동향

Diabetes, Endocrinology and Metabolic Diseases

발주처

국가

분야

과학기술과 인문사회

접수기간

~

URL


Diabetes, Endocrinology and Metabolic Diseases Primary Sponsor: Department of Health and Human Services Deadline: 4/1/2001; 8/1/2001; 12/1/2001 KEYWORDS National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) The NIDDK supports research in diabetes, endocrinology and metabolic diseases; digestive diseases and nutrition; and kidney, urologic and hematologic diseases. For additional information about areas of interest to the NIDDK, please visit our home page at http://www.niddk.nih.gov. Diabetes, Endocrinology and Metabolic Diseases The Division of Diabetes, Endocrinology and Metabolic Diseases supports basic and clinical research on the etiology, pathogenesis, prevention, diagnosis, and treatment of diabetes mellitus and its complications; endocrine diseases; osteoporosis; cystic fibrosis, and other metabolic disorders; as well as research on basic endocrine and metabolic processes. Research topics of potential interest to small businesses include, but are not limited to: A. Development and characterization of animal models for diabetes, obesity, or complications of diabetes. B. Development of non-invasive or minimally invasive methods for monitoring blood glucose; implantable glucose sensors; improved insulin delivery methods or devices; improved insulin formulations; or integration of sensor and delivery systems to create an artificial pancreas. C. Development a cell culture model of the human pancreatic beta cell that will have the following salient features: (1) stably maintain its physiologic responsiveness to glucose and othe secretagogues, (2) accurately reflect in vivo signaling through cell surface and nuclear receptors relevant to the regulation of insulin production and secretion, (3) maintain responsiveness to growth factors and cytokines normally active in the development and maintenance of the pancreatic beta cell, and (4) retain contact growth inhibition as in the in vivo situation. D. Development of novel methods for beta-cell expansion, use of islet stem cells for allografting, or short or long term culture of pancreatic tissues for islet cell transplantation. E. Development of antibodies to cell surface markers on mammalian stem/progenitor cells from the pancreas that will facilitate the prospective identification and purification of these cells. F. Development of quantitative clonogenic assays both in vivo and in vitro that will allow characterization of potential stem/progenitor cells of the pancreas. G. Development of tests for islet viability, using functional genomics, proteomics, or other methods, and of improved methods to enhance viability of islets prior to implantation, methods to improve engraftment of islets, or methods to protect isle grafts though immunomodulation/tolerance induction or immuno-isolation. H. Development of improved methods for whole pancreas transplantation such as improved protective measures, less toxic drugs, immunomodulation or tolerance induction. I. Development of novel or improved methods for monitoring metabolic control in diabetes. J. Development of non-invasive imaging methods for in vivo measurement of pancreatic beta cell mass, function, inflammation or perfusion, for use in both endogenous pancreas and transplanted pancreatic tissue/islet cells. K. Development of assays to detect viruses in pancreatic or lymphoid tissue to study the etiology of type 1 diabetes. L. Development of techniques or products useful in prevention of type 1 diabetes, including strategies for vaccination or immunomodulation/tolerance induction. M. Development of novel methods for the large scale production of GAD or other potential immunoprotective proteins for use in clinical trials. N. Development of improved methods of HLA typing, assays for predictive autoantibodies, and other tests for use in identifying patients at risk of developing type 1 diabetes. O. Development and testing of new strategies to detect the onset and monitor the progression of the late complications of diabetes, particularly neuropathy. P. Development of surrogate markers for identification of disease states and disease progression, and for use as endpoints in clinical trials of diabetes and its complications; osteoporosis; and cystic fibrosis. Q. Development and testing of new strategies to prevent the late complications of diabetes, including new modalities to prevent the development of or promote complete, rapid healing of diabetic foot ulcers. R. Development of DNA chip array technologies and other new methods to identify and analyze differential gene expression in cells and tissues affected by diabetes mellitus and its complications. S. Development of new vectors, gene inactivation techniques, and other novel methodologies for gene therapy of diabetes and its complications. T. Development of methods to maximize the ability of patients and providers to implement recommended therapy for diabetes and achieve desirable outcomes, including strategies to enhance diabetes self-management, to address social and cultural barriers to adherence, to improve communication between patients and care providers, and to develop alternative models of health care delivery (such as computer-aided management or telemedicine). U. Development of new drugs or innovative strategies to reduce peripheral insulin resistance in type 2 diabetes. V. Development of quantitative measures for the evaluation of health behavior modification programs, such as methods to measure dietary intake and physical activity, in the prevention and control of diabetes. W. Development of non-peptide agonists and antagonists for hormone and neuropeptide receptors with potential utility in structural studies or for therapeutic use in the treatment of endocrine disorders, including obesity. X. Identification of new ligands for previously unclassified (orphan) receptors and/or partial agonists or antagonists with therapeutic potential. Y. Development of Selective Receptor Modulators (SRMs) with tissue-specific action. Z. Development of nonradioactive techniques for measuring hormones. AA. Development of new techniques for simultaneous measurement of multiple hormones in a single solution. BB. Development of new tests or reagents for diagnosis of endocrine disorders. CC. Development of new or improved technologies for physiologic and metabolic measurements in transenic mice, including miniaturized assays, metabolic cages, and new imaging strategies. DD. Development of analytical and display tools which could be used with large clinical data sets, imaging date, microarray assays, or genomic data. EE. Development of new, automated techniques for protein crystallization. FF. Development of new approaches to the modeling, analysis, and prediction of three-dimensional protein structure (including membrane proteins). GG. Development of novel methods for determination of the three-dimensional structure of transporter proteins or protein families. HH. For cystic fibrosis, NIDDK is interested in research in the following areas: 1. Development of specific inhibitors of CFTR. 2. Development of measures or endpoints that can be used for evaluating the success of therapy for cystic fibrosis, including gene therapy. 3. Development or improvement in diagnostic tests for cystic fibrosis. 4. Animal or cell models useful for the study of cystic fibrosis, including use of transgenic technology. 5. Identification or characterization of potential therapeutic modalities capable of ameliorating the molecular defects in cystic fibrosis, including agents to improve trafficking and function of mutant CFTR, to enhance function of channels which may serve as alternatives to CFTR, to enhance other cell processes impaired by mutations in CFTR, and to correct the molecular defects (such as impaired anti-microbial peptide activity) leading to the infection and inflammation characteristic of cystic fibrosis. 6. Development or improvement in approaches to gene therapy for cystic fibrosis through optimization of gene delivery systems to improve tropism for target cells, increase the efficiency and duration of transgene expression, and mitigate potential toxicity, or evaluation of safety and efficacy of methods for gene therapy of cystic fibrosis in animals models or human subjects. 7. Development of products useful in assessing or improving nutritional status in patients with cystic fibrosis, including improvement of pancreatic enzyme preparations. 8. Development and validation of effective strategies to improve compliance with therapy and promote health-enhancing behavior for people with cystic fibrosis. 9. Development, testing, and validation of educational materials for use in conjunction with (1) carrier detection or (2) neonatal screening or other methods for diagnosis of cystic fibrosis useful for helping people understand the risks, benefits and imitations of the test and the interpretation of the results. II. For other inherited metabolic disorders, e.g., defects of urea cycle enzymes and enzymes of purine and pyrimidine metabolism, glycogen and lipid storage diseases, organic and aminoacidurias, NIDDK is interested in research leading to: 1. Development of restriction fragment length polymorphisms and polymerase chain reaction techniques for diagnostic reagents and tests and adaptation of these techniques to prenatal diagnosis in fetal cells isolated from maternal blood. 2. Production of large quantities of enzymes by recombinant DNA technology in bacteria cell lines or transgenic animals as a first step toward production of an orphan drug. 3. Design and synthesis of chemical "activators" for mutant enzymes. 4. Design and synthesis of new, stabilized, biological active peptides and proteins useful for enzyme replacement therapy. 5. Development of stabilized enzymes through in vitro site-directed mutagenesis or enzymatic modification. 6. Development of animal models of genetic diseases that mimic the pathophysiology of the human disease and can be used to assess treatments. 7. Improvements in transfection efficiency, level of gene expression or duration of gene expression for currently used gene therapy vectors. 8. Development of packaging cell lines which will package replication defective viruses to higher titers or package viral DNA with new or altered viral envelope proteins to improve cell targeting. 9. Development of new vectors including AAV, lentivirus or Herpes virus with improved ability to transduce non-dividing cells such as hematopoietic stem cells, neurons, hepatocytes or lung epithelium. 10. Development of efficient homologous recombination techniques to allow insertion of a corrected gene in its normal location. 11. Improvements in experimental delivery systems such as liposomes or conjugates for receptor-mediated endocytosis to increase efficiency of targeted DNA delivery and increase duration of expression. For additional information on research topics, contact: Diabetes, Endocrinology and Metabolic Diseases Dr. Barbara Linder National Institute of Diabetes and Digestive and Kidney Diseases Democracy 2, Room 699 Bethesda, MD 20892 (301) 594-0021; Fax: (301) 480-3503 Email: bl99n@nih.gov Digestive Diseases and Nutrition Dr. Judith Podskalny National Institute of Diabetes and Digestive and Kidney Diseases Democracy 2, Room 667 (301) 594-8876; Fax: (301) 480-8300 Email: jp53s@nih.gov Kidney, Urologic and Hematologic Diseases Dr. James Scherbenske National Institute of Diabetes and Digestive and Kidney Diseases Democracy 2, Room 613 Bethesda, MD 20892 (301) 594-7719; Fax: (301) 480-3510 Email: js255f@nih.gov For administrative and business management questions, contact: Mr. George Tucker, M.B.A. Grants Management Specialist National Institute of Diabetes and Digestive and Kidney Diseases Democracy 2, Room 635 (301) 594-8853; Fax: (301) 480-3504 Email: gt35v@nih.gov NOTE: The Solicitations listed on this site are partial copies from the various SBIR agency solicitations and are not necessarily the latest and most up-to-date. For this reason, you should always use the suggested links on our reference pages. These will take you directly to the appropriate agency information where you can read the official version of the solicitation you are interested in. The official link for this page is: http://grants.nih.gov/grants/funding/sbir.htm. Solicitation closing dates are: April 1, August 1, and December 1, 2001.