Provided herein are compositions and methods for reducing toxicity associated with TAR DNA-binding protein 43. Certain embodiments of the present disclosure are related to compositions that treat, inhibit, reduce, prevent, or delay a disease or condition associated with TDP-43 toxicity, such as cystic fibrosis or neurodegenerative diseases. Certain embodiments of the present disclosure are related to methods of treating, inhibiting, reducing, preventing, or delaying a disease or condition associated with TDP-43 toxicity by administering compounds of any one of Formulas (I), (II), (III), (IV), (V), (VI), (VII), or (VIII) to a subject in need.

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.

The present invention provides novel mutations of the CFTR gene related to cystic fibrosis or to conditions associated with cystic fibrosis. Also provided are probes for detecting the mutant sequences. Methods of identifying if an individual has a genotype containing one or more mutations in the CFTR gene are further provided.

Qualitative and quantitative methods are for the detection of alginate oligomers in body fluids based on analyzing the Fourier transform infrared spectroscopy (FTIR) spectrum of a body fluid sample, for example a sputum sample, at a specific wave number range and, more particularly, certain specific characteristic wavenumbers.

Qualitative and quantitative methods are for the detection of alginate oligomers in body fluids based on analyzing the Fourier transform infrared spectroscopy (FTIR) spectrum of a body fluid sample, for example a sputum sample, at a specific wave number range and, more particularly, certain specific characteristic wavenumbers.

The invention relates to an assay for diagnosing a disease or affliction that affects fluid uptake or secretion or for studying the effectiveness of one or more drugs for treating the disease or affliction, wherein the assay comprises measuring swelling of one or more organoids.

Described are compounds for targeting proteases, e.g. serine proteases and their use in the diagnostic methods and methods for treatment of respiratory diseases such as cystic fibrosis. The compounds have the structure [H]—[B]-[A]; wherein [H] is a hydrophilic group, [B] is a subsite recognition group and [A] is a binding group; wherein A has the formula: —C(0)—CH.sub.2—NR.sup.1—COOR.sup.2 and wherein [B] has the structure: (i) —[CO—CH.sub.2—NR.sup.3]m-, or (ii) -[AA1-AA2]- or (iii) -(AA1-C0-CH.sub.2NR.sup.3)— or (iv) —(CO—CH.sub.2—NR.sup.3-AA1)- or (v) —(C0—CH.sub.2—NR.sup.4-AA1-AA3)-.

Disclosed herein are methods for detecting protein expression in an individual diagnosed with cystic fibrosis. The methods, in certain aspects, include the steps of obtaining a sample from said individual and detecting expression in said sample of each protein of a protein set. The method may further include the step of determining expression level of one or more proteins of the protein set. The disclosed methods may be used to predict one or more clinical parameters in an individual having cystic fibrosis.

The invention relates to an assay for diagnosing a disease or affliction that affects fluid uptake or secretion or for studying the effectiveness of one or more drugs for treating the disease or affliction, wherein the assay comprises measuring swelling of one or more organoids.

The present invention relates to the field of fibrosis and inflammation and more particularly to the use of ADAM12 (A Disintegrin and Metalloproteinase 12) inhibitors to prevent or treat inflammation-induced fibrosis. The present invention also relates to the use of ADAM12 as a marker for inflammation-induced fibrosis and to the ablation of ADAM12 expressing cells as therapeutic approach to interfere with the development of pro-fibrotic cells.