Excessive deposition of extracellular matrix is a hallmark of Idiopathic pulmonary fibrosis (IPF), it is advantageous to target the cells and the mechanisms associated with this process. By targeting myofibroblasts (specialized contractile fibroblasts) that are key for the development of IPF with drugs conjugated with fibroblast activation protein (FAP), this technology helps minimize the production of extracellular matrix in the lungs and provides a new treatment option for patients diagnosed with IPF.

Provided herein are antibody molecules that bind specifically to C-MET and related nucleic acid molecules, vectors and host cells. Also provided herein are medical uses of such antibody molecules.

The present invention relates to a new assay to diagnose nonalcoholic steatohepatitis (NASH), NASH progression and NASH fibrosis stage.

Staphylococcus nepalensis releases corisin, a peptide conserved in diverse Staphylococci, that induces apoptosis of lung epithelial cells. Therefore, methods and apparatus for detecting the presence of corisin in a biological sample of a patient are disclosed, as well as pharmaceutical compositions, such as antibodies, and methods for treating patents having or suspected of having fibrosis.

Provided herein are, inter alia, compositions and methods for identifying and using agents capable of inhibiting myofibroblast transition as well as methods for treating diseases associated with the same in a subject in need thereof.

It has been discovered that plasma samples from endometriosis patients contain a number of markers whose abundance is different from those in healthy individuals. It has also been discovered that, by measuring the abundance of those markers, whether or not a subject is affected by endometriosis can be diagnosed, the extent of endometrial fibrosis or adhesion in a subject can be determined, pain of a patient affected or suspected of being affected by endometriosis can be predicted, and pathological conditions of the patient can be monitored.

This disclosure relates to devices, assays, and methods related to airway inflammation caused by polymorphonuclear neutrophils (PMNs). In certain embodiments, the disclosure relates to a model device that emulates the changes in airway cell physiology due to transmigration of PMNs from blood to the cells at the air-liquid interface. In certain embodiments, the airway cells are supported on a collagen layer wherein the collagen layer is further supported by a porous polymer from which PMNs can migrate. In certain embodiments, the disclosure contemplates adding bacteria, fungi and/or viruses to the device to emulate disease states. In certain embodiments, the disclosure relates to the use of the model system to test compounds to identify drug candidates and diagnose subjects with airway-related diseases and conditions.

The present disclosure provides methods of inducing desmoplastic stroma to express a normal phenotype by detecting increased levels of NetG1 or NGL1 in tumor or in desmoplastic stroma isolated from a human subject, and/or detecting NetG1 in circulating extracellular vesicles, and/or detecting increased pFAK in the stroma, and treating the human subject with a therapeutic regimen; and by detecting NetG1 in a microvesicle isolated from a human subject, and/or treating the human subject with a therapeutic regimen.

The present invention provides an antibody to a fibrosis-related molecule and medical application thereof. The antibody of the present invention is an antibody that binds to CHL1 protein and an antibody that neutralizes the binding of the CHL1 protein to a fibroblast.

The present disclosure relates to antibody molecules that bind specifically to C-MET and related nucleic acid molecules, vectors and host cells. Also provided are medical uses of such antibody molecules. The claimed anti C-Met antibodies of the present application have been selected by in silico engineering. Some of the antibodies have been generated and further characterized after expression in mammalian expression system