Methods for detecting a mycobacterial infection in a patient are disclosed. These methods include the step of detecting lipoarabinomannan (LAM) and/or derivatives thereof in a biological sample from the patient. Methods for diagnosing disease, including nontuberculous mycobacterial infection (NTM), and kits for the described methods are also provided.

The invention relates to in vitro methods for detecting bacteremia, for selecting a therapy for a subject with cystic fibrosis or for a subject with systemic inflammatory response syndrome and for selecting a subject with cystic fibrosis or with systemic inflammatory syndrome for a particular therapy based on the expression levels of a gene selected from tumor necrosis factor alpha (TNFα), IL-1b, IL-10, CCL2, interferon beta (IFN-β), IL-17, IL-2, IL-4 and VEGF in a blood sample from the subject. The invention also relates to a kit comprising a TLR-4 agonist and a reagent specific for determining the level of at least one cytokine selected from the group consisting of tumor necrosis factor alpha (TNFα), IL-1b, IL-10, CCL2, interferon beta (IFN-β), IL-17, IL-2, IL-4 and VEGF and to the uses of this kit.

The present invention is directed to modified CFTR proteins or fragments thereof that contain single or multiple amino acid mutations to improve the structural stability of such CFTR proteins and/or fragments. Specifically, the modified CFTR proteins or fragment thereof differ from the wild-type human CFTR protein or fragment thereof by the presence of four or more mutations selected from V150D, M470V, S492P, F494N, S495P, A534P, I539T, G550E, G551D, R553Q, R555K, Q637R, S1255L, K1334G, S1359A, E1371Q, H1402S, Q1411D, and any combination thereof, such that the stability of the polypeptide is increased relative to that of the wild-type human CFTR polypeptide or fragment thereof.

A method to determine the severity of a disease of chronic inflammation in a patient, comprising the steps of (1) collection or preparation of a bodily fluid, tissue or lavage and (2) measurement of ALX receptor ligands or ALX receptor expression in the fluid, tissue, or lavage, wherein the level of ALX receptor ligands predicts a clinical outcome or choice of treatment modality, is disclosed.

Disclosed herein are microfluidic devices that may be used to mimic human organ systems, in particular, pancreatic function, and methods of using same. In particular, disclosed are microfluidic devices that may include a first chamber having a plurality of pancreatic ductal epithelial cells (PDECs), a second chamber having a plurality of pancreatic islets, and a permeable membrane fluidly connecting the chambers. The disclosed devices and methods may be used for the study of pancreatic cell function, for the development of therapeutics, or for the development of personalized therapeutics wherein the cells of the device are obtained from an individual in need of such treatment.

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.

The invention pertains to the use of a specific biomarker of elastin degradation (desmosine) that measures the extent and progression of chronic obstructive pulmonary disease (COPD). In addition to potentially serving as a screening procedure for COPD, it provides a real-time measure of COPD drug efficacy and may therefore supersede the use of less sensitive tests such as pulmonary function studies and computed tomography. Equally important, the current invention constitutes a marked improvement for measuring desmosine in tissues and body fluids by greatly shortening the time for detection of this molecule in liquid chromatography-tandem mass spectrometry (LC-MS-MS) assays that are the gold standard for such measurements. Unlike previous methods, the invention allows for the use of LC-MS-MS without modification, so the method can be applied to any laboratory that uses this equipment for other measurements. This would include forensic facilities that need to determine if undiagnosed COPD played a role in the loss of life.

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.

Provided herein are methods of making and using a number of different types of liver cells.

The present invention relates to a method of determining the effectiveness of a compound in a subject for treatment of cystic fibrosis comprising the steps of a) determining a first excretion level of bicarbonate in a first urine sampling obtained from a subject having cystic fibrosis; where said first urine sampling has been obtained prior to said subject has been treated with a compound for treatment of cystic fibrosis; b) determining a second excretion level of bicarbonate in a second urine sampling from said subject; where said second urine sampling is obtained after said subject has been treated with said compound for a predetermined time period; and c) determining the effectiveness of the compound against cystic fibrosis by comparing said first excretion level of bicarbonate to said second excretion level of bicarbonate; wherein said compound is considered as effective if said second excretion level of bicarbonate is above said first excretion level of bicarbonate and said compound is considered ineffective if said second excretion level of bicarbonate is below or at the same excretion level as said first excretion level of bicarbonate. The present invention also relates to a method for sub-categorizing cystic fibrosis.