The present disclosure relates to transgenic Caenorhabditis elegans including, in sensory neurons, Channelrhodopsin 2 (ChR2)::Green Fluorescence Protein (GFP) DNA in which the ChR2 gene and the GFP gene are linked, a method of producing the same, a method of regulating the lifespan thereof, and a method of screening an aging regulation candidate by using the same. The present disclosure may also provide an animal model for research into prevention/treatment of aging-related diseases by regulating the lifespan of an animal on a subject level and a method of screening a drug candidate for prevention/treatment of aging-related diseases.

An organ for transplantation having a kidney, a ureter, and a urinary bladder and an organ structure in which a first ureter, a first urinary bladder, a second ureter and a second urinary bladder are sequentially connected to a kidney can produce urine and excrete the produced urine, and thus is useful for transplantation.

The present invention relates to the field of seizures. More specifically, the present invention provides compositions and methods for treating refractory seizures in neonates. In one embodiment, the method comprises the steps of (a) administering to the patient an amount of a KCC2 agonist and/or trkB antagonist effective to restore KCC2 expression to normal physiological levels; and (b) administering to the patient an effective amount of an anti-seizure medication.

The present invention relates to methods of treating or preventing angiogenesis-related diseases by the administration of stem cells and/or progeny cells thereof.

Provided are a knockout mouse, a method for screening a substance for suppressing mesial temporal lobe epilepsy, and a method for selecting a technique for suppressing mesial temporal lobe epilepsy. A knockout mouse 30 or more days of age that has lost the function of the Girdin gene in at least the nervous tissues and exhibits the phenotypes of (1), (2), and (3) below. (1) hippocampal sclerosis should be present, (2) extrahippocampal brain damage should be limited, and (3) spontaneous epilepsy that can be said to be of hippocampal origin should be present.

The present invention provides compositions and methods for treating joint disorders that are characterized by an inflammatory component. In some aspects, the compositions and methods are to prevent the progression of osteoarthritis and other arthritides and to treat osteoarthritis and other arthritides in a mammalian joint.

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.

A method of preparing a mouse model of herpes using a herpes simplex virus and hydrocortisone, and a mouse model of herpes prepared the method are disclosed. When the preparation method is used, an animal model in which the symptoms of herpes clearly appear can be prepared, and thus the animal model can be widely used in the development of therapeutic agents for herpes simplex virus infection. A use of the mouse model in screening and developing a candidate therapeutic agent is also disclosed.

Deferred treatment of nerve injuries is provided. Accordingly, there is provided a method of deferred treatment of a nerve injury in a subject in need thereof, the method comprising implanting at least 1 week following onset or diagnosis of the nerve injury in the subject a composition comprising a hyaluronic acid, a laminin polypeptide and an antioxidant at or near the nerve injury of the subject.

The present disclosure provides adeno-associated vims (AAV) vectors and uses thereof. In certain embodiments, the AAV vectors comprise a nucleic acid that encodes an antagonist against a family with sequence similarity 19, member A5 (FAM19A5) protein, e.g., anti-FAM19A5 antibody, e.g., anti-FAM19A5 scFv.