation of an inflammatory response to schistosome eggs.

MIB Abstract ID Number: 15304

PreMedline Identifier: 18285496

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