Abstract: The present invention provides a method for treating inflammation in a subject which comprises administering to the subject soluble receptor for advanced glycation endproduct (sRAGE) in an amount effective to inhibit binding of advanced glycation endproducts (AGEs) to RAGE thereby treating inflammation in the subject. The present invention also provides for a method for treating inflammation in a subject which comprises administering to the subject an agent in an amount effective to inhibit the interaction between receptor for advanced glycation endproduct (RAGE) and its ligand thereby treating inflammation in the subject.

Abstract: The present invention provides for a transgenic non-human animal whose cells contain a DNA sequence comprising: (a) a nerve tissue specific promoter operatively linked to a DNA sequence which encodes amyloid-beta peptide alcohol dehydrogenase (ABAD), and (b) a nerve tissue specific promoter operatively linked to a DNA sequence encoding a mutant human amyloid precursor protein hAPP695, hAPP751 and hAPP770 bearing mutations linked to familial Alzheimer's disease in humans, wherein the non-human animal exhibits at least one phenotype from the group consisting of: reduced basal synaptic transmission; inhibited synaptic plasticity; increased neuronal stress; elevated 4-hydroxynonenal in cerebral cortex; increased heme oxygenase type I in cerebral cortex; decreased synaptophysin in cerebral cortex; decreased micortubule-associated protein 2 in cerebral cortex; and increased levels of activated caspase 3 antigen in cortical neurons.

Abstract: The present invention provides an isolated nucleic acid encoding an endoplasmic reticulum associated amyloid-beta peptide binding (ERAB) polypeptide. The ERAB polypeptide may comprise human ERAB polypeptide. The present invention provides a purified ERAB polypeptide, as well as a method for treating a neurodegenerative condition in a subject which comprises administering to the subject an agent in amount effective to inhibit ERAB polypeptide binding to amyloid-beta peptide so as to thereby treat the neurodegenerative condition.

Abstract: The invention provides a method for reducing damage to an ischemic tissue which comprises contacting cells of the tissue with an inhibitor of Early Growth Response Factor-1 Protein (Egr-1). In addition, the invention provides a method for reducing vascular injury during reperfusion of an ischemic tissue in a subject which comprises contacting the tissue with a compound which inhibits expression of Early Growth Response Factor-1 (Egr-1) protein in the tissue so as to reduce vascular injury in the tissue during reperfusion. wherein the inhibitor is a nucleic acid consisting essentially of the polynucleotide sequence 5?-CTTGGCCGCTGCCAT-3? (SEQ ID NO:1). In one embodiment of the invention, the subject has suffered a stroke, or a myocardial infarction. In another embodiment of the invention, the subject is undergoing or has undergone angioplasty, cardiac surgery, vascular surgery, or organ transplantation.

Abstract: The present invention provides for a transgenic non-human animal whose cells contain a recombinant DNA sequence comprising a nerve tissue specific promoter operatively linked to a DNA sequence which encodes amyloid-beta peptide alcohol dehydrogenase (ABAD), and exhibits at least one phenotype from the group consisting of: overexpression of ABAD, elevated levels of basal ATP; protection from metabolic or ischemic stress.

Abstract: The present invention provides a method for decreasing cerebral vasoconstriction in a subject suffering from chronic or acute cerebral amyloid angiopathy which comprises administering to the subject an inhibitor of receptor for advanced glycation endproduct (RAGE) in an effective amount to inhibit transcytosis of amyloid &bgr; peptides across the blood-brain barrier in the subject, thereby decreasing cerebral vasoconstriction in the subject. The invention further provides for a method for ameliorating neurovascular stress in a subject which comprises administering to the subject an effective amount of an inhibitor of receptor for advanced glycation endproduct (RAGE), so as to increase cerebral blood flow in the subject, thereby ameliorating neurovascular stress in the subject.

Abstract: The present invention provides a method for treating symptoms of diabetes in a diabetic subject which comprises administering to the subject a therapeutically effective amount of an agent which inhibits binding of advanced glycation endproducts to any receptor for advanced glycation endproducts so as to treat chronic symptoms of diabetes in the subject.

Abstract: The present invention provides a method for treating symptoms of diabetes in a diabetic subject which comprises administering to the subject a therapeutically effective amount of an agent which inhibits binding of advanced glycation endproducts to any receptor for advanced glycation endproducts so as to treat chronic symptoms of diabetes in the subject.

Abstract: The present invention provides for a purified endothelial monocyte activating polypeptide II, wherein the polypeptide has an apparent molecular weight of about 20,000 Daltons. The present invention also provides for an effector cell activating protein comprising a polypeptide having an amino acid sequence wherein at least four amino acid residues are the same as RIGRTVT and are in the same relative positions. The invention also provides for a DNA which encodes the effector cell activating protein. The invention also provides for methods of inducing inflammation in a subject and methods of treating tumors in a subject. The invention also provides for a pharmaceutical composition which comprises the endothelial monocyte activating polypeptide II and a carrier.

Abstract: The present invention provides a method for decreasing cerebral vasoconstriction in a subject suffering from chronic or acute cerebral amyloid angiopathy which comprises administering to the subject an inhibitor of receptor for advanced glycation endproduct (RAGE) in an effective amount to inhibit transcytosis of amyloid &bgr; peptides across the blood-brain barrier in the subject, thereby decreasing cerebral vasoconstriction in the subject. The invention further provides for a method for ameliorating neurovascular stress in a subject which comprises administering to the subject an effective amount of an inhibitor of receptor for advanced glycation endproduct (RAGE), so as to increase cerebral blood flow in the subject, thereby ameliorating neurovascular stress in the subject.

Abstract: The invention provides for a non-human transgenic animal whose cells contain a recombinant DNA sequence comprising: (a) a nerve tissue specific promoter operatively linked to a DNA sequence which encodes human receptor for advanced glycation endproducts (RAGE), and (b) a nerve tissue specific promoter operatively linked to a DNA sequence encoding a mutant human amyloid precursor protein hAPP695, hAPP751 and hAPP770 bearing mutations linked to familial Alzheimer's disease in humans, wherein said non-human transgenic animal exhibits at least one phenotype from the group consisting of: increased expression of M-CSF gene in cerebral cortex; increased expression of IL-6 gene in cerebral cortex; increased neuronal stress; increased neurotoxicity; neuron loss; increased level of activated form of caspase 3 in brain; and increased level of phosphorylated tau protein in brain.

Abstract: The present invention provides a method for treating symptoms of diabetes in a diabetic subject which comprises administering to the subject a therapeutically effective amount of an agent which inhibits binding of advanced glycation endproducts to any receptor for advanced glycation endproducts so as to treat chronic symptoms of diabetes in the subject.

Abstract: This invention provides a purified endothelial monocyte activating polypeptide (EMAP II). It further provides a method of obtaining purified endothelial monocyte activating polypeptide (EMAP II), a method of making antibodies to it and a method of detecting it. This invention also provides an effector cell activating protein which contains an amino acid sequence homologous to RIGRIVT and a method of detecting same. This invention also provides a method of treating a tumor in a subject by administering an effective dose of endothelial monocyte activating polypeptide (EMAP II).

Abstract: The present invention provides a method for treating inflammation in a subject which comprises administering to the subject soluble receptor for advanced glycation endproduct (sRAGE) in an amount effective to inhibit binding of advanced glycation endproducts (AGEs) to RAGE thereby treating inflammation in the subject. The present invention also provides for a method for treating inflammation in a subject which comprises administering to the subject an agent in an amount effective to inhibit the interaction between receptor for advanced glycation endproduct (RAGE) and its ligand thereby treating inflammation in the subject.

Abstract: The present invention provides a method for decreasing cerebral vasoconstriction in a subject suffering from chronic or acute cerebral amyloid angiopathy which comprises administering to the subject an inhibitor of receptor for advanced glycation endproduct (RAGE) in an effective amount to inhibit transcytosis of amyloid &bgr; peptides across the blood-brain barrier in the subject, thereby decreasing cerebral vasoconstriction in the subject. The invention further provides for a method for ameliorating neurovascular stress in a subject which comprises administering to the subject an effective amount of an inhibitor of receptor for advanced glycation endproduct (RAGE), so as to increase cerebral blood flow in the subject, thereby ameliorating neurovascular stress in the subject.

Abstract: The present invention provides an isolated nucleic acid encoding an endoplasmic reticulum associated amyloid-beta peptide binding (ERAB) polypeptide. The ERAB polypeptide may comprise human ERAB polypeptide. The present invention provides a purified ERAB polypeptide, as well as a method for treating a neurodegenerative condition in a subject which comprises administering to the subject an agent in amount effective to inhibit ERAB polypeptide binding to amyloid-beta peptide so as to thereby treat the neurodegenerative condition.

Abstract: This invention provides a purified endothelial monocyte activating polypeptide (EMAP II). It further provides a method of obtaining purified endothelial monocyte activating polypeptide (EMAP II), a method of making antibodies to it and a method of detecting it. This invention also provides an effector cell activating protein which contains an amino acid sequence homologous to RIGRIVT and a method of detecting same. This invention also provides a method of treating a tumor in a subject by administering an effective dose of endothelial monocyte activating polypeptide (EMAP II).

Abstract: This invention provides a method of selectively decreasing pulmonary vascular resistance in a subject by administering endobronchially a drug chosen from among cAMP analogs, cGMP analogs, phosphodiesterase inhibitors, nitric oxide precursors, nitric oxide donors, and nitric oxide analogs.

Abstract: This invention provides a method of selectively decreasing pulmonary vascular resistance in a subject by administering endobronchially a drug chosen from among cAMP analogs, cGMP analogs, phosphodiesterase inhibitors, nitric oxide precursors, nitric oxide donors, and nitric oxide analogs.

Abstract: This invention provides a purified endothelial monocyte activating polypeptide (EMAP II). It further provides a method of obtaining purified endothelial monocyte activating polypeptide (EMAP II), a method of making antibodies to it and a method of detecting it. This invention also provides an effector cell activating protein which contains an amino acid sequence homologous to RIGRIVT and a method of detecting same. This invention also provides a method of treating a tumor in a subject by administering an effective dose of endothelial monocyte activating polypeptide (EMAP II).