The present disclosure provides methods of determining whether a subject treated for hypertension should continue hypertension treatment. In exemplary embodiments, the method comprises measuring the level of at least two of the following in a urine sample obtained from the subject: (i) Alpha—1 microglobulin (aim); (ii) kidney injury molecule (KIM—1); and (iii) Chitinase-3-like protein (YKL-40); wherein the subject should continue the hypertension treatment, when the levels are decreased or unchanged, relative to a control level, and wherein the subject should discontinue or decrease the hypertension treatment, when the levels are increased, relative to a control level. Related methods, kits, assay systems, systems comprising machine readable instructions, computer-readable storage media, and methods implemented by a processor in a computer are furthermore provided herein.

The present invention relates to a method for assessing a status of a wound of a patient, comprising the steps of determining a concentration of one or more inflammatory markers selected from glucose and eotaxin-1 in a sample from the wound, wherein the sample comprises or consists of wound fluid and the one or more inflammatory markers may indicate an inflammation within the wound, ii. determining a concentration of one or more bacterial markers in the sample, wherein the one or more bacterial markers may indicate a colonization of the wound with metabolically active bacteria, iii. assessing the status of the wound based on the concentrations of the one or more inflammatory markers and the one or more bacterial markers, wherein the status of the wound is assessed as being inflamed or not inflamed and as being colonized with metabolically active bacteria or not colonized with metabolically active bacteria. This diagnostic method allows a reliable, specific and detailed assessment of the status of the wound.

Presented herein are systems and methods for developing classifiers useful for predicting response to particular treatments. For example, in some embodiments, the present disclosure provides a method of treating subjects suffering from an autoimmune disorder, the method comprising administering an alternative to anti-TNF therapy to subjects who have been determined to be non-responsive via a classifier established to distinguish between responsive and non-responsive prior subjects in a cohort who have received the anti-TNF therapy.

A new, stable trimeric TNFα structure is disclosed with distorted symmetry which can bind to the TNFR1 receptor to attenuate signalling therefrom, which can be used in the treatment and/or prevention of diseases associated with the soluble TNFα/TNFR1 interaction. Membrane-bound TNFα is not affected in its ability to signal through TNFR2, and thus the new structure of TNFα may be used in therapies which do not significantly raise the risk of infection or malignancy.

The present invention relates to the finding that TL1A enhances differentiation of TH17 cells, and enhance IL17 secretion from TH17 cells. In one embodiment, the present invention provides a method of treating an inflammatory disease comprising determining the presence of a TL1A signaling profile, and treating the disease by administering a composition comprising a therapeutically effective dosage of one or more inhibitors of TL1A or TH17 cell differentiation. In another embodiment, the disease is characterized by TH17 differentiation.

A method for screening compounds for their ability to interact with transmembrane proteins is provided. Also provided is a method for determining whether proteins such as transmembrane proteins are able to oligomerise.

The present disclosure provides antibodies that specifically bind to human OX40 receptor (OX40) and compositions comprising such antibodies. In a specific aspect, the antibodies specifically bind to human OX40 and modulate OX40 activity, e.g., enhance, activate, or induce OX40 activity, or reduce, deactivate, or inhibit OX40 activity. The present disclosure also provides methods for treating disorders, such as cancer, by administering an antibody that specifically binds to human OX40 and modulates OX40 activity, e.g., enhances, activates, or induces OX40 activity. Also provided are methods for treating autoimmune or inflammatory diseases or disorders, by administering an antibody that specifically binds to human OX40 and modulates OX40 activity, e.g., reduces, deactivates, or inhibits OX40 activity.

The application relates to methods of treating chronic viral infection by modulating Tim-3 activity. In addition, the present application relates to methods of diagnosing or monitoring immune system activity or function, chronic viral infection and inflammatory disease using Tim-3 expression.

The present invention relates to the field of molecular biology, cell biology, and cancer biology. Specifically, the present invention relates to methods of treating myelodysplastic syndrome (“MDS”) with a farnesyltransferase inhibitor (FTI) that include determining whether the subject is likely to be responsive to the FTI treatment based on the Th1/Th2 balance and additional characteristics.

Disclosed herein are systems and methods for detecting ocular analytes in vitreous humor or aqueous humor. Specifically exemplified are systems having a sample acquisition device that is inline with an analyte detection device. The system embodiments allow for the easy procurement and testing of samples. In a typical embodiment, the analyte detection device includes a sample staging chamber and a test chamber that comprises reagents that specifically interact with the analyte. The test chamber may include a sample pad, a conjugate pad having at least one conjugate reagent specific to the analyte loaded thereon, an assay platform having a substrate with at least one test region having a test reagent immobilized thereon, the test reagent being specific to the analyte; and an optional absorbent pad.