The invention relates to an in vitro method for the diagnosis of acute pancreatitis (AP) in a subject by detection of Glycoprotein 2 isoform alpha (GP2a) protein. In particular the invention pro-vides an in vitro method for the diagnosis of acute pancreatitis (AP) in a subject by detection of Glycoprotein 2 isoform alpha (GP2a) protein, comprising providing a sample of a human subject exhibiting symptoms of having pancreatic disease, wherein said sample is obtained from the subject within 72 hours of the appearance of said symptoms, providing an affinity reagent directed against GP2a, contacting said sample with said affinity reagent thereby capturing GP2a from said sample, and determining the concentration of GP2a from said sample, wherein determining a concentration of GP2a in said sample that is greater than the average concentration of GP2a in control samples, such as in a group of healthy individuals, indicates the presence of AP and the absence of one or more of chronic pancreatitis, pancreatic cancer, gastrointestinal cancer, liver cancer, neuroendocrine tumor, sarcoma, peptic ulcer or peritonitis. The invention further provides a kit and a system developed for carrying out the claimed method and determining the concentration of GP2a and performing an automated analysis of one or more samples.

The invention features compositions and methods for characterizing inflammatory bowel disease and inflammatory bowel disease subtypes, such as well Crohn's disease and ulcerative colitis. In one aspect, the invention provides a panel for characterizing inflammatory bowel disease, the panel including two or more (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 20, 25) capture molecules each bound to a substrate, wherein each capture molecule specifically binds a marker polypeptide selected from one or more of the following: CD3, CD4, CDS, CD24, CD25, CD27, CD38, CD44, CD45RA, CD45RO, CD127, CD161, CTLA-4, CXCR3, CCR4, CCR6, CCR7, FOXP3, HLA-DR, IFNγ, IL-10, IL-17A, IL-21, IL-22, CD11c, IL23p19, CD66b, CD163, CD44, ckit, CD16, NKp46, AHR, and TNFα, or a polynucleotide encoding said marker polypeptide.

The present invention relates to compositions and methods for binding and inhibiting renalase. In one embodiment, the renalase binding molecule inhibits renalase activity. Thus, in diseases and conditions where a reduction of renalase activity is beneficial, such inhibitory renalase binding molecules may act as therapeutics.

The presently claimed invention relates to materials and methods for diagnosing a chronic inflammatory disease in a patient comprising testing a biological sample from the patient for a level of a first neurovascular biomarker of lymphatic activation and diagnosing the patient as having the chronic inflammatory disease if the tested level of the first neurovascular biomarker of lymphatic activation is less than a first normal level.

A system and method for using new biomarkers to assess individual diseases is provided. In one embodiment of the present invention, absolute quantification of annotated metabolites by mass spectrometry is used to identify certain biomarkers and derivatives thereof (i.e., signatures), which are then used to screen for, diagnose, predict, prognose, and treat various diseases, including, but not limited to, breast cancer, ovarian cancer, colorectal cancer, pancreatic cancer, and acute graft-versus-host disease.

The inventors have produced two high specificity and high affinity monoclonal antibodies that bind to human neuromedin U (NMU). Methods and compositions are provided for treating an individual in need thereof (e.g., an individual who is obese and/or has diabetes) by administering an anti-NMU/NMUR agent (e.g., an anti-NMU antibody). For example, methods and compositions are provided for increasing circulating insulin in an individual. Methods and compositions are also provided for detecting neuromedin U (NMU) (e.g., in a biological sample such as serum). Methods and compositions are also provided for predicting whether an individual will develop diabetes and/or PDAC, and for identifying an individual who would benefit from administration of an anti-NMU/NMUR agent.

Necrotizing Enterocolitis (NEC) biomarkers, NEC biomarker panels, and methods for obtaining a NEC signature for a sample are provided. Also provided are methods, compositions, and kits for making a Necrotizing Enterocolitis (NEC) assessment of an individual, e.g. for diagnosing NEC in a patient, prognosing NEC in a patient, treating an NEC patient, etc. These methods find use in a number of applications, such as diagnosing and treating infants who are suspected of having NEC, intestinal perforation (IP), or sepsis.

This invention describes a method for early diagnostics of severe pancreatitis using cell membrane damage detection mechanisms. The method involves a non-invasive testing of human urine or other body fluids samples of patients that are suspected to be affected by acute pancreatitis. The invention is based on heat shock protein HSP-70, 90, 60, and 27 role of action in disease progression.

The present invention relates to methods and compositions for identifying subjects treated with or considered for treatment with checkpoint blockade therapeutic agents that are at higher or lower risk for developing checkpoint therapy associated colitis, by analyzing the intestinal microbiome of those subjects. It is based, at least in part, on the discovery that the abundance of certain intestinal microbiota of the phyla Bacteroidetes, including the bacteria in the families Bacteroidaceae, Rikenellaceae, and Barnesisllaceae, and/or an increase or decrease in microbial genetic pathways involved in polyamine transport and/or B vitamin biosynthesis (e.g., (riboflavin (B2), pantothenate (B5) and thiamine (B1)) are associated with the likelihood of developing checkpoint therapy associated colitis.

The purpose of the present invention is to provide a simple and highly accurate method for detecting pancreatic exocrine dysfunction with minimal invasiveness to a subject. The method comprising in vitro measurement of two APOA2 protein variants, mutants thereof and/or fragments thereof in a body fluid sample derived from the subject and detection of the presence or absence of pancreatic exocrine dysfunction on the basis of the measured amounts, and a detection kit for pancreatic exocrine dysfunction including antibodies that can specifically bind to said proteins are provided.