A method for changing a condition of an eyelid of a mammal excluding a human, a model animal for evaluating a therapeutic or prophylactic effect against an eyelid disease obtained by the method, a method for producing the model animal, a method of screening using the model animal and a substance having a therapeutic or prophylactic effect against an eyelid disease selected by the method of screening, and a therapeutic or prophylactic agent against an eyelid disease containing the substance as an active ingredient.

The present invention concerns methods and means to produce humanized antibodies from transgenic non-human animals. The invention specifically relates to novel immunoglobulin heavy and light chain constructs, recombination and transgenic vectors useful in making transgenic non-human animals expressing humanized antibodies, transgenic animals, and humanized immunoglobulin preparations.

In one aspect, the disclosure provides methods, cells and transgenic non-human mammals for the production of fusion proteins comprising one or more polypeptide fused to an Fc domain, as well as the fusion proteins comprising one or more polypeptide fused to an Fc domain obtained from these methods, cells and transgenic non-human mammals.

This disclosure relates to transgenic rabbit models of cystic fibrosis, and methods of using these rabbits and their derivatives.

The invention relates to obtaining a preparation of recombinant human PLTP from the milk of a transgenic animal containing in its genome one or more copies of a transgene comprising a polynucleotide coding for human PTLP, placed under transcriptional control of a promoter permitting its specific expression in the cells of the mammary glands of said animal. The recombinant human PLTP preparation obtained can be used in the prevention or treatment of septic shock.

Methods, uses, and compositions for manipulating genomic DNA. Some of the embodiments of the invention provide for making a founder animal that is completely free of all unplanned genetic modifications. Some embodiments are directed to removing genetic faults in established breeds without making other alterations to the genome. Other embodiments are directed to particular tools or processes such as TALENs or CRISPR with a preferred truncation. One embodiment involves introducing a targeted targeting endonuclease system and a HDR template into a cell (optionally with a mismatch in the binding of the targeting endonuclease and the targeted site). Another embodiment includes processes of making a genetically modified livestock animal comprising a genome that comprises inactivation of a neuroendocrine gene selective for sexual maturation, with the inactivation of the gene preventing the animal from becoming sexually mature. One embodiment includes compositions and methods for making livestock with a polled allele, including migrating a polled allele into a bovine species without changing other genes or chromosomal portions.

An apparatus for unilateral spinal cord compression includes a fixed member and a movable member that moves longitudinally along the fixed member by using a linear actuating mechanism to compress a portion of spinal cord encompassed by the movable member and the fixed member.

The present invention relates to methods and compositions for improving nuclease mediated homologous recombination (HR). The invention is directly relevant to basic biomedical research, transgenic animal production, regenerative medicine, gene therapy, and other disciplines where HR is involved.

The present disclosure pertains to the field of animal disease models, specifically to a method for constructing an animal model of open-angle glaucoma. In this model, the pathogenesis of open-angle glaucoma is mimicked by inducing necroptosis in trabecular meshwork cells through the injection of IFN- into the anterior chamber. This process leads to the inhibition of trabecular meshwork activity and functional impairment, resulting in elevated intraocular pressure and subsequent optic nerve changes indicative of glaucoma. The pathophysiological alterations observed in the animal model closely resemble those seen in human open-angle glaucoma, including chamber angle opening, trabecular meshwork dysfunction, increased intraocular pressure, and loss of RGCs.