Provided are a method for producing a spermatogenic stem cell-like cell from a primordial germ cell-like cell derived from an isolated pluripotent stem cell in vitro, the method including (1) a step of coculturing a primordial germ cell-like cell with a gonad somatic cell in suspension to give reconstituted testis, and (2) a step of culturing the obtained reconstituted testis at gas/liquid interface to induce a DDX4-positive and PLZF-positive cell in the reconstituted testis; and
a method for producing a GSC-like cell, including dissociating a spermatogenic stem cell-like cell obtained by the method from the reconstituted testis, and culturing the cell under conditions that can induce a germline stem cell from the spermatogenic stem cell.

The application relates to methods for determining a parameter such as toxicity and pharmacokinetic behavior for a pharmaceutical compound against a disease or disorder. The test animals being used are non-human animals not suffering from or is not showing symptoms or signs of the disorder and which do not provoke an immune response against said pharmaceutical compound. These animals are obtainable by administration of a peptide comprising an oxidoreductase motif further comprising an NKT peptide epitope or an MHC class II T cell epitope of said pharmaceutical compound, wherein said motif and said epitope are separated by a linker of between 0 and 4 amino acids.

Provided herein are compositions, methods, and devices for the treatment and prevention of atrial fibrillation (AF) using gene therapy techniques. In particular, oxidative stress (OS) and parasympathetic nervous system signaling are inhibited to prevent and/or reverse the electrical remodeling that underlies AF.

The subject invention provides materials and methods for producing animals with short hair length. In a preferred embodiment, this is accomplished by altering in the animal the nucleotide sequence that encodes the prolactin receptor (PRLR) protein such that a truncated version of the protein is produced. Advantageously, and surprisingly, the truncated protein produced according to the subject invention retains lactogenic functionality, but causes the animal to have a short-hair coat.

In some aspects, the disclosure relates to the reactivation of inactive X chromosomes (Xi). In some embodiments, the disclosure provides compositions and methods for the reactivation of inactive X chromosomes. In some embodiments, the compositions and methods described by the disclosure may be useful for the treatment of dominant X-linked diseases.

A system, apparatus, and/or method of determining a health condition of an animal is provided. First data may be received from a first sensor device. The first data may be indicative of an animal event of an animal. Second data may be received from a second sensor device. The second sensor may be separate and/or distinct from the first sensor device. The second data may confirm an occurrence of the animal event. The animal event may be a discharge event and/or a feeding event. The occurrence of the animal event may be identified based on the first data and the second data. The occurrence of the animal event may be displayed via a display device. A health condition of the animal may be determined based on the animal event. The determination of the health condition may be based on a quantity and/or a duration of the animal event.

Genetically modified non-human animals and methods and compositions for making and using the same are provided, wherein the genetic modification comprises a humanization of an endogenous signal-regulatory protein gene, in particular a humanization of a SIRP gene. Genetically modified mice are described, including mice that express a human or humanized SIRP protein from an endogenous SIRP locus.

Genetically modified non-human animals comprising a humanized interleukin-15 (IL-15) gene. Cells, embryos, and non-human animals comprising a human IL-15 gene. Rodents that express humanized or human IL-15 protein.

The present invention relates to the field of nephrology. More specifically, the present invention provides compositions and methods useful for the study and treatment of acute kidney injury. In one embodiment, the present invention provides a knockout animal whose genome comprises a deletion of exon 2 and exon 3 of kelch-like ECH-associated protein 1 (KEAP1) in T-cells. In another embodiment, a method for treating a subject diagnosed with AKI comprising the steps of (a) isolating T-cells from the subject; (b) activating Nrf2 expression in the isolated T-cells; and (c) administering the T-cells back to the subject.

A transgenic cat with a phenotype characterized by the substantial absence of the major cat allergen, Fel d I. The phenotype is conferred in the transgenic cat by disrupting the coding sequence of the target gene with a specialized construct. The phenotype of the transgenic cat is transmissible to its offspring.