The disclosure provides methods for determining liver fibrosis development, risk and prognosis.

The present invention relates to methods for diagnosing, determining, or monitoring liver diseases and conditions based on the blood concentration of circulating epithelial cells in and their gene expression.

The present disclosure provides methods of treating subjects having a liver disease, and methods of identifying subjects having an increased risk of developing a liver disease.

Provided is a monoclonal antibody specifically reactive with a C-terminal neo-epitope of PIIINP comprised in a C-terminal amino acid sequence CPTGXQNYSP-COOH (SEQ ID NO: 4) in which X is Gly or Pro, and where the monoclonal antibody does not recognize or bind an elongated version of the C-terminal amino acid sequence CPTGXQNYSPQZ-COOH (SEQ ID NO: 5), in which Z is absent or is one or more amino acids of the sequence of collagen type III. Also provided is a method of immunoassay for detecting in a biological sample the C-terminal neo-epitope of PIIINP generated by N-protease cleavage of intact type III procollagen, by contacting the sample with the monoclonal antibody, and determining the amount of binding of the antibody.

Provided are compositions related to HSD17B13 variants, including nucleic acid molecules and polypeptides related to variants of HSD17B13, and cells comprising those nucleic acid molecules and polypeptides. Also provided are methods related to HSD17B13 variants. Such methods include methods for detecting the presence of the HSD17B13 rs72613567 variant in a biological sample comprising genomic DNA, for detecting the presence or levels of any one of variant HSD17B13 Transcripts C, D, E, F, G, and H, and particularly D, in a biological sample comprising mRNA or cDNA, or for detecting the presence or levels of any one of variant HSD17B13 protein Isoforms C, D, E, F, G, or H, and particularly D, in a biological sample comprising protein. Also provided are methods for determining a subject's susceptibility to developing a liver disease or of diagnosing a subject with liver disease.

The present disclosure relates generally to methods for using pexidartinib and related Risk Evaluation and Mitigation Strategy (REMS), while reducing the occurrence of hepatotoxic adverse events.

An in vitro cell culture substrate is disclosed. The substrate comprises a decellularized tissue-specific extracellular matrix, wherein the tissue-specific extracellular matrix is derived from fibrotic tissue. A method of method of assessing an in vitro fibrotic cell culture is also disclosed. The method comprises providing one or more substrates comprising decellularized tissue-specific extracellular matrix derived from fibrotic tissue, where each substrate is provided in segregated manner. The method further comprises culturing native cells in each substrate to form a fibrotic cell culture. The method further comprises assessing at least one characteristic of each fibrotic cell culture.

A method is provided to measure modulation of bile salt export transport and/or formation activity in hepatocyte or stable cell line preparations by test agents including but not limited to drugs, drug candidates, biologicals, food components, herb or plant components, proteins, peptides, DNA, RNA. Furthermore, the method is to determine modulation of bile salt export transport and/or formation activity not only by said test agents, but further their metabolites or bio transformed products formed in situ. The bile salt export transport and/or formation activity modulation includes but not limited to inhibition, induction, activation and/or regulation. The method can be practiced to identify test agents, which have potential to cause liver injury, drug-drug interactions, and/or can be used as therapeutic agents for the treatment of cholestasis, abnormality of bile salt metabolism, liver diseases and cholesterol abnormality.

A method for identifying a kidney transplant recipient at an increased risk of developing interstitial fibrosis or tubular atrophy which comprises obtaining a post-transplant urine sample from the kidney transplant recipient; measuring the level of clusterin in the urine sample; comparing the level of clusterin in the patient sample to the level of clusterin in a control sample from the urine of a non-fibrotic kidney transplant recipient; diagnosing a kidney transplant recipient with a clusterin level that is significantly higher than the clusterin level in the control as being at an increased risk of developing interstitial fibrosis or tubular atrophy.

Provided herein are peptides and variant peptides that exhibit enhanced activity at the GLP-1 receptor, as compared to native glucagon.