Provided herein are methods for determining a metabolic rate for at least one endogenous short-chain fatty acid in a subject, for diagnosing a pulmonary disease in a subject and for diagnosing a neurological disorder in a subject. Generally in the methods stable isotope labeled short-chain fatty acid are pulsed and metabolic rates are calculated in a first baseline blood sample and in a series of second blood samples obtained at intervals. The metabolic rates provide information about fatty acid metabolism and production.

In some aspects, the invention provides methods of treating a subject in need of treatment for a chronic complement-mediated disorder. In some aspects, the invention provides methods of treating a subject in need of treatment for a Th17-associated disorder. In some aspects, the invention provides methods of treating a subject in need of treatment for a chronic respiratory system disorder. In some aspects, the invention provides methods of administering a complement inhibitor to a subject. In some embodiments, a method of treating a subject comprises administering multiple doses of a complement inhibitor to the subject according to a dosing schedule that leverages the prolonged effect of complement inhibition in chronic respiratory disorders. In some embodiments, a subject has chronic obstructive pulmonary disease. In some embodiments, a subject has asthma.

This disclosure provides a robust, sensitive, and specific assay for the detection and measurement of periostin levels in samples obtained from human patients having, or suspected of having an IL-13-mediated disease or disorder. The disclosure further provides novel antiperiostin monoclonal antibodies that recognize at least isoforms 1, 2, 3, 4, 7, and 8 of human periostin, and assay kits comprising one or more of these antibodies.

Methods and kits for screening, diagnosing, detecting or predicting a patient outcome/risk variable for a lung transplant recipient after transplant or an EVLP outcome by measuring biomarker levels of one or more biomarkers selected from IL-6, IL-8, sTNFR1 and sTREM-1 in EVLP perfusate are described. The methods involve for example, i. obtaining one or more test EVLP perfusate samples of a donor lung; ii. determining in one or more test EVLP perfusate sample of a donor lung, a polypeptide level of one or more biomarkers selected from IL-8, IL-6, sTNFR1 and sTREM-1; and iii. a) comparing the polypeptide level of the one or more biomarkers in the perfusate sample with a control or cut-off level, wherein the differential level is indicative of outcome/risk of after transplant or of an EVLP outcome; or b) using the polypeptide level of one or several of the one or more biomarkers in combination, as part of an algebraic calculation of outcome/risk.

A method for diagnosing and/or stratifying the risk of infections or chronic diseases of the respiratory tract and lungs, particularly lower respiratory tract infections and chronic obstructive pulmonary disease, in which method provasopressin (proAVP) or fragments or partial peptides thereof, especially copeptin or neurophysin II, is/are determined. Suitable biomarker combinations for in-vitro diagnosis are also included.

Implementations are related to providing image selection suggestions. In some implementations, a method includes receiving first user input indicative of selection of one or more first images in an image library and determining one or more first image characteristics of the one or more first images. The method further includes identifying one or more second images in the image library. Each image of the one or more second images is associated with at least one second image characteristic that matches at least one of the one or more first image characteristics. The method further includes causing a user interface to be displayed. The user interface includes the one or more second images and enables selection of the one or more second images by a user.

Pulmonary hypertension is a progressive disease of various origins that is associated with vascular remodelling and results in right heart dysfunction. Accumulating evidence indicates important roles of immune cells and inflammatory chemokines in the pathogenesis and progression of pulmonary hypertension. We have identified CCL21 as anti-remodelling efficacy biomarker for pulmonary hypertension. CCL21 was found to be highly sensitive and specific in discriminating pulmonary hypertension patients from matched controls. CCL21 was upregulated in pulmonary hypertension and down-regulated with treatment with an anti-remodelling agent.

Described are compositions and methods for diagnosing acute exacerbations of chronic obstructive pulmonary disease (AECOPD). Multiple reaction monitoring mass spectrometry (MRM-MS) was used to quantify the amount of protein biomarkers in plasma samples from human subjects. The amount of the biomarkers in the sample can distinguish AECOPD from a stable or convalescent state of COPD, or from a subject without COPD.

Provided herein are methods and compositions relating, in part, to the generation of human progenitor cells committed to the lung lineage and uses of such cells for treatment of lung diseases/disorders or injury to the lung. Whether an adult stem cell can be isolated from human adult lung remains controversial in the art and at present, methods for isolating and using adult lung stem cells from humans lack reproducibility. Thus, the methods and compositions described herein are advantageous over the present state of knowledge in the art and permit the generation of human lung progenitor cells for treatment, tissue engineering, and screening assays.

The invention provides methods of treating or preventing pulmonary fibrosis or idiopathic pulmonary fibrosis (IPF) by administering an anti-EphA3 antibody to a patient. Moreover, the invention provides methods of identifying a candidate for treatment with an anti-EphA3 antibody by evaluating BAL fluid for EphA3 positivity are also disclosed. The invention further provides methods of measuring the efficacy of treatment by evaluating the reduction of the disease markers of fibrosis in a pulmonary fibrosis or IPF patient treated with an anti-EphA3 antibody are also disclosed.