The present disclosure relates to a method for preparing an Alzheimer's disease (AD) animal model, including: selecting healthy male human ApoE4 transgenic mice, and intraperitoneally injecting a 4 mmol/L Al(mal).sub.3 solution at a volume of 10 ml/kg, with aluminum exposure for 60 days, and interval time of 2 days for every 5 days, to obtain an AD animal model co-induced by genetic and environmental factors which are interacted without being simply superimposed. The AD animal model established according to the method of the examples in the present disclosure can express the characteristic pathological changes of AD and has the characteristics of learning and memory impairment. The AD animal model provided by the present disclosure can be used for drug screening and AD mechanism research, and has the advantages of stable properties, prominent reproducibility, easy operation, and low cost.

This disclosure relates to a genetically modified rodent and use thereof as a rodent model. More specifically, this disclosure relates to rodent (e.g., mouse or rat) comprising a loss of function mutation in an endogenous Crnn (cornulin) gene, and to use of such a rodent animal as a rodent model of skin inflammation disorders (e.g., psoriasis),

The present invention relates to the field of biotechnology, in particular to application of a GPR45 gene. The present invention discloses, for the first time, a correlation between GPR45 and obesity and also discloses that obesity may be caused if the GPR45 gene is knocked out or the expression of the GPR45 gene is reduced. Moreover, an obese mouse model is established by adopting a method of blocking the expression of the GPR45 gene for the first time, which is more similar to the mechanism underlying the obesity of human, is thus an ideal model for obesity basis and clinical application researches and can be well applied in screening of drugs for treating obesity.

The present invention provides a therapeutic agent for a muscle weakness symptom (sarcopenia) or a metabolic disease, containing a -crystallin (CRYM) inhibitory substance as an active ingredient. The inhibitory substance is selected from the group consisting of an antisense nucleic acid against CRYM, an RNAi-inducing nucleic acid against CRYM and a ribozyme against CRYM, expression vectors of these, an antagonist antibody against CRYM, and a low molecular weight compound that inhibits activity of CRYM.

A transgenic mouse that is engineered by one or more genetic modifications that delete endogenous Adam6a and Adam6b genes in a male mouse, which mouse comprises in its genome only one exogenous Adam6 transgene, and expresses an ADAM6 protein comprising at least 90% sequence identity to SEQ ID NO:1 or SEQ ID NO:2, which Adam6 transgene is functional in a male mouse.

A system is provided comprising a plurality of C. elegans cultures, where each culture comprises a transgenic C. elegans strain that models a mammalian disease or condition. Methods of using a system, e.g., for characterizing microbial strains of a mammalian microbiome and determining whether such microbial strains affect a mammalian disease or disorder.

This invention relates to the engineering of animal cells, preferably mammalian, more preferably rat, that are deficient due to the disruption of tumor suppressor gene(s) or gene product(s). In another aspect, the invention relates to genetically modified rats, as well as the descendants and ancestors of such animals, which are animal models of human cancer and methods of their use.

Disclosed are non-naturally occurring zebrafish, such as transgenic zebrafish, which comprise a mutation in the rhodopsin (rho) gene. Also disclosed are methods of identifying compounds useful in treating retinal-specific defects and disorders, such as degeneration. Further disclosed are methods of identifying mutations in the rhodopsin gene that can cause retinal-specific defects.

Disclosed are non-naturally occurring zebrafish, such as transgenic zebrafish, which comprise a mutation in the rhodopsin (rho) gene. Also disclosed are methods of identifying compounds useful in treating retinal-specific defects and disorders, such as degeneration. Further disclosed are methods of identifying mutations in the rhodopsin gene that can cause retinal-specific defects.

Provided herein are material and methods for changing gene expression in select sex chromosomes. The materials and methods of the subject invention can be used to produce non-human transgenic animals that produce progeny of a predetermined gender and to generate non-human transgenic animals that produce single-sexed semen.