The present application is directed to the use of a VEGF-C inhibitor, a VEGFR-2 inhibitor and/or a VEGFR-3 inhibitor as a prophylactic or therapeutic for the treatment of eye disorders such as a maculopathy and pathogenic ocular neovascularisation. The application is also directed to the use of a VEGF-C measurement from a biological sample from a mammalian subject as a predictive marker, a selected marker, a responsive marker or a tracking marker for a disease or condition selected from the group consisting of a maculopathy and pathogenic ocular neovascularization.

The present subject matter provides compositions, formulations, and methods for inhibiting, treating, or preventing aberrant angiogenesis in a subject.

The present invention relates to a neovascular-targeting contrast medium composition and a method for preparing same. The neovascular-targeting contrast medium composition according to the present invention exhibits high binding force to neovascularization-associated α.sub.vβ.sub.3 integrin, excellent tissue permeability and biostability, enables simple measurement in vitro, in vivo, or ex vivo, and thus is effective in the detection of neovascularization and in diagnosing diseases associated therewith, and therefore may be usefully employed in the relevant industries.

The invention includes, in part, methods and compounds for diagnosing diseases and conditions characterized by altered threonyl-tRNA synthetase (TARS) activity, which include, but are not limited to diseases and conditions in which angiogenesis is altered. In some embodiments of the invention, a level of a TARS molecule is determined and compared to a control level of TARS to assess onset, progression, and/or regression of a disease or condition associated with altered TARS activity.

The invention includes, in part, methods and compounds for diagnosing diseases and conditions characterized by altered threonyl-tRNA synthetase (TARS) activity, which include, but are not limited to diseases and conditions in which angiogenesis is altered. In some embodiments of the invention, a level of a TARS molecule is determined and compared to a control level of TARS to assess onset, progression, and/or regression of a disease or condition associated with altered TARS activity.

Disclosed are an α.sub.vβ.sub.3 integrin targeting single-domain antibody and various applications thereof. The α.sub.vβ.sub.3 integrin targeting single-domain antibody exhibits high binding ability to α.sub.vβ.sub.3 integrin related to angiogenesis, excellent tissue permeability, and biostability compared to conventional antibodies. Further, the single-domain antibody may be combined with fluorescent particles and thus may be easily measured in vitro, in vivo or ex vivo, and may be effective in detecting angiogenesis and diagnosing angiogenesis related diseases, therefore it may be usefully used in related industries.

The present disclosure relates to antibodies, for example monoclonal antibodies, and their use in clinical patient evaluation and therapy. The present disclosure further relates to a method for modulating the activity of human CXCL-1 protein (hereinafter, referred to as CXCL1). In an aspect, antibodies described herein are capable of being used as a medicament for the prevention and/or treatment of diseases involving CXCL1 function, for example, pathological angiogenesis and inflammatory diseases.

The present subject matter provides compositions, formulations, and methods for inhibiting, treating, or preventing aberrant angiogenesis in a subject.

The invention includes, in part, methods and compounds for treating diseases and conditions characterized by elevated threonyl-tRNA synthetase (TARS) activity, which include, but are not limited to diseases and conditions in which angiogenesis is elevated as compared to normal. In some embodiments of the invention, a level of a TARS molecule is determined and compared to a control level of TARS to assess a treatment for a disease or condition characterized by elevated TARS activity.

Detection of under-expression of selected genes in NK cells is used to confirm a hypoxic tumor microenvironment that is ordinarily suppressive with respect to ADCC and cytotoxic cell killing of NK cells. Most notably, while hypoxia is known to upregulate HIF-1α and genes under the control of HIF-1α, hypoxia in a tumor microenvironment led to under-expression of selected genes, including HIF-1α. Thus, gene expression analysis of certain genes on NK cells can be used to detect conditions in a tumor that would indicate use of haNK cells.