The inventions provide the art with novel treatments of various airway conditions such as asthma wherein pathological production of mucus is implicated. Disclosed are novel inhibitors of miR-200 micro-RNAs, including inhibitors of miR-141. These miRNAs promote pathological mucus production and other airway dysfunction. They may be targeted by antagomirs which disrupt their activity. Additionally, they may be targeted by compositions with disrupt the gene expression of the targeted miR.

This document relates to methods and materials involved in treating a mammal having a gastrointestinal disorder (e.g., an irritable bowel syndrome (IBS) such as post-infection IBS (PI-IBS)). For example, one or more protease inhibitors and/or one or more microorganisms that produce one or more protease inhibitors can be administered to a mammal having, or at risk of developing, a gastrointestinal disorder to treat the mammal.

A knock-in non-human mammal comprising a recombinant androgen receptor (AR) cassette containing an exogenous human polyglutamine (polyQ) tract encoding sequence in exon 1, wherein the human polyQ tract encoding sequence is stably integrated into the genome of the animal. Also provided are recombinant cells, fertilized eggs and tissues. The resulting animal displays a wide range of phenotypes, best characterized as Metabolic Syndrome and can be used in screening and other assays.

The present invention is related to short-term renal injury models and methods for creating these models. The models and methods can be used for identifying, testing or characterizing candidate molecules with respect to their suitability to treat renal injury. The methods comprise a step of inducing, in a test subject, renal injury by administering subcutaneously a bolus of a renal injury inducer, in a dosage sufficiently high to induce renal injury. Different types of readout for renal injury are provided such as albumin creatinine ratio (ACR) determined in a urine sample taken from the subject, or the development of transcutaneous fluorescence after injection of a fluorescent molecule. Based on the readout the degree of renal injury and/or alteration of GFR can be determined.

The present invention provides a method for treating a fibrotic lung disease or fibrotic lung condition in a subject that involves an increase in NEU1 expression and/or activity, comprising administering to the subject an effective amount of an agent that inhibits the activity of NEU 1 sialidase, thereby treating the fibrotic lung disease or fibrotic lung condition in the subject.

Provided is a drug target for idiopathic pulmonary fibrosis, and the use thereof. The drug target is AREG signaling in AT2 cells of the lung. The drug target can be used to screen drugs for treating and/or preventing pulmonary fibrosis, in particular, idiopathic pulmonary fibrosis (IPF) of animals and human beings.

The present invention relates to a method for constructing an animal model of pulmonary fibrosis, in particular, idiopathic pulmonary fibrosis (IPF), the constructed animal model using the said method, and a method for screening the candidate drugs for treating pulmonary fibrosis, in particular, idiopathic pulmonary fibrosis (IPF).

The invention includes compositions and methods for the treating or preventing endometriosis in a subject in need thereof. In one aspect, the invention relates to compositions and methods for inhibiting microRNA451a.

The present disclosure provides use of a histone deubiquitinase in preparing a drug for preventing aging and treating aging-related diseases and relates to the technical field of biological medicines. The histone H2A deubiquitinase MYSM1 has a nucleotide sequence shown as SEQ ID NO. 1. It is verified that MYSM1 protein deficiency causes significant aging of mice and induces the aging-related diseases; and the MYSM1 can promote DNA injury repair, prevent cellular senescence and suppress chronic inflammation. Proved by a result of using an adeno-associated virus expressing mouse-derived MYSM1 as a gene therapy, the MYSM1 may remarkably prolong the lifespan of the mice, reduce the process and the number of senescent cells, improve normal functions of tissues and organs, reduce occurrence and development of the aging-related diseases, which proves that the MYSM1 has a good application prospect in delaying aging and treating the aging-related diseases.

A system is provided comprising a plurality of C. elegans cultures, where each culture comprises a transgenic C. elegans strain that models a mammalian disease or condition. Methods of using a system, e.g., for characterizing microbial strains of a mammalian microbiome and determining whether such microbial strains affect a mammalian disease or disorder.