The present invention relates to a method for treating or alleviating an osteoporosis in a subject. The method comprises steps of identifying the subject having the osteoporosis, and administering to the subject an effective amount of a composition that increases a level of Discoidin Domain Receptor 1 (DDR1) protein in the subject.

Systems and methods relate to transgenic organisms and their use as biosensors are described. In some embodiments, the systems and methods include a first population of transgenic organisms that includes a first constitutively expressed reporter gene, and a first transgene that includes a first inducible promoter from a response pathway gene, wherein the first inducible promoter is coupled to a first reporter gene. Other embodiments are described.

Provided herein are rapid, reliable methods for generating mice (or other species) that develop tumors of known genotype with respect to two or more mutated, tumor-associated genes using blastocyst complementation.

The invention provides for transgenic donor animals (e.g., pigs) whose cells, tissues and organs have a better long-term survival when transplanted into a human patient. The transgenic donor animal carries one or more human transgenes which is expressed only when the endogenous gene of the donor animal is knocked out shortly before a graft is harvested for transplantation. This genetic switch allows the donor animal to remain healthy during the majority of its lifetime, while still allowing expression of the human transgene for optimal transplant tolerance in a human recipient. The transgene may encode a cytokine receptor, an adhesion molecule, or a complement regulatory protein.

Provided herein are methods of generating sterile male insects. The methods include generating a insect stock comprising females with two X chromosomes each having the same centromere with male insects comprising an X chromosome and a Y chromosome each having the same centromere and mating parental male insects having an X:Y/O genome with normal females, thereby producing the sterile male insects.

The invention relates to a vector comprising: a 5 nucleic acid that is homologous to a genomic sequence 5 of a stop codon of a constitutively expressed gene; an exogenous nucleic acid; a 3 nucleic acid that is homologous to a genomic sequence 3 of the stop codon of the constitutively expressed gene; a translation interruption-reinitiation signal operably linked to the 5 nucleic acid and the exogenous Targeting nucleic acid, wherein the translation interruption-reinitiation signal is capable of replacing the stop codon of the constitutively expressed gene.

Pericytes are mural cells of brain capillaries that degenerate in multiple neurological disorders. Pericytes regulate neurovascular functions, but their role in the adult brain and disease is still poorly understood because of the lack of adequate pericyte-specific experimental models. All current pericyte-deficient models are not pericyte specific, and carry an inherited embryonic trait. Here, the Inventors generated an inducible pericyte-specific Cre line using a double-promoter strategy. The Inventors ablated adult mouse pericytes expressing Cre-dependent diphtheria toxin receptor after toxin administration. Pericyte ablation led to a rapid dysregulation of cerebral blood flow and blood-brain barrier breakdown. This was followed by behavioral deficits and neurodegenerative changes. These findings show that circulatory deficits leading to secondary neurodegeneration develop immediately after pericyte loss.

Systems and methods relate to transgenic organisms and their use as biosensors are described. In some embodiments, the systems and methods include a first population of transgenic organisms that includes a first constitutively expressed reporter gene, and a first transgene that includes a first inducible promoter from a response pathway gene, wherein the first inducible promoter is coupled to a first reporter gene. Other embodiments are described.

The invention is directed to compositions and methods for treating or reducing the likelihood of the development of epilepsy in an individual. The method comprises administering to the central nervous system of an individual in need of such treatment a therapeutically effective amount of an agent capable of increasing the expression and/or activity of miR-128.

Non-human animal genomes, non-human animal cells, and non-human animals comprising a humanized coagulation factor XII (F12) locus and methods of making and using such non-human animal genomes, non-human animal cells, and non-human animals are provided. Non-human animal cells or non-human animals comprising a humanized F12 locus express a human coagulation factor XII protein or a chimeric coagulation factor XII protein, fragments of which are from human coagulation factor XII. Methods are provided for using such non-human animals comprising a humanized F12 locus to assess in vivo efficacy of human-coagulation-factor-XII-targeting reagents such as nuclease agents designed to target human F12. A short isoform of F12 that is produced locally in the brain, and methods of using the short isoform, are also provide.