Managing and treating elevated OS biomarkers in mammals such as companion animals with at least one of the supplements alpha-lipoic acid, carnitine, co-enzyme Q-10, ginger, green tea, licorice, milk thistle, garlic, honey. resveratrol, soybeans, tomatoes, turmeric, vitamin D, vitamin E or selenium. Diagnosing an oxidative stress (OS) in a mammal comprises collecting a sample; screening the sample to detect the presence of an OS biomarker, selectively isoprostane and other antioxidants such as HODE microRNAs. TAC: GSH, MDA, and TNF-alpha. The sample can be saliva.

A system for identifying, monitoring and matching patients with appropriate treatments using a systemic mediator-associated physiologic test profile are provided. The system of the present invention increases the likelihood of demonstrating clinical efficacy in clinical trial datasets.

The present invention relates to a method of in vitroprediction of the in vivoefficacy in a patient of treatment with a drug product based on an overall assessment of the properties patients own immune cells when exposed to the drug product with and/0 or without stimulation; the drug product when exposed to said patients own immune cells; and any preexisting antibodies against said drug product in said patient.

T cell surface marker, CRTH2, is a target for treating Postural Orthostatic Tachycardia Syndrome, a hemodynamic abnormality. Targeting CRTH2 permits control of disease symptoms in POTS, for which no FDA approved treatment is currently available. Cell surface expression on certain T cell subsets characterizes the syndrome. Cell surface expression can be conveniently determined in plasma samples using flow cytometry.

T cell surface marker, CRTH2, is a target for treating Postural Orthostatic Tachycardia Syndrome, a hemodynamic abnormality. Targeting CRTH2 permits control of disease symptoms in POTS, for which no FDA approved treatment is currently available. Cell surface expression on certain T cell subsets characterizes the syndrome. Cell surface expression can be conveniently determined in plasma samples using flow cytometry.

The present disclosure relates to methods of inhibiting vimentin activity, methods of screening for new vimentin inhibitors and uses of new vimentin inhibitors.

Provided are methods of analysing markers of eosinophil levels and/or markers of neutrophil levels in a blood sample from a patient suffering from an exacerbation of inflammation of a respiratory condition to determine the levels of eosinophils and/or neutrophils respectively. The methods may involve selecting an appropriate treatment. Systems and kits for performing the analysis are also provided.

Provided are methods of analysing markers of eosinophil levels and/or markers of neutrophil levels in a blood sample from a patient suffering from an exacerbation of inflammation of a respiratory condition to determine the levels of eosinophils and/or neutrophils respectively. The methods may involve selecting an appropriate treatment. Systems and kits for performing the analysis are also provided.

Molecules for inhibiting arachidonate 15-lipoxygenase (ALOX-15) gene products including dsRNA (dsRNA) agents such as small interfering RNAs (siRNAs), antisense oligonucleotides, and small molecule inhibitors for therapeutic use. Additionally provided are methods to inhibit the expression of a target gene by administering these agents for the treatment of diseases involving ALOX-15 gene products.

Disclosed is a method of measuring the prostaglandin E main urinary metabolite (PGE-MUM), in which a mixture solution of a urine sample treated with alkali can directly be subjected to an antigen-antibody reaction system in an immunoassay of PGE-MUM, without neutralization and dilution followed by dispensation. The method of measuring PGE-MUM includes the steps of: a) mixing a urine sample with an alkaline aqueous solution, and b) subjecting the mixture solution resulting from a) to an immunoassay using a bicyclo PGE-MUM-immobilized or anti-bicyclo PGE-MUM antibody-immobilized solid phase to measure PGE-MUM in the urine sample, wherein the immunoassay is performed in a weakly-acidic basal buffer solution in the presence of a second pH buffering agent which exerts a buffering effect in the basic range and is different from the pH buffering agent contained in the basal buffer solution, and in the presence of a cationic surfactant.