The present disclosure provides methods and compositions that find use in facilitating a diagnosis of chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) in a subject. The methods and compositions involve measurement of at least one of proteins: IL-16, IL-7, VEGF, CXCL9, CX3CL1, CCL24, CCL19, and CCL11 in a body fluid sample of a subject suspected of having CFS/ME. Levels of one or more of the aforementioned proteins can be used to facilitate a diagnosis of a CFS/ME and/or confirm a diagnosis of CFS/ME. The methods and compositions of the present disclosure also find use in screening subjects for clinical trials and facilitating treatment decisions for a subject.

The instant disclosure provides biomarkers and methods for identifying subjects at risk of developing cytokine release syndrome (CRS), neurotoxicity, or both after adoptive immunotherapy to guide preemptive intervention, modified therapy, or the like. For example, adverse event biomarkers may be measured in a subject before pre-conditioning chemotherapy, before immunotherapy (e.g., adoptive immunotherapy infusion comprising a chimeric antigen receptor (CAR)-modified T cell), or shortly after pre-conditioning chemotherapy and/or immunotherapy. Exemplary biomarkers include temperature, cytokine levels and endothelial activation biomarkers, such as angiopoietin-2, von Willebrand factor (vWF), ratio of angiopoietin-2 to angiopoietin-1, and ratio of ADAMTS13 to vWF. Also provided are methods of treating subjects identified as at risk of developing cytokine release syndrome (CRS), neurotoxicity, or both to minimize such potential adverse events.

The purpose of the present invention is to provide a method for predicting the effectiveness of an angiogenesis inhibitor in a subject suffering from a tumor. Provided is a method comprising a step of testing for the presence or absence of an a mutation or loss of expression of B-Raf and PTEN in a sample of tumor tissue from the subject. By using the presence or absence of or a mutation or loss of expression of B-Raf and PTEN as an indicator, this method enables the antitumor effectiveness of the angiogenesis inhibitor to be predicted without administering the angiogenesis inhibitor to the subject.

The invention provides methods and systems for detecting a biomarker in a synovial fluid wherein the system also includes a control to ensure that the test sample is indeed synovial fluid. The biomarkers and the control for synovial fluid can be identified using proteomic methods, including but not limited to antibody based methods, such as an enzyme-linked immunosorbant assay (ELISA), a radioimmunoassay (RIA), or a lateral flow immunoassay.

The invention provides methods and systems for detecting a biomarker in a synovial fluid wherein the system also includes a control to ensure that the test sample is indeed synovial fluid. The biomarkers and the control for synovial fluid can be identified using proteomic methods, including but not limited to antibody based methods, such as an enzyme-linked immunosorbant assay (ELISA), a radioimmunoassay (RIA), or a lateral flow immunoassay.

A method for predicting the risk of recurrence of Atrial Fibrillation in a subject based on measuring the amount of the biomarker Angiopoietin-2 (Ang-2) and optionally of at least one further biomarker in a sample from the subject is described. Also described is a method of diagnosing Atrial Fibrillation in a subject suspected to suffer from Atrial Fibrillation based on measuring the amount of the biomarker Angiopoietin-2 (Ang-2) and optionally of at least one further biomarker in a sample from the subject. Also described are devices adapted to carry out the method of the present disclosure.

Recent literature on SARS-CoV-2 pathogenesis has suggested that the induction of substantial acute respiratory distress phenotypes is driven by a mismatched inflammatory response together with broad vascular dysfunction. While several detailed reports implementing multi-omic approaches have provided insight into the immune cell phenotypes involved in these processes, risk stratifying markers specific to COVID-19 and the vasculature have not been explored. Provided herein is a comprehensive, multi-omics-based description of the molecular antecedents to COVID-19 mortality, yielding new insights pertaining to the vasculature while highlighting the urgent need for clinical translation of novel biomarkers for disease prognosis.

An anti-Ang2 antibody or an antigen-binding fragment thereof that specifically binds to an angiogenesis-inducing factor Angiopoietin-2 (Ang2) and complexes with a Tie2 receptor and Ang2, and related methods and compositions.

Methods of treating cancers comprising administering a fibroblast growth factor receptor 1 (FGFR1) extracellular domain (ECD) and/or an FGFR1 ECD fusion molecule are provided. Methods of treating cancers comprising administering a fibroblast growth factor receptor 1 (FGFR1) extracellular domain (ECD) and/or an FGFR1 ECD fusion molecule and at least one anti-angiogenic agent are provided.

The present invention relates to a method for predicting the risk of a subject of rapidly progressing to chronic heart failure and/or of hospitalization due to chronic heart failure and/or death. The method is based on the determination of at least one biomarker selected from the group consisting of a BNP-type peptide, IGFBP7 (IGF binding protein 7), a cardiac Troponin, soluble ST2 (sST2), FGF-23 (Fibroblast Growth Factor 23), and Growth Differentiation Factor 15 (GDF-15), in a sample of a subject. The method may further encompass the assessment of the presence or absence of (i) abnormal midwall fractional shortening or (ii) left ventricular hypertrophy. Further envisaged by the present invention are devices adapted to carry out the present invention.