An application of a UTX gene in preparation of drugs for preventing or treating lipid diseases. The invention further discloses a method for knocking out a UTX gene from a mouse liver. The invention further discloses a UTX overexpression adenovirus as well as a preparation method and an application thereof. The invention further discloses a method for upregulating UTX expression in a mouse liver. The invention further discloses therapeutic action of UTX overexpression on HFD induced hyperlipidemia and NAFLD. The invention provides an available laboratory basis for preparing lipid-lowering drugs, so that the UTX can be used for preparing drugs affecting the lipid, and a new research method is provided for researching the occurrence and development of dyslipidemia.

Methods and compositions for the prevention and treatment of liver damage or disease in a subject in need thereof are provided. The methods involve providing the sulfated oxysterol 25-hydroxycholesterol-3-sulfate (25HC3S) to the subject e.g. by 1) administering 25HC3S to the subject; or 2) overexpressing, in the subject, the hydroxysterol sulfotransferase enzyme SULT2B1b, which catalyzes the sulfation of 25-hydroxycholesterol (25HC) to form 25HC3S.

An object of the present invention is to provide a pharmaceutical composition or food or drink composition comprising an active ingredient that suppresses functional expression of Oscar protein. Another object of the present invention is to provide a pharmaceutical composition or food composition for preventing or treating kidney disease A further object of the present invention is to provide a pharmaceutical composition or food or drink composition that suppresses functional expression of Oscar in a living organism in order to suppress functional expression of FGF23. A still further object of the present invention is to provide a method for evaluating an effect, in the body, of an active ingredient that suppresses functional expression of Oscar protein. The above objects are achieved by at least one member selected from the group consisting of antagonists of the Oscar protein; genome editing systems that target Oscar gene; at least one RNA molecule selected from the group consisting of siRNA, shRNA, and miRNA that target Oscar mRNA, or vectors capable of expressing the RNA molecule; and antibodies that specifically bind to the Oscar protein and suppress function of the Oscar.

The present invention relates to a composition for the diagnosis of a degenerative brain disease, comprising hpmA, which is a substance derived from Proteus, Shigella, Klebsiella pneumoniae, or Citrobacter, preferably a Proteus mirabilis strain, from a biological sample of a subject. In addition, the present invention relates to a method for providing information for the diagnosis of a degenerative brain disease such as Parkinson's disease, brain neuritis (neuroinflammation), or Alzheimer's disease, by measuring the amount of hpmA.

To identify a microorganism causing the development of primary sclerosing cholangitis associated with ulcerative colitis. A Klebsiella pneumoniae strain inducing inflammation in the liver.

Aspects of the disclosure relate to a composition comprising 20-60% w/w of fat combined with a nitric oxide synthase inhibitor. Method aspects of the disclosure relate to a method for inducing heart failure with preserved ejection fraction in an experimental laboratory animal, the method comprising administering a composition of the disclosure or a composition comprising 10-60% w/w of fat and a composition comprising a nitric oxide synthase inhibitor to the laboratory animal.

Provided are a knockout mouse, a method for screening a substance for suppressing mesial temporal lobe epilepsy, and a method for selecting a technique for suppressing mesial temporal lobe epilepsy. A knockout mouse 30 or more days of age that has lost the function of the Girdin gene in at least the nervous tissues and exhibits the phenotypes of (1), (2), and (3) below. (1) hippocampal sclerosis should be present, (2) extrahippocampal brain damage should be limited, and (3) spontaneous epilepsy that can be said to be of hippocampal origin should be present.

Methods for the treatment or prevention of disease, such as fatty liver disease and obesity, are described including the modulation the amount of CTRP1 in a subject. Novel mouse strains are also described.

The present invention provides a simple and rapid construction of an animal model of constipation and use thereof. The construction method comprises: irritating a rat via tail-clamping and then gavaging the rat with 3.5-7 mg/kg of loperamide the next day, wherein the tail-clamping irritation treatment is as follows: clamping a tail 2-4 times every day for 25-35 min each time continuously for 3-5 days. The present invention obtains a method for constructing a rat model of constipation caused by liver depression and spleen deficiency by combining the tail-clamping irritation treatment and loperamide gavage treatment. The method has a short modeling period, is simple to operate, has a low cost, and effectively overcomes stress reaction of a rat. Besides, the constructed rat model of constipation caused by liver depression and spleen deficiency has various mechanisms, being stable, reliable and high in repeatability.

The invention relates to a viral expression construct and related viral vector and nucleic acid molecule and composition and to their use wherein said construct and vector are suitable for expression in a mammal and comprise a nucleotide sequence encoding a Fibroblast growth factor 21 (FGF21) to be expressed in liver, adipose tissue and/or skeletal muscle.