Abstract:
The invention provides a method of reducing infarct size and/or limiting, decreasing and/or inhibiting reperfusion injury and/or ameliorating heart failure in a patient comprising administering a pharmaceutically effective amount of at least one compound capable of inhibiting AC5 to the patient. The compound capable of inhibiting AC5 is particularly effective when administered during or after reperfusion in patients suffering from an ischemic injury.
Abstract:
Nitric oxide biosynthesis-inhibiting anti-inflammatory and anti-microbial compounds of Formula (3) and Formula (4) wherein R1 and R2 are independently selected from optionally substituted thienyl, optionally substituted furyl, optionally substituted —CH═CH-thienyl and optionally substituted provided that R2 is substituted with as nitro group Treatment methods utilizing the compounds, and methods of synthesis of the compounds are also disclosed.
Abstract:
The present invention relates to methods of inducing differentiation of mammalian bone marrow stromal cells into neuronal cells by contacting marrow stromal cells with a neuronal differentiation-inducing compounds. Neuronal differentiation-inducing compounds of the invention include anti-oxidants such as, but not limited to, beta-mercaptoethanol, dimethylsulfoxide, butylated hydroxyanisole, butylated hydroxytoluene, ascorbic acid, dimethylfumarate, and n-acetylcysteine. Once induced to differentiate into neuronal cells, the cells can be used for cell therapy, gene therapy, or both, for treatment of diseases, disorders, or conditions of the central nervous system.
Abstract:
The present invention is a dentinal drug delivery composition composed of cationic and/or neutral porous particles containing an effective amount of a therapeutic agent, a method for using the dentinal drug delivery to provide a dental treatment, and a method for identifying anti-inflammatory agents capable of diffusing through dentin.
Abstract:
The present invention provides a novel method of treatment for treating brain disorders that manifest oxidative stress by providing targeted populations of neurons with the ability to catabolize the acetylated amino acid derivative, N-acetylaspatic acid (NAA) and further supply extraphysiological levels of ATP to neurons via the targeted expression of the NAA catabolic enzyme aspartoacylase (ASPA) in neurons and astrocytes.
Abstract:
The present invention relates to diagnostic, prognostic and clinical methods of distinguishing high-risk IPMN from more benign IPMN as well as high-grade PanIN and PDAC from low-grade PanIN with moderate sensitivity and very high specificity using Das-1 and related antibodies.
Abstract:
The present invention relates to methods of screening for compounds that bind RNA molecules. In particular, the methods of the invention comprise screening a library of test compounds, each of which is attached to a solid support, with a dye-labeled RNA molecule to form a dye-labeled target RNA:support-attached test compound complex. By virtue of the dye label on the target RNA, the support becomes labeled and can be separated from unlabeled solid supports. The present invention further relates to methods of inhibiting an RNA-protein interaction, to methods of screening for compounds that increase or decrease the production of a protein, and to methods of screening for a compound that is capable of treating or preventing a disease whose progression is associated with an in vivo binding of a test compound to a target RNA.
Abstract:
Site-specific modified proteins and method for producing site-specific modified proteins using amino acid analogs are disclosed. Methods for labeling proteins at a desired site in the presence of nucleophilic side chains, including lysine and cysteine side chains, are also disclosed. Methods for labeling the site-specific modified proteins are also disclosed.
Abstract:
A regulated deployment of a toxin gene for developmental programmed cell death in bacteria is described. M. xanthus is demonstrated to have a solitary mazF gene that lacks a cotranscribed antitoxin gene. Deletion of mazF results in elimination of the obligatory cell death during development causing dramatic reduction in spore formation. Surprisingly, MrpC functions as a MazF antitoxin and a mazF transcription activator. Transcription of mrpC and mazF is negatively regulated via MrpC phosphorylation by a Ser/Thr kinase cascade. Various methods of exploiting this novel pathway are described herein.