The disclosure provides methods of generating a murine model of neonatal necrotizing enterocolitis, whereby the generated murine animal exhibits at least one symptom of neonatal necrotizing enterocolitis. The disclosure also provides methods to measure transfusion effects on anemia and methods for identifying and isolating an agent useful for the treatment or prevention of neonatal necrotizing enterocolitis.

An object of the present invention is to provide a non-human model animal rich in stromal tissue, a cell structure useful for producing the above-described non-human model animal, a method for evaluating a test substance in which the above-described non-human model animal is used, and a method for producing the above-described non-human model animal. According to the present invention, a cell structure is provided which contains a biocompatible macromolecular block and at least a cancer cell and a mesenchymal cell, and in which a plurality of the above-described biocompatible macromolecular blocks are arranged in gaps between a plurality of the above-described cells.

The present invention relates to the identification of a microRNA family, designated miR-29a-c, that is a key regulator of fibrosis in cardiac tissue. The inventors show that members of the miR-29 family are down-regulated in the heart tissue in response to stress, and are up-regulated in heart tissue of mice that are resistant to both stress and fibrosis. Also provided are methods of modulating expression and activity of the miR-29 family of miRNAs as a treatment for fibrotic disease, including cardiac hypertrophy, skeletal muscle fibrosis other fibrosis related diseases and collagen loss-related disease.

The present invention relates to an animal model having hypoparathyroidism and a method for producing the same. According to the present invention, the animal model having hypoparathyroidism is economical and efficient in that it can demonstrate a pathophysiology of hypoparathyroidism and maintain a survival of animals without any distortion of the pathophysiology by supplying an optimal calcium content diet.

The present invention relates to methods and assays for identifying agents useful in the treatment of fibrotic diseases, in particular diseases related to fibroblast migration and differentiation. The invention provides polypeptide and nucleic acid TARGETs, siRNA sequences based on these TARGETs and antibodies against the TARGETs. The invention is further related to pharmaceutical composition comprising siRNA sequences based on the TARGETs and antibodies against the TARGETs for use in the treatment of fibrotic disease. The invention further provides in vitro methods for inhibition of fibroblast migration and differentiation.

The disclosure is in the field of cell therapy, more in particular, stem cell transplantation therapy. The disclosure provides methods and compositions for improving the efficacy of stem cell transplantation therapy by reducing the inflammatory activity of a stem cell transplant. More in particular, the disclosure provides a method for preparing a stem cell transplant with reduced inflammatory activity comprising a step of suspending a composition comprising stem cells in a fibrinogen-depleted plasma and/or in a fibrinogen and C-reactive protein-depleted plasma.

Disclosed herein include methods for preventing, inhibiting, reducing, or treating cardiac ischemic injury. The method comprises administering a therapeutic composition comprising a plurality of microRNA (miR) antagonists to a subject before, during, and/or after a cardiac ischemic event. The method can comprise administration of the therapeutic composition as two doses separated by an interval.

The invention relates to methods of treating an individual suffering from a structural cardiac muscle defect, comprising providing cardiomyocytes of at least part of the cardiac muscle of the individual with a high mobility group A (HMGA) protein to thereby promote proliferation of said cardiomyocytes. The invention further relates to an expression construct for functional expression of said HMGA protein, a pharmaceutical composition, comprising HMGA or said expression construct, and to a method of culturing cardiomyocytes in vitro, comprising providing cardiomyocytes with a HMGA protein or the expression construct.

Disclosed herein is a method of promoting sustained survival, sustained regeneration, in a lesioned mature neuron, sustained compensatory outgrowth in a neuron, or combinations thereof. The method comprises contacting the lesioned mature neuron with an effective amount of an inhibitor of PTEN and an effective amount of an inhibitor of SOCS3 to thereby promote survival and/or regeneration and/or compensatory outgrowth of the neuron. Therapeutic methods of treatment of a subject with a neuronal lesion by administration of a therapeutically effective amount of an inhibitor of PTEN and a therapeutically effective amount of an inhibitor of SOCS3, are also disclosed, as are pharmaceutical compositions and devices for use in the methods.

The subject invention concerns materials and methods for treating a person or animal having cognitive impairment. In one embodiment, the method comprises administering an effective amount of one or more inflammatory mediator(s), for example, fms-related tyrosine kinase 3 (Flt3) ligand, interleukin-6 (IL-6), macrophage migration inhibitory factor (MIF), interleukin-1 (IL-1), interleukin-3 (IL-3), erythropoietin (EPO), vascular endothelial growth factor A (VEGF-A), hypoxia-inducible transcription factor (HIF-1alpha), insulin like growth factor-1 (IGF-1), tumor necrosis factor (TNF), granulocyte colony-stimulating factor (G-CSF), granulocyte/macrophage colony-stimulating factor (GM-CSF), macrophage colony-stimulating factor (M-CSF), Stem Cell Factor (SCF), Darbepoetin (ARANESP), and metalloproteinases, to an animal or person in need of treatment.