117 results about "Male mice" patented technology

Mice are provided that comprise a reduction or deletion of ADAM6 activity from an endogenous ADAM6 locus, or that lack an endogenous locus encoding a mouse ADAM6 protein, wherein the mice comprise a sequence encoding an ADAM6 or ortholog or homolog or fragment thereof that is functional in a male mouse. In one embodiment, the sequence is an ectopic ADAM6 sequence or a sequence that confers upon a male mouse the ability to generate offspring by mating. Mice and cells with genetically modified immunoglobulin heavy chain loci that comprise an ectopic nucleotide sequence encoding a mouse ADAM6 or functional fragment or homolog or ortholog thereof are also provided.

Mice are provided that comprise a reduction or deletion of ADAM6 activity from an endogenous ADAM6 locus, or that lack an endogenous locus encoding a mouse ADAM6 protein, wherein the mice comprise a sequence encoding an ADAM6 or ortholog or homolog or fragment thereof that is functional in a male mouse. In one embodiment, the sequence is an ectopic ADAM6 sequence or a sequence that confers upon a male mouse the ability to generate offspring by mating. Mice and cells with genetically modified immunoglobulin heavy chain loci that comprise an ectopic nucleotide sequence encoding a mouse ADAM6 or functional fragment or homolog or ortholog thereof are also provided.

The present invention is to provide a non-human animal model of systemic lupus erythematosus wherein generation of anti-double stranded DNA antibody and anti-single stranded antibody is induced, and that is made to spontaneously develop glomerulonephritis and arthritis, and a screening method for a therapeutic agent for systemic lupus erythematosus wherein the non-human animal model is used. FcγRIIB deficient mouse that is not made to spontaneously develop autoimmune pathology although its autoantibody response is enhanced is backcrossed into C57BL / 6J (B6) mouse for 12 generations to generate FcγRIIB deficient B6 mouse, the FcγRIIB deficient B6 male mouse is intercrossed with lpr / B6 female mouse, and thus obtained FcγRIIB+ / − / lpr+ / − mice were further crossed to generate a mouse model of systemic lupus erythematosus.

This invention provides a method for constructing type ii animal model of mucopolysaccharide storage disease, which comprises synthesizing the oligonucleotide strand and annealing annealing the pUC57 T7 SgRNA with it, then connect to gain a sgRNA expression vector according to the mouse iDS gene design target; to obtain a mouse fertilized egg; mix the transferred Cas9mRNA and sgRNA to obtain an RNA mixture, microinject the RNA mixture to the cytoplasm of that fertilized egg, then implant the it into the female mice to get a F0 generation mice; extract the genomic DNA of them and use them as a template to carry out PCR reaction. The product was digested and the mutant ones were selected to determine Founder Mice; Founder Mice and those wild male mice were mated to obtain F1 mice. The invention also provides an animal model constructed by this method and the usage of the model in the study of mucopolysaccharide sequestration type ii.

The invention discloses a new method for improving transgenic efficiency of animals. In the transgenic method, the sperm cells and the oocytes are used as vectors, through improvement of the method, the exogenous genes are respectively led to the sperm cells and the oocytes and the exogenous genes carried by the sperm cells and the oocytes are further integrated in the embryos through fertilization process, thus improving the efficiency of leading the exogenous genes to the nuclei and then realizing high efficiency expression. The method is characterized by respectively transfecting female and male reproductive cell systems by adopting a point injection method before the female and male mice mate with each other and then selecting the male mice 1-5 days and 35-40 days after surgery and the female mice 1-7 days after surgery to mate with each other to obtain the transgenic mouse offspring. By adopting the method, transgenosis of sheep is explored, the transgenic efficiency of big mammals can be improved and a new approach is provided for breeding in the animal husbandry. In the method, a transgenic system adopting female and male reproductive cells for joint mediation is explored.

The invention discloses a method for building a mouse model with multiple-generation obesity and fatty liver pathologic change. The method comprises the steps of: respectively feeding mice with normal food (NC) and high-fat food (HF) to obtain F0-generation mice, namely an NCF0 group and an HFF0 group; feeding female mice with different foods until sexual maturity, breeding with male mice fed with normal food to obtain F1-generation mice, namely an NCF1 group and an HFF1 group; after ablactation, respectively and continuously feeding the two groups of mice with normal food and high-fat food, respectively feeding female mice with normal food and high-fat food until sexual maturity, breeding with male mice fed with normal food to obtain F2-generation mice, namely an NCF2 group and an HFF2 group; and after ablactation, respectively and continuously feeding the NCF2 group and HFF2 group of mice with normal food and high-fat food. The specific modeling route is shown in Figure 1. The result shows that the obesity degree, insulin resistance degree and fatty liver pathologic change degree of the mice fed with high-fat food are progressively increased generation by generation.

The invention discloses an anti-breeding rodenticide. Melia azedarach oil is served as an anti-breeding agent, and the weight percent of the melia azedarach oil in the anti-breeding rodenticide accouts for 0.08%-0.1%. Through researching the intrinsic rules and hormone regulation mechanism of mouse breeding as well as studying the toxicological and function mechanism of a vegetable anti-breeding agent, ideal anti-breeding agent-melia azedarach oil is screened. The anti-breeding rodenticide is low in effective dosage, makes mice infertile, and has the advantages of low toxicity index, high safety, no harm to human being and animals and no secondary poisoning. After the anti-breeding rodenticide is eaten 10 days later, main reproductive organs-testicles of male mice generate the following variation: the organ coefficient gets small, the sperm amount is reduced, the seminiferous tubule diameter is thinned, lumens are reduced, germinal epithelium thickness is thinned, and interstitial cells are decreased; and ovarial organ coefficient of female mice is obviously reduced, and the corpus luteum in an ovarial structure is contracted. Dead fetus are increased after male and female mice coition, and the breeding number is greatly decreased.

The invention belongs to the technical field of poison bait for deratization and particularly relates to poison bait for inhibiting mouse breeding and a preparation method of the poison bait. The poison bait for inhibiting mouse breeding comprises a poison layer and a food layer, wherein the food layer wraps the poison layer; the poison layer is prepared from drospirenone, quinestrol and an auxiliary material; the content of drospirenone is 0.005%-0.01% of the total weight of the poison bait, the content of quinestrol is 0.001%-0.01% of the total weight of the poison bait, the content of the auxiliary material is 5%-30% of the total weight of the poison bait, and the balance is the food layer. The poison bait for inhibiting mouse breeding has little influence on mouse behaviors, can inhibit breeding of female and male mice, has more lasting efficacy and contains fewer poisons.

Mice, tissues, cells, and genetic material are provided that comprise a humanized heavy chain immunoglobulin locus, a humanized light chain locus that expresses a universal light chain, and a gene encoding an ADAM6 or ortholog or homolog or functional fragment thereof. Mice are provided that express humanized heavy chains comprising human variable domains, and that express humanized light chains comprising human variable domains wherein the light chains are derived from no more than one, or no more than two, light chain V and J or rearranged V / J sequences. Fertile male mice that express antibodies with universal light chains and humanized heavy chains are provided. Methods and compositions for making bispecific binding proteins are provided.

The invention discloses a unilateral ureteral ligation recanalisation animal model and a building method thereof. The method comprises the following steps of: 1) preparing an elastic plastic tube; and 2) after implanting an elastic plastic fat pad into the left ureter of an SD male mouse to pressurize to perform ligation obstruction, performing a surgery 7 days later for the second time, in the surgery, taking out the elastic plastic tube, dredging the left ureter to release the left kidney obstruction and separate the envelope of the left kidney at the same time, and ligaturing the right ureter with a NO. 4 thread. In addition, the invention also discloses the animal model built by the method. The animal model can reduce renal functions and cause renal tubule mesenchyme fibrosis change. The model building period is short; the response is quick; the cost is low; the model is convenient to use; the performance of the model is stable; the repeatability is good; pathomorphological changes of kidney after obstruction can be observed; the functional level of the kidney can be studied; and the relation between the pathomorphological changes and the functional level can be embodied; and the animal model provides a new study target for clinical research and development of medicaments for preventing and treating renal fibrosis.

The invention discloses a method for establishing an animal model of type 2 diabetes. The steps are as follows: (1) prepare lipopolysaccharide solution with physiological saline, and the concentration is 100 μg / ml; Feed and inject lipopolysaccharide solution at the same time; (3) measure the body weight of the male mice after the 28th day; (4) fast the male mice for 8 hours after measuring the body weight, and separate serum to measure blood sugar and insulin; (5) evaluate insulin Resistance ability and evaluation of glucose-stimulated insulin secretion ability; (6) On the 30th day and the 32nd day, the male mice were given intraperitoneal injection of STZ solution once; (7) When the random blood sugar> 16.8mmol / L, the type 2 diabetic animal was determined The model is built. The present invention skillfully selects the lipopolysaccharide in Escherichia coli 0111:B4 subspecies, cooperates with common feed feeding and STZ injection, and successfully establishes the type 2 diabetes animal model. The invention is easy to operate, and the cost of building a model is low, and the molding rate is high and the molding cycle is short.

The invention provides a method of producing a non-obese diabetic (insulin-dependent diabetes mellitus) animal model. The method comprises overexpressing NIK (NF-kappa-B-inducing kinase) gene in pancreatic beta cells of an animal. Compared with existing non-obese diabetic (NOD) mouse models, beta-NIK-OE male mice herein have the advantages of good stability, short period, low expense and the like,and are applicable to the research on diabetic pathogenesis, the research on diabetic complications and the screening of diabetes drugs.

The present invention is to provide a non-human animal model of systemic lupus erythematosus wherein generation of anti-double stranded DNA antibody and anti-single stranded antibody is induced, and that is made to spontaneously develop glomerulonephritis and arthritis, and a screening method for a therapeutic agent for systemic lupus erythematosus wherein the non-human animal model is used. FcγRIIB deficient mouse that is not made to spontaneously develop autoimmune pathology although its autoantibody response is enhanced is backcrossed into C57BL / 6J (B6) mouse for 12 generations to generate FcγRIIB deficient B6 mouse, the FcγRIIB deficient B6 male mouse is intercrossed with lpr / B6 female mouse, and thus obtained FcγRIIB+ / − / lpr+ / − mice were further crossed to generate a mouse model of systemic lupus erythematosus.