Provided are a method and a composition for preventing or treating atopic dermatitis through administration of monoclonal stem cells and a method for screening atopic dermatitis patients suitable for administration of monoclonal stem cells and predicting prognosis of patients. According to the method for the subfractionation culture and proliferation of stem cells of the disclosure, large quantities of desired monoclonal mesenchymal stem cells can be obtained in a short period of time through rapid proliferation of monoclonal mesenchymal stem cells. In addition, the monoclonal mesenchymal stem cells thus obtained can be administered to atopic dermatitis patients according to a prescribed administration cycle, guidelines, and dose to effectively ameliorate atopy symptoms in the patients. Moreover, by using a marker to identify patient groups particularly suitable for the treatment and selectively administering the monoclonal mesenchymal stem cells to the patient groups, an excellent therapeutic effect for atopic dermatitis can be achieved.

The present disclosure relates to a kit for quantitative detection using a fluorescent microarray, and belongs to the technical field of protein detection. The kit of the present disclosure includes a detection plate and a detection antibody coupled with fluorescent microspheres, where the detection plate is provided with a plurality of reaction chambers; the reaction chamber is provided with an opening, and an inner bottom surface of the reaction chamber is provided with a plurality of detection sites that are arranged side by side along a length direction of the reaction chamber at an interval. The kit of the present disclosure may detect allergen-specific IgE, IgG and IgA with high sensitivity, as well as rapidly and quantitatively detect an allergen-specific antibody IgE, IgG and IgA concentration in human serum or plasma, and may screen dozens of allergens at a time.

The invention relates to methods of treating ichthyosis in a subject with an inhibitor of the interleukin 36 (IL-36) pathway, and methods of selecting a subject for therapy with the IL-36 pathway inhibitor.

Provided is an ST2 antigen binding protein, such as a mouse, human, chimeric or humanized antibody or antigen binding fragment thereof that specifically binds to ST2. Also provided are nucleic acid molecules encoding the above-mentioned antibodies and antigen binding fragments thereof, and an expression vector and host cell for expressing the antibodies or antigen binding fragments thereof. Further provided are methods for preparing and using the antibodies and antigen binding fragments thereof. The methods comprise treating and preventing IL33/ST2-mediated related diseases or conditions.

The present disclosure provides methods of treating lung disease subjects that are likely to respond to an IL-33 antagonist, an interleukin-4 receptor alpha antagonist, or an IL-13 receptor antagonist, based on the subject's IL-33 Asthma polygenic risk score.

Isolated human monoclonal antibodies which bind to IL-8 (e.g., human IL-8) are disclosed. The human antibodies can be produced in a hybridoma, transfectoma or in a non-human transgenic animal, e.g., a transgenic mouse, capable of producing multiple isotypes of human monoclonal antibodies by undergoing V-D-J recombination and isotype switching. Also disclosed are pharmaceutical compositions comprising the human antibodies, non-human transgenic animals, hybridomas, and transfectomas which produce the human antibodies, and therapeutic and diagnostic methods for using the human antibodies.

Methods of determining infection type are disclosed. In one embodiment, the method comprises measuring the amount of TRAIL and/or IP10 no more than two days from symptom onset.

Disclosed herein are methods in which an individual with multiple sclerosis (MS) can be classified into one of six subject groups, each subject group predictive for the patient's responsiveness to an interferon-β (IFN-β) therapy. The individual with MS can be classified according to the individual's serum marker levels, e.g., at baseline or following treatment with therapy. Depending on the classification, the individual with MS can be treated with standard therapies (e.g. IFN-β) or one or more alternative therapies with or without IFN-β.

A method for detection or monitoring status of silent brain ischemia (SBI) and cerebrovascular health. The assay reagents and methods described herein provide a specific indicator of cerebral microvascular disease, enabling clinicians to identify patients at risk for the development of SBI. A method of treating a subject having silent brain ischemia and/or metabolic syndrome comprises administering to the subject aspirin therapy, blood pressure therapy, body weight management, and/or a program of diet and exercise when levels of two or more SBI markers are elevated. Described herein are molecules that are produced by cerebral endothelial cells exposed to chronic vascular risk factors including obesity, hyperlipidemia, hypertension, and glucose intolerance. These stress molecules produced by cerebral endothelial cells are detectable in the serum and serve as diagnostic indicators of brain-specific endothelial cell damage and correlate with MRI indicators of silent stroke and impaired cognitive function.

The current disclosure provides use of high dose nicotinamide adenine dinucleotide (NAD) precursor regimens for reduction of inflammation in human patients with preexisting inflammation. The NAD precursor can be nicotinamide riboside (NR) and the high dose regimen can include at least 1000 or 2000 mg/day for at least 9 days.