Abstract: The present invention is directed to a tumor suppressor protein which has been designated hamartin and to the gene, TSC1, which encodes this protein. Mutations in the gene have been found to be associated with certain types of tuberous sclerosis and this has served as a basis for a diagnostic method designed to identify patients that have, or are likely to develop, symptoms associated with this disease. The introduction of the TSC1 gene and subsequent expression of hamartin into cells may be used as a means for treating tuberous sclerosis and other conditions characterized by abnormal cellular growth.

Abstract: The present invention discloses compositions containing natural human extracellular matrices and methods for the use thereof. More particularly, the present invention provides compositions and methods for the repair of skin defects using natural human extracellular matrix by injection.

Abstract: The invention provides a human preproneurotensin/neuromedin N (HPPN) and polynucleotides which identify and encode HPPN. The invention also provides expression vectors, host cells, antibodies, agonists, and antagonists. The invention also provides methods for treating or preventing disorders associated with expression of HPPN.

Abstract: The invention proposes a method for detecting and/or quantifying, in a biological sample, a cytotoxic factor, in particular a gliotoxic factor, with respect to adherent target cells, in particular macroglial cells, the toxicity of which causes the death by apoptosis of said cells. The method comprises providing an initial fraction of the sample, optionally enriched with the toxic factor by previous treatment, incubating the initial toxic factor with a reference culture medium comprising adherent target cells, and detecting and/or quantifying in the adherent target cells killed by apoptosis, by flow cytometry, at least one direct or indirect characteristic associated with the apoptotic adherent cells of the whole or part of the incubated medium, which, if it is present and/or is quantified, qualifies the sample as positive, i.e. as containing said toxic factor. The initial biological sample is preferably a urine specimen.

Abstract: The present invention contemplates therapeutic compositions containing a fibrinogen homolog capable of binding to endothelial cells in an RGD-independent manner that inhibits fibrinogen binding to endothelial cells. Also described are therapeutic compositions containing an ICAM-1 homolog capable of binding to fibrinogen in an RGD-independent manner that inhibits fibrinogen binding to endothelial cells. Methods of inhibiting endothelial cell and fibrinogen mediated inflammation within a patient by administering a homolog of this invention are also contemplated.

Abstract: The present invention relates to the identification, cloning and sequencing of nucleic acid molecules encoding an isoform of the enzyme glutamic acid decarboxylase and further relates to the use of these molecules and/or peptides and polypeptides encoded thereby in diagnostic tests for Insulin Dependent Diabetes Mellitus and other diseases in which glutamic acid decarboxylase is an autoantigen and in the treatment of patients suffering from these diseases.

Abstract: FK506 and geldanamycin promote nerve regeneration by a common mechanism that involves the binding of these compounds to polypeptide components of steroid receptor complexes other than the steroid hormone binding portion of the complex (FKBP52 and hsp90, respectively). These and other agents cause hsp90 dissociation from steroid receptor complexes or block association of hsp90 with steroid receptor complexes.

Abstract: Methods for detecting human factor VIII or factor VIII-like polypeptides in and isolating it from solutions such as blood or conditioned media are disclosed, together with reagents suitable for the purpose comprising binding moieties that recognize human factor VIII and/or a factor VIII-like polypeptide and form a binding complex therewith. Preferred polypeptide binding moieties are particularly disclosed.