Abstract: It is demonstrated herein that inhibitors of immune checkpoints and CHI3L1 are synergistic. Accordingly, described herein are methods and compositions relating to combinatorial therapies for cancer, e.g., comprising an inhibitor of CHI3L1; and an inhibitor of an immune checkpoint protein. In some embodiments, the CHI3L1 inhibitor can be an antibody or antibody reagent as described herein.

Abstract: The methods and assays described herein relate to the diagnosis, prognosis, and treatment of subjects with emphysema, COPD, and/or cigarette-induced lung damage. In some embodiments, the methods and assays relate to subjects with a decreased level of NLRX1 expression. In some embodiments, the methods and assays relate to the administration of an agonist of NLRX1 and/or an inhibitor of MAVS.

Abstract: Described herein are methods and compositions relating to anti-Chi3L1 antibodies, antibody reagents, and antigen-binding fragments thereof which display superior properties, e.g., high sensitivity, high specificity, high binding affinity, neutralization activity ex vivo and in vivo (e.g., blocks Chi3L1-induced MAPK and AKT signaling). Methods of treatment, e.g., of treating cancer, obesity, and/or asthma by administering the compounds described herein are also provided.

Abstract: Described herein are methods, assays, and systems related to the prognosis, diagnosis, and treatment of Hermansky Pudlak Syndrome (HPS) and, e.g., pulmonary fibrosis in a subject. As described herein, subjects with HPS who have, will develop, or are most at risk or developing pulmonary fibrosis have elevated levels of CHI3L1. In some embodiments, the methods comprise administering an agonist of IL-13R?2 or an inhibitor of CRTH2 to the subject.

Abstract: Described herein are methods, assays, and systems related to the prognosis, diagnosis, and treatment of Hermansky Pudlak Syndrome (HPS) and, e.g., pulmonary fibrosis in a subject. As described herein, subjects with HPS who have, will develop, Cor are most at risk or developing pulmonary fibrosis have elevated levels of CHI3L1. In some embodiments, the methods comprise administering an agonist of IL-13R?2 or an inhibitor of CRTH2 to the subject.

Abstract: The methods and assays described herein relate to the diagnosis, prognosis, and treatment of subjects with emphysema, COPD, and/or cigarette-induced lung damage. In some embodiments, the methods and assays relate to subjects with a decreased level of NLRX1 expression. In some embodiments, the methods and assays relate to the administration of an agonist of NLRX1 and/or an inhibitor of MAVS.

Abstract: The technology described herein is directed to methods of treating, e.g., obesity and/or asthma which relate to the interacting roles of Chi3L1 and Sirt1 in controlling adipose tissue and respiratory health.

Abstract: Disclosed herein are compositions and methods for detecting nonalcoholic steatohepatitis (NASH) measuring CHI3L1 levels. In some embodiments, the methods described herein can distinguish NASH from nonalcoholic fatty liver disease. CHI3L1 levels can also be used to monitor treatment progress in patients having NASH. Also disclosed herein are compositions and methods for treating NASH by targeting CHI3L1.

Abstract: The present invention provides compositions and methods for the detection, treatment, and prevention of a kidney injury. The invention relates to the discovery that chitinase 3-like 1/Brp-39/YKL-40 serves as both a biomarker for the degree of kidney injury and a critical mediator of a reparative response in the kidney.

Abstract: The present invention includes compositions and methods for the treatment of inflammatory disease (e.g., asthma, COPD, inflammatory bowel disease, atopic dermatitis, atopy, allergy, allergic rhinitis, scleroderma, and the like), relating to inhibiting a chitinase-like molecule. The invention further includes methods to identify new compounds for the treatment of inflammatory disease, including, but not limited to, asthma, COPD and the like. This is because the present invention demonstrates, for the first time, that expression of IL-13, and of a chitinase-like molecule, mediates and/or is associated with inflammatory disease and that inhibiting the chitinase-like molecule treats and even prevents, the disease. Thus, the invention relates to the novel discovery that inhibiting a chitinase-like molecule treats and prevents an inflammatory disease.

Abstract: The present invention provides methods of treating a subject diagnosed with, or at risk for developing, pathogenic fibrosis, particularly pulmonary fibrosis. The method of the invention comprises administering to the subject a compound or composition which inhibits semaphorin (SEMA) 7A, SEMA 7A receptors, or downstream effectors. A SEMA 7A inhibitor comprises an antibody, a soluble SEMA 7A receptor, an siRNA, a ribozyme, an antisense, an aptamer, a peptidomimetic, a small molecule, a soluble receptor, or any combinations thereof.

Abstract: The invention includes methods of treating oxidant-mediated acute lung injury in a subject by administration of a chitinase-like protein molecule, or an activator thereof. The invention also includes methods of assessing the level of a chitinase-like protein molecule in a subject as a marker of the prognosis of a subject suffering from acute lung injury.

Abstract: The present invention includes compositions and methods for the treatment of inflammatory disease (e.g., asthma, COPD, inflammatory bowel disease, atopic dermatitis, atopy, allergy, allergic rhinitis, scleroderma, and the like), relating to inhibiting a chitinase-like molecule. The invention further includes methods to identify new compounds for the treatment of inflammatory disease, including, but not limited to, asthma, COPD and the like. This is because the present invention demonstrates, for the first time, that expression of IL-13, and of a chitinase-like molecule, mediates and/or is associated with inflammatory disease and that inhibiting the chitinase-like molecule treats and even prevents, the disease. Thus, the invention relates to the novel discovery that inhibiting a chitinase-like molecule treats and prevents an inflammatory disease.

Abstract: The present invention provides compositions and methods for the detection, treatment, and prevention of a kidney injury. The invention relates to the discovery that chitinase 3-like 1/Brp-39/YKL-40 serves as both a biomarker for the degree of kidney injury and a critical mediator of a reparative response in the kidney.

Abstract: The present invention includes compositions and methods for the treatment of Th1 and/or Th2 mediated inflammatory diseases, relating to inhibiting CCR5. This is because the present invention demonstrates, for the first time, that expression of IFN-?, IL-13, and CCR5, mediates and/or is associated with Th1 and/or Th2 inflammatory diseases and that inhibiting CCR5 treats, and even prevents, the diseases. Thus, the invention relates to the novel discovery that inhibiting CCR5 treats and prevents Th1 and/or Th2 mediated inflammatory disease.

Abstract: The present invention provides a method for the treatment or prophylaxis of T-helper type 2 (Th2)-mediated disorders using antagonists of IL-11.

Abstract: The present invention includes compositions and methods for the treatment of Th1 and/or Th2 mediated inflammatory diseases, relating to inhibiting CCR5. This is because the present invention demonstrates, for the first time, that expression of IFN-?, IL-13, and CCR5, mediates and/or is associated with Th1 and/or Th2 inflammatory diseases and that inhibiting CCR5 treats, and even prevents, the diseases. Thus, the invention relates to the novel discovery that inhibiting CCR5 treats and prevents Th1 and/or Th2 mediated inflammatory disease.

Abstract: An apparatus includes first and second input terminals configured to be coupled to one of multiple types of input sources. The apparatus also includes a diode and a resistor coupled in series between the first and second input terminals. The apparatus further includes a plurality of switches each coupled to at least one of the diode and the resistor. The switches are configured to be opened and closed to reconfigure the apparatus depending on the type of input source. The switches could include a first switch coupled to the first input terminal, a current source, and a first side of the diode. The switches could also include a second switch coupled to the current source, a second side of the diode, and a first side of the resistor. In addition, the switches could include a third switch coupled to the second input terminal and a second side of the resistor.

Abstract: The present invention encompasses compositions and compounds as well as methods of their use for the regulation of a VEGF-induced tissue response. A VEGF-induced tissue response may include angiogenesis, inflammation, increased vascular permeability, increased vascular leak, hemorrhage, or mucus metaplasia. As such, the present invention encompasses methods of treating diseases where a VEGF-induced tissue response is part of the disease's clinical presentation. Specifically, the present invention provides compounds and compositions as well as methods for treating acute lung injury (ALI), acute respiratory distress syndrome (ARDS), asthma, chronic obstructive pulmonary disease (COPD), obstructive sleep apnea (OSA), idiopathic pulmonary fibrosis (IPF), tuberculosis, pulmonary hypertension, pleural effusion, and lung cancer.

Abstract: The present invention is based on the discovery that a single nucleotide polymorphism (SNP) present the chitinase 3-like 1 gene (CHI3L1) encoding YKL-40 or a regulatory domain of the CHI3L1 gene, is associated with elevated YKL-40 levels, as well as an increased risk for developing a lung disorder, including asthma, bronchial hyperresponsivity, and/or reduced lung function.