4589 results about "Animal model" patented technology

Methods and compositions for detecting and localizing light originating from a mammal are disclosed. Also disclosed are methods for tracking light emission to selected regions, as well as for tracking entities within the mammal. In addition, animal models for disease states are disclosed, as are methods for localizing and tracking the progression of disease or a pathogen within the animal, and for screening putative therapeutic compounds effective to inhibit the disease or pathogen.

The invention concerns HER<HIL><PDAT>2</BOLD><PDAT>-transgenic non-human mammals, animal models for screening drug candidates for the treatment of diseases and disorders associated with the overexpression of HER<HIL><PDAT>2</BOLD><PDAT>. In particular, the invention concerns animal models designed to test drug candidates for the treatment of HER<HIL><PDAT>2</BOLD><PDAT>-overexpressing cancers, including breast cancer, that are not responding or poorly responding to current treatments.</PTEXT>

Disclosed are antisense oligonucleotide, polynucleotide, and peptide nucleic acid compounds that specifically bind to mammalian mRNA encoding a beta1-adrenoceptor polypeptide and that are useful in the control and/or treatment of cardiac dysfunction, hypertension, hypertrophy, myocardial ischemia, and other cardiovascular diseases in an affected mammal, and preferably, in a human subject. The antisense compounds disclosed herein, and pharmaceutical formulations thereof, provide sustained control of beta1-adrenoceptor expression over prolonged periods, and achieve therapeutic effects from as little as a single dose. Administration of these antisense compositions to approved animal models resulted in a decrease in blood pressure, but no significant change in heart rate. Use of such antisense compositions in the reduction of beta1-adrenoceptor polypeptides in a host cell expressing beta1-adrenoceptor-specific mRNA, and in the preparation of medicaments for treating human and animal diseases, and in particular, hypertension and other cardiac dysfunction is also disclosed.

The present invention features non-human transgenic animal models for Alzheimer's disease (AD) and CAA, wherein the transgenic animal is characterized by 1) overexpression of bioactive transforming growth factor-beta1 (TGF-beta1) or 2) both overexpression of bioactive TGF-beta1 and expression of a human amyloid beta precursor protein (APP) gene product. The transgenic animals may be either homozygous or heterozygous for these alterations. Bigenic animals are further characterized by development of AD-associated and/or CAA-associated pathology within about two to three months of age.

The present invention relates to an adult mammal which exhibits growth or replication of abnormal cells in a target tissue or organ by over-expressing Hedgehog protein in such target tissue or organ. The present invention also relates to a method of preparing an adult animal model of prostate cancer. The invention further relates to a method of evaluating an agent for treating prostate cancer.

The invention in some aspects relates to isolated nucleic acids, compositions, and kits useful for identifying adeno-associated viruses in cells. In some aspects, the invention provides kits and methods for producing somatic transgenic animal models using recombinant AAV (rAAV) to an animal having at least one transgene that expresses a small interfering nucleic acid or at least one binding site for a miRNA.

A method of determining the voltage and current output required for the application of specific and selective electric and electromagnetic signals to diseased articular cartilage in the treatment of osteoarthritis, cartilage defects due to trauma or sports injury, or used as an adjunct with other therapies (cell transplantation, tissue-engineered scaffolds, growth factors, etc.) for treating cartilage defects in the human knee joint and a device for delivering such signals to a patient's knee. An analytical model of the human knee is developed whereby the total tissue volume in the human knee may be determined for comparison to the total tissue volume of the diseased tissue in the animal model using electric field and current density histograms. The voltage and current output used in the animal model is scaled based on the ratio of the total tissue volume of the diseased tissue of the human to the total tissue volume of the diseased tissue in the animal model and the resulting field is applied to the diseased tissue of the human using at least two electrodes applied to the knee or a coil or solenoid placed around the knee. The voltage of the signal applied to the electrodes, coil or solenoid is varied based on the size of the knee joint; larger knee joints require larger voltages to generate the effective electric field.

Nucleic acid vectors encoding light-gated cation-selective membrane channels, in particular channelrhodopsin-2 (Chop2), converted inner retinal neurons to photosensitive cells in photoreceptor-degenerated retina in an animal model. Such treatment restored visual perception and various aspects of vision. A method of restoring light sensitivity to a retina of a subject suffering from vision loss due to photoreceptor degeneration, as in retinitis pigmentosa or macular degeneration, is provided. The method comprises delivering to the subject by intravitreal or subretinal injection, the above nucleic acid vector which comprises an open reading frame encoding a rhodopsin, to which is operatively linked a promoter and transcriptional regulatory sequences, so that the nucleic acid is expressed in inner retinal neurons. These cells, normally light-insensitive, are converted to a light-sensitive state and transmit visual information to the brain, compensating for the loss, and leading to restoration of various visual capabilities.

The present invention relates to a method of producing a non-human animal model of hypertrophic scarring. This involves producing an incision in a non-human animal and applying mechanical strain over the incision under conditions effective to produce hypertrophic scarring, thereby producing a non-human animal model of hypertrophic scarring. The present invention also relates to a method of determining the efficacy of an agent for prevention or treatment of a disease condition. This method involves providing a non-human animal having an incision over which mechanical strain is applied under conditions effective to produce hypertrophic scarring, administering an agent to the incision, and determining whether the agent is efficacious for prevention or treatment of a disease condition. Also provided is a non-human animal model of hypertrophic scarring. This involves a non-human animal having an incision over which mechanical strain has been applied under conditions effective to produce hypertrophic scarring.

A robotic architecture for capturing the autonomous performance advantages the animal models enjoy in the natural environment is disclosed. A biomimesis process is employed to allow selective utilization of basic physical components and adaptation of a common control paradigm for each of different vehicle types. The biomimetic architecture involves five functional elements: a basic biomorphic plant for capturing the biomechanical advantages of the model organism; a neural circuit-based controller consisting of a finite state machine; myomorphic actuators producing linear graded force in response to trains of current pulses for mediating movements; labeled line code output by neuromorphic sensors; and a reactive behavioral sequencer executing command sequences defined within a behavioral library.

The invention discloses the transgenic animal model for pathological anxiety, the method to generate this model, the method to test drugs and drug candidates for the treatment of pathological anxiety and the method to use Wfs1 as target for screening of new anxiolytic drugs to treat pathological anxiety. This animal model is useful to test potential drug candidates for the treatment of diseases caused by pathological anxiety and to screen therapeutic compounds for the psychiatric disorders caused by reduces stress-tolerance and deficiency in adaptation to environmental challenges.

The present invention relates to compositions and methods for inhibiting unwanted angiogenesis, particularly those of ocular tissues. The treatment, inhibition, and/or prevention of choroidal neovasculature (CNV) is provided, along with an animal model for CNV and imaging techniques that permit the screening of potential agents as anti-angiogenesis and anti-CNV agents.

The application identifies novel fragments of alpha-synuclein in patients with Lewy Body Disease (LBD) and transgenic animal models thereof. These diseases are characterized by aggregations of alpha-synuclein. The fragments have a truncated C-terminus relative to fill-length alpha-synuclein. Some fragments are characterized by a molecular weight of about 12 kDa as determined by SDS gel electrophoresis in tricine buffer and a truncation of at least ten contiguous amino acids from the C-terminus of natural alpha-synuclein. The site of cleavage preferably occurs after residue 117 and before residue 126 of natural alpha-synuclein. The identification of these novel fragments of alpha-synuclein has a number of application in for example, drug discovery, diagnostics, therapeutics, and transgenic animals.

Behavioral pharmacological data with the compound of formula (I), a novel and selective 5HT2A/2C receptor inverse agonist, demonstrate in vivo efficacy in models of psychosis and dyskinesias. This includes activity in reversing MK-801 induced locomotor behaviors, suggesting that this compound may be an efficacious anti-psychotic, and activity in an MPTP primate model of dyskinesias, suggesting efficacy as an anti-dyskinesia agent. These data support the hypothesis that 5HT2A/2C receptor inverse agonism may confer antipsychotic and anti-dyskinetic efficacy in humans, and indicate a use of the compound of formula (I) and related agents as novel therapeutics for Parkinson's Disease, related human neurodegenerative diseases, and psychosis.

The invention provides a method for establishing a humanized rat drug evaluation animal model. According to the method, a multidrug resistance gene 1 (Abcb1)-knocked-out genetically engineered rat is obtained through a microinjection method by virtue of a CRISPR/Cas9 gene knockout technology and 153kb bacterial artificial chromosome (BAC) fragments containing a humanized Abcb1 promoter and cDNA is simultaneously inoculated into the rat genome through the microinjection method by virtue of a large fragment transgenic technology to obtain a transgenic rat capable of stably expressing human Abcb1 and the genetically engineered rat and the transgenic rat are hybridized to establish the humanized rat drug evaluation animal model. RT-PCR analysis shows that Abcb1 expression profiles of humanized Abcb1 rat are significantly different from those of the rat endogenous Abcb1. The method has the beneficial effects that the humanized rat capable of expressing human Abcb1 is obtained and the rat is used for expressing human Abcb1 genes and has closer expression profiles to those of human so that the model can be well used for the efficacy evaluation of newly developed drugs.

The combination of an interleukin-6 (IL-6) antagonist and an antiproliferative drug is described. In its preferred embodiment, the present invention describes the combination of an IL-6 superantagonist, particularly a superantagonist totally incapable of binding gp130 and an antiproliferative drug belonging to the glucocorticoid class (SANT-7 and dexamethasone). The combination according to the present invention has shown surprising synergism in an animal model of multiple myeloma and the ability to overcome the resistance to the antiproliferative drug developed by myeloid cells. The combination according to the present invention is useful for the preparation of a medicament for the treatment of tumours, particularly IL-6-dependent tumours.

The invention discloses a method for culturing normal human lung tissue and a lung cancer tissue organoid in an in-vitro manner. The method includes: acquiring fresh human-derived lung tissue cells, and performing collagen digestion on the fresh human-derived lung tissue cells to obtain single cells; culturing human lung tissue and the lung cancer tissue organoid under in-vitro 3D culture conditions; performing H&E staining to determining the structure and form, and using q-PCR to detect related gene expression; using immunofluorescent staining to authenticate cell sources and detect related protein expression. The invention further discloses a method for building a mouse animal model based on the organoid. The method for culturing the normal human lung tissue and the lung cancer tissue organoid and the method for building the mouse animal model have the advantages that the methods are significant to the building of large-scale and good-consistency human-derived in-situ lung cancer animal models, and a good basis and related application prospect are provided for the fundamental researches of lung cancer.

The invention provides a method for establishing an obese rat animal model based on a CRISPR (clustered regularly interspaced short palindromic repeat) gene knockout technology. The method comprises the following steps: (1) establishing an Lep/Lepr gene knockout rat model; (2) carrying out the authentication and related analysis on the obese rat animal model; (3) evaluating the energy metabolism and the body fat rate of the obese rat animal model. According to the method, a CRISPR/Cas system is used for respectively or simultaneously knocking out Lep and LepR genes so as to obtain the rat model modified by a corresponding target gene, so that the understanding of gene regulation in the obesity morbidity process can be deepened, and the high-level animal model can be provided for the translational medicine and the new medicine research and development.