Compositions of peritoneal dialysis solutions and metabolizing enzymes, and their uses to treat disorders associated with elevated levels of metabolites are disclosed. Animal models of hyperoxalemia are also disclosed.

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.

A composition of matter comprising an adeno-associated virus (AAV) or other human compatible virus, encoding the gene for Sialidase Neu3, B3Galt4, St3Gal2, or combinations thereof, and a neuron specific promoter, wherein the composition is suitable for administration to a patient comprising injecting the AAV or other human compatible virus into the brain by intracranial stereotaxic injunction; wherein the AAV's encoding for the Sialidase Neu3, B3Galt4, St3Gal2, or combinations thereof enhance and/or normalize levels of GM1 in neurons, providing both therapeutic relief and disease modifying effects in specific areas of the brain relevant to particular neurodegenerative diseases.

The disclosure relates to therapeutic proteins and pharmaceutical compositions comprising said proteins, which have utility in treating various human diseases. In particular aspects, the disclosed therapeutic proteins are useful for treating human gastrointestinal inflammatory diseases and gastrointestinal conditions associated with decreased epithelial cell barrier function or integrity. Further, the disclosed therapeutic proteins are useful for treating human inflammatory bowel disease, including inter alia, Crohn's disease and ulcerative colitis.

Fish embryos may be successfully vaccinated or therapeutically treated if the therapeutic agent is injected into the yolk sac. Therapeutic agents may be directly injected or released from microspheres and enter the circulation and tissues. Injection into the yolk sac, combined with the use of carriers, allows for a continued, controlled release of therapeutic agents and processing of antigens. Fish vaccination or therapeutic treatment, selecting fish embryos post fertilization at the one-cell to eyed egg stage of development, and injecting the yolk sac with carriers associated with an antigen(s) or therapeutic agent(s), may be fully automated.

The present disclosure relates to a method for preparing a Graves' ophthalmopathy phenotype animal model, the method including a step of administering zymosan A to a subject other than humans, a Graves' ophthalmopathy phenotype animal model prepared thereby, and a method for screening a therapeutic material for alleviation or treatment of Graves' ophthalmopathy. By using the method for preparing a Graves' ophthalmopathy phenotype animal model, which includes a step of administering zymosan A to a subject other than humans according to the present disclosure, an experimental animal model for Graves' ophthalmopathy, which simultaneously exhibits blepharitis, orbital tissue inflammation, and exophthalmos, may be obtained. In addition, the animal model prepared by the preparation method of the present disclosure may be advantageously used for researching the development of a therapeutic agent for Graves' ophthalmopathy the etiology of which has not been yet accurately revealed.

Disclosed herein are methods of treatment for an intraocular pressure (IOP)-associated condition in a subject, that include administering to the subject an effective amount of a tissue plasminogen activator (tPA) therapeutic agent. In one embodiment, the IOP-associated condition is glaucoma. The administration of a tPA therapeutic agent can be an extended administration intended to cause a reduction in IOP in the subject for a period of at least one day to a year or more, relative to IOP levels in the subject prior to administration of the tPA therapeutic agent. The tPA therapeutic agent can be, for example, tPA, a tPA derivative, a small molecule direct or indirect tPA agonist, or a gene therapy vector.

The present invention provides a model animal for establishing an effective therapy for a protein aggregation disease typified by Alzheimer's disease and the like.

More specifically, the present invention provides the followings: (A) a non-human animal that exhibits a degenerative symptom attributed to protein aggregation, wherein the degenerative symptom attributed to protein aggregation is induced by misfolding of the protein and said degenerative symptom is promoted; and (B) a method for producing the non-human animal that exhibits the degenerative symptom attributed to the protein aggregation, comprising the following (1) and (2): (1) inducing misfolding of the protein to cause the degenerative symptom attributed to the protein aggregation in the non-human animal, and (2) giving a treatment to promote the degenerative symptom attributed to the protein aggregation in the non-human animal.

The present invention relates to a composition for treating neuroinflammatory disease comprising a complement component 8 gamma protein or a fragment thereof, and more particularly, to use for treating neuroinflammatory disease of a complement component 8 gamma protein or a fragment thereof which exhibits an effect of reducing the expression of inflammatory cytokines in microglia.

The composition of the present invention has effects of reducing Alzheimer's abnormal behavior patterns and reducing the secretion of neuroinflammatory cytokines in brain microglia and thus can be very usefully used for development of an agent for preventing or treating neuroinflammatory disease.

Methods of preparing mammalian enteroids, and methods producing T. gondii oocysts in vitro and in vivo in heterologous systems, are provided.