Abstract: The invention features a method of inhibiting formation of atherosclerotic lesions by administering to a mammal, e.g., a human patient who has been identified as suffering from or at risk of developing atherosclerosis, a compound that reduces expression or activity of AFABP.

Abstract: The present invention relates to a treatment for myocardial infarction and blood clots within a patient, and more specifically to a therapy which enhances clot lysis comprising administering to a patient an antibody directed to &agr;2-antiplasmin crosslinked to fibrin (&agr;2AP-FX) which does not inhibit plasma &agr;2-antiplasmin (&agr;2AP). The invention also relates to a treatment for enhancing clot lysis comprising administering an antibody directed toward &agr;2-antiplasmin crosslinked to fibrin which does not inhibit plasma &agr;2AP together with a thrombolytic agent.

Abstract: Methods of treating a mammal having a condition characterized by vascular smooth muscle cell proliferation, where the mammal is treated with progesterone or an agonist thereof. Also disclosed are methods of screening compounds useful for inhibiting vascular smooth muscle cell proliferation.

Abstract: Disclosed is a polypeptide termed UBCE2A that catalyzes the covalent attachment of ubiquitin to the transcription factor E2A, thereby triggering the degradation of E2A. Also disclosed are DNAs encoding UBCE2A.

Abstract: The present invention relates to a treatment for myocardial infarction and blood clots within a patient, and more specifically to a therapy which enhances clot lysis comprising administering to a patient an antibody directed to &agr;2-antiplasmin crosslinked to fibrin (&agr;2AP-FX) which does not inhibit plasma &agr;2-antiplasmin (&agr;2AP). The invention also relates to a treatment for enhancing clot lysis comprising administering an antibody directed toward &agr;2-antiplasmin crosslinked to fibrin which does not inhibit plasma &agr;2AP together with a thrombolytic agent.

Abstract: The present invention relates to a treatment for myocardial infarction and blood clots within a patient, and more specifically to a therapy which enhances clot lysis comprising administering to a patient an antibody directed to &agr;2-antiplasmin crosslinked to fibrin (&agr;2AP-FX) which does not inhibit plasma &agr;2-antiplasmin (&agr;2AP). The invention also relates to a treatment for enhancing clot lysis comprising administering an antibody directed toward &agr;2-antiplasmin crosslinked to fibrin which does not inhibit plasma &agr;2AP together with a thrombolytic agent.

Abstract: The invention provides an isolated DNA which regulates vascular smooth muscle cell-specific transcription of a polypeptide-encoding sequence to which it is operably linked

Abstract: A mouse model for vein graft stenosis useful for identifying compounds which reduce or prevent such stenosis, consisting of a mouse engrafted with an autogenous vein which exhibits detectable stenosis within 30 days of transplantation. Also disclosed are therapeutic methods for inhibiting the development of vein graft stenosis.

Abstract: A substantially pure DNA comprising a sequence encoding a smooth muscle cell LIM (SmLIM) polypeptide, methods of diagnosing vascular injury by detecting a decrease in SmLIM gene expression, and methods of inhibiting vascular smooth muscle cell proliferation.

Abstract: A substantially pure DNA comprising an endothelial cell-specific promoter sequence capable of directing endothelial cell-specific transcription of a polypeptide-encoding sequence or an antisense template to which it is operably linked.

Abstract: The present invention relates to a treatment for myocardial infarction and blood clots within a patient, and more specifically to a therapy which enhances clot lysis comprising administering to a patient an antibody directed to .alpha.2-antiplasmin crosslinked to fibrin (.alpha.2AP-FX) which does not inhibit plasma .alpha.2-antiplasmin (.alpha.2AP). The invention also relates to a treatment for enhancing clot lysis comprising administering an antibody directed toward .alpha.2-antiplasmin crosslinked to fibrin which does not inhibit plasma .alpha.2AP together with a thrombolytic agent.

Abstract: Hybrid immunoglobulin-enzyme molecules are provided which are composed of antibodies, or derivatives or fragments thereof, which specifically bind an arterial or venous thrombus that are operably linked to the enzymatically active portions of thrombolytic enzymes such as plasminogen activators. In a preferred embodiment the hybrid molecules specifically bind to fibrin and have fibrinolytic activity. The hybrid molecules of the present invention may be produced by any means, including chemical conjugation, or by means of recombinant DNA, genetic engineering and/or hybridoma technology. Methods for making and using the molecules in diagnosis and therapy are also disclosed.

Abstract: A substantially pure DNA comprising a sequence encoding a smooth muscle cell LIM (SmLIM) polypeptide, methods of diagnosing vascular injury by detecting a decrease in SmLIM gene expression, and methods of inhibiting vascular smooth muscle cell proliferation.

Abstract: A mouse model for transplant arteriosclerosis useful for identifying compounds which reduce or prevent such arteriosclerosis, consisting of a mouse engrafted with a histoincompatible artery which exhibits detectable arteriosclerosis within 30 days of transplantation. Also disclosed are therapeutic methods for inhibiting the development of transplant arteriosclerosis in mammalian recipients of allografted organs.

Abstract: Compositions and methods for inhibiting the activation and/or active state of a precursor protein are provided. Compositions provided can bind to a cleavage site of a precursor protein. Also provided are compounds useful for generating inhibitor compositions. Application of the invention to the treatment of myocardial infarction and other thrombotic conditions is specifically provided. Further provided are antibodies specific for active Factor XIII.

Abstract: Hybrid immunoglobulin-enzyme molecules are provided which are composed of antibodies, or derivatives or fragments thereof, which specifically bind an arterial or venous thrombus that are operably linked to the enzymatically active portions of thrombolytic enzymes such as plasminogen activators. In a preferred embodiment the hybrid molecules specifically bind to fibrin and have fibrinolytic activity. The hybrid molecules of the present invention may be produced by any means, including chemical conjugation, or by means of recombinant DNA, genetic engineering and/or hybridoma technology. Methods for making and using the molecules in diagnosis and therapy are also disclosed.

Abstract: The present invention relates to a treatment for myocardial infarction and blood clots within a patient, and more specifically to a therapy which enhances clot lysis comprising administering to a patient an antibody directed to .alpha.2-antiplasmin crosslinked to fibrin (.alpha.2AP-Fx) which does not inhibit plasma .alpha.2-antiplasmin (.alpha.2AP). The invention also relates to a treatment for enhancing clot lysis comprising administering an antibody directed toward .alpha.2-antiplasmin crosslinked to fibrin which does not inhibit plasma .alpha.2AP together with a thrombolytic agent.

Abstract: A method of inhibiting arteriosclerosis or smooth muscle cell proliferation by identifying an animal having an artery suspected of needing such inhibition and contacting the artery with an apoptosis-inducing amount of an antioxidant.

Abstract: Heterobifunctional antibodies having dual specificities, one specificity directed against a thrombus, and the other specificity directed against a thrombolytic agent are disclosed. The invention also relates to methods of using these heterobifunctional antibodies to lyse a thrombus.

Abstract: A chimeric molecule that contains a fibrin-binding portion of an antibody covalently linked to an inhibitor of thrombin, which molecule is administered to inhibit thrombus formation and growth.