Abstract: Systems for predicting a drug delivery profile as described herein include at least one drug pump and/or a controllable valve that produce a drug flow and dispense at least a first drug. The system also includes at least one carrier fluid pump and/or another controllable valve that produces a carrier fluid flow, a flow junction structure configured to receive the drug flow and the carrier fluid flow to produce a mixed flow, and a fluid path for carrying the mixed flow between the flow junction structure and a delivery point. The system further includes a processing device configured to predict the drug delivery profile at the delivery point based on determining a predicted time variation of drug concentration at the delivery point using at least a model of the mixed flow. The model includes a plurality of parameters related to propagation of the mixed flow through the fluid path.

Abstract: In accordance with the present invention, EC progenitors can be used in a method for regulating angiogenesis, i.e., enhancing or inhibiting blood vessel formation, in a selected patient and in some preferred embodiments for targeting specific locations. For example, the EC progenitors can be used to enhance angiogenesis or to deliver an angiogenesis modulator, e.g. anti- or pro-angiogenic agents, respectively to sites of pathologic or utilitarian angiogenesis. Additionally, in another embodiment, EC progenitors can be used to induce reendothelialization of an injured blood vessel, and thus reduce restenosis by indirectly inhibiting smooth muscle cell proliferation.

Abstract: Improvements on the basic method used for BEAMing increase sensitivity and increase the signal-to-noise ratio. The improvements have permitted the determination of intrinsic error rates of various DNA polymerases and have permitted the detection of rare and subtle mutations in DNA isolated from plasma of cancer patients.

Abstract: In accordance with the present invention, EC progenitors can be used in a method for regulating angiogenesis, i.e., enhancing or inhibiting blood vessel formation, in a selected patient and in some preferred embodiments for targeting specific locations. For example, the EC progenitors can be used to enhance angiogenesis or to deliver an angiogenesis modulator, e.g. anti- or pro-angiogenic agents, respectively to sites of pathologic or utilitarian angiogenesis. Additionally, in another embodiment, EC progenitors can be used to induce reendothelialization of an injured blood vessel, and thus reduce restenosis by indirectly inhibiting smooth muscle cell proliferation.

Abstract: Methods and products for identifying subjects at risk of acute kidney injury (AKI) are provided according to the invention. Included, for instance, are diagnostic kits and methods involving the use of at least two AKI associated markers.

Abstract: Provided herein are an isolated or enriched population of tumor initiating cells derived from normal cells, cells susceptible to neoplasia, or neoplastic cells. Methods of use of the cells for screening for anti-hyperproliferative agents, and use of the cells for animal models of hyperproliferative disorders including metastatic cancer, diagnostic methods, and therapeutic methods are provided.

Abstract: As described below, the present invention features compositions and methods for increasing TNFR2/p75 receptor signaling to reduce inflammation. Methods for increasing TNFR2/p75 expression or signaling may also be used to increase the survival of resident cells or transplanted stem cells (e.g., bone marrow derived or peripheral blood derived stem cells) in a damaged tissue.

Abstract: As described below, the present invention features methods for reprogramming somatic cells and related therapeutic compositions and methods.

Abstract: The present invention features compositions and methods of treating or preventing hypertension or a cardiac indication. In particular embodiments, the invention provides E2F2 as a new therapeutic target for the treatment of hypertension or a cardiac indication, and methods of increasing the expression and/or activity of E2F2.

Abstract: The present invention relates to a novel method of inhibiting gap junction-mediated signaling in pyramid cells. Pyramidal gap junctions are quickly and reversibly inhibited by beta-amyloid or biologically active fragments thereof. The present invention also relates to the use of beta-amyloid as an anticonvulsant for the treatment of epilepsy and other pathological hypersynchrony conditions in humans and non-human animals.

Abstract: The present invention generally provides compositions and methods that are useful for the treatment or prevention of a neoplasm, and screening methods that can be used to detect compounds that modulate the activity of a DJ-I gene.

Abstract: The invention provides compositions comprising genetically modified bone marrow cells and related therapeutic and diagnostic methods. Transduced bone marrow cells can be therapeutically administered to a subject, such as a human patient to provide for the expression of an encoded protein in the subject in need thereof.

Abstract: According to aspects of the invention, methods for preventing or treating kidney damage are provided. Compositions for the prevention or treatment of kidney damage are also provided. Aspects of the invention relate to methods for screening the toxicity of a radio-contrast agent. Kits for the treatment or prevention of kidney damage are also provided.

Abstract: Tumors can be directed into a vasculogenic program and used to regenerate tissues in a verterbrate host, identify factors originating from the tumor that are useful for tissue regeneration, and to generate such factors for use in a subject apart from the tumor itself.

Abstract: The present invention generally provides methods for preventing, treating or reducing the severity of symptoms associated with tissue ischemia by administering a CXCR4 antagonist in combination with at least one nucleic acid encoding a morphogen or effective fragment thereof. In one embodiment, the methods include elevating peripheral blood endothelial progenitor cells (EPCs), bone marrow-derived stem cells (BMSCs), or both cell types. The invention has a wide spectrum of applications including reducing or eliminating tissue ischemia, especially tissue ischemia associated with a myocardial infarct (heart attack).

Abstract: The invention features compositions and methods that are useful for preventing or treating a cardiac disease or for promoting cardiac health following a myocardial infarction. The invention further features compositions and methods for promoting angiogenesis, cell proliferation, and/or decreasing apoptosis in muscle tissue, such as cardiac tissue. The invention provides for the expression of human growth hormone in cardiac muscle following a myocardial infarction.

Abstract: The invention generally provides screening methods for the identification of therapeutic compounds useful for the treatment of a neurodegenerative disease, and related prophylactic and therapeutic compositions and methods.

Abstract: The present invention encompasses methods for inhibiting TNF-alpha expression with N-substituted dopamine derivatives. In this method a cell is administered a pharmaceutically effective amount of N-acetyl dopamine derivatives or N-alkyldopamine derivatives and a pharmaceutically acceptable carrier for treating a cell, preferably in an animal or human suffering from overexpression or abundant TNF-alpha. The N-acetyldopamine derivative or N-alkyldopamine derivatives may be administered alone or in combination with N-acetylserotonin (NAS) or other compound to inhibit TNF-alpha expression. Also disclosed is a method of treating a TNF-alpha related disease and/or disorder using such a compound.

Abstract: Methods for enhancing angiogenesis in a mammal using hepatocyte growth factor (“HGF”) are provided. In the methods, HGF can be administered to mammals suffering from, for instance, vascular insufficiency or arterial occlusive disease. Articles of manufacture and kits containing HGF are also provided.

Abstract: This invention relates to methods and compositions for the treatment of apoptotic cell-death. In particular the invention relates to Akt molecules and their use in inhibiting apoptotic cell-death in cardiomyocytes, skeletal myocytes and/or vascular endothelial cells. In view of these discoveries, Akt molecules can be used to inhibit apoptotic cell-death of any of the foregoing cells, and in particular, to treat conditions (e.g., myocardial infarction) that result in increased apoptotic cell-death of cardiomyocytes, skeletal myocytes and/or vascular endothelial cells.