Provided herein are method and kits for identifying thrombus origin based on temporal thrombin activity assay, and use thereof for optimizing post-ischemic event treatment, and further preventing recurrence of secondary ischemic events.

Provided herein are methods for the diagnosis, prognosis, and treatment of thrombosis in subject having or suspected of having systemic lupus erythematosus including determination of a level of platelet-bound complement C4d, C3 level, and one or both of a level of antiphosphatidyl serine/prothrombin complex and/or lupus anticoagulant.

Provided is a reagent for assaying a thrombin-antithrombin complex (TAT) in a blood sample from a subject by latex agglutination assay. The reagent includes a polycation. As a result, TAT complexes can be precisely assayed while circumventing the effect of heparin. The polycation is, for example, hexadimethrine bromide, chitosans, modified dextran, aminodextran, hydroxymethyl cellulose trimethylamine, lysozyme, spermine, spermidine, polylysine, polyarginine, polyornithine, protamine sulfate, hydroxyethyl cellulose trimethylamine, heparin-binding protein, polyallylamine, polyallylamine hydrochloride, poly(diallyl dialkyl amine), polyamideamine, polyamine, polyvinylbenzyltrimethylammonium chloride, polydiallyldimethylammonium chloride, polyethyleneimine, polypropyleneimine, polypropylethyleneimine, polyimidazoline, polyvinylamine, polyvinyl pyridine, poly(acrylamide/methacryloxypropyltrimethylammonium bromide), poly(diaryldimethylammonium chloride/N-isopropylacrylamide), poly(dimethylaminoethyl acrylate/acrylamide), poly(dimethylaminoethyl methacrylate), polydimethylaminoepichlorohydrin, polyethyleneiminoepichlorohydrin, polymethacryloxyethyl-trimethylammonium bromide, hydroxypropylmethacryloyloxyethyl dimethyl ammonium chloride, poly(methyldiethylaminoethylmethacrylate/acrylamide), poly(methyl/guanidine), polymethylvinylpyridinium bromide, poly(vinylpyrrolidone-dimethylaminoethyl methacrylate), or polyvinylmethylpyridinium bromide.

The invention relates to a method of determining the bleeding risk of a subject comprising: a. contacting a first sample from the subject with an activation mixture comprising (I) TIX-5, (II) factor Xa or an activation agent for activating directly or indirectly the conversion of factor X to factor Xa, and (III) a phospholipid mixture, b. determining the value of a coagulation function parameter of said sample, c. comparing the coagulation function parameter with a control value, d. determining the bleeding risk based on a comparison between the value of said coagulation function parameter of said first sample and said control value.

Specific single nucleotide polymorphisms (SNPs) in the human genome, and their association with deep vein thrombosis (DVT) and related pathologies, such as pulmonary embolism (PE), in relation with hormonal preparations (i.e. combined contraceptives, hormone replacement therapeutics) and hormone levels (i.e. during pregnancy and post-partum).

A fusion protein being a lipid-free reference standard having good long-term storability, which is used for measuring the quantity or quality of modified HDL, and a method for accurately, repeatability and reliably measuring high-density lipoprotein using the same. In the fusion protein, a complete protein sequence or partial fragment protein sequence for ApoA I is linked directly or via a spacer to a LOX-1 binding protein sequence that binds to a lectin-like oxidized LDL receptor: LOX-1. The method for measuring a modified high-density lipoprotein in a test sample is a method for measuring a modified high-density lipoprotein through binding of the modified high-density lipoprotein to LOX-1 and an anti-APOA I antibody, wherein, using the fusion protein as a reference standard for the modified high-density lipoprotein, the modified high-density lipoprotein in the test sample is determined by comparison with the reference standard through optical detection and/or radiation dosage detection.

The present invention provides an in vitro method for the assessment of functional protein S levels in a sample. The present invention also provides kits for use in the determination of functional protein S levels in a sample. Also provided is a method of treatment based on the determination of functional protein S levels, followed by administration of a therapeutic agent.

In some embodiments, the invention provides methods for detecting an aberrant fibrinolysis condition in a patient. The method includes subjecting a blood sample from the patient to a viscoelastic analysis in the presence of a known amount of a thrombolytic agent, to obtain a coagulation characteristic value of the patient; and comparing the coagulation characteristic value of the patient to a coagulation characteristic value of a healthy individual, the coagulation characteristic value of the healthy individual obtained by subjecting a blood sample from a healthy individual to the viscoelastic analysis in the presence of the known amount of the thrombolytic agent, wherein a difference in the coagulation characteristic value of the patient as compared to the coagulation characteristic value of the healthy individual identifies the patent as having aberrant fibrinolysis. In some embodiments, the invention also provides a container adapted for detecting an aberrant fibrinolysis condition in a blood sample using viscoelastic analysis comprising an interior having a coating comprising a thrombolytic agent.

The disclosure provides biomarker proteins, a change in the concentration or activity level of which are associated with atypical hemolytic uremic syndrome (aHUS) or clinically meaningful treatment of aHUS with a complement inhibitor. Also provided are compositions and methods for interrogating the concentration and/or activity of one or more of the biomarker proteins in a biological fluid. The compositions and methods are useful for, among other things, evaluating risk for developing aHUS, diagnosing aHUS, determining whether a subject is experiencing the first acute presentation of aHUS, monitoring progression or abatement of aHUS, and/or monitoring response to treatment with a complement inhibitor or optimizing such treatment.

The disclosure relates to methods for detecting PNH Type II cell populations in biological samples as well as methods for determining whether a patient is at an increased risk for developing thrombocytopenia or thrombosis based on the percentage of PNH Type II cells in the patient's blood. The disclosure also features reagents and conjugates for use in the methods.