A method for assaying a heparin-induced thrombocytopenia (HIT) in a patient's serum or plasma sample, the method comprising: incubating a mix of platelets with the patient's serum or plasma sample in the presence of either a low concentration of heparin or a high concentration of heparin; incubating a mix of platelets in the presence or absence of a platelet activator; quantifying platelets and activated platelets in the mixes; calculating percentage of activated platelets within the platelets for each of the mixes; calculating a heparin platelet activation (HEPLA) index using the calculated percentages; measuring and calculating HEPLA indices of serum or plasma samples from donors not suffering from HIT; calculating cut-off values from the HEPLA indices of serum or plasma samples from donors not suffering from HIT, and determining whether a patient suffers of HIT or not by comparing the HEPLA index of the patient with the cut-off values.

Disclosed are methods and systems for measuring serotonin in a sample using liquid chromatography and mass spectrometry.

A system and method are provided for harvesting target biological substances. The system includes a substrate and a first and second channel formed in the substrate. The channels longitudinally extending substantially parallel to each other. A series of gaps extend from the first channel to the second channel to create a fluid communication path passing between a series of columns with the columns being longitudinally separated by a predetermined separation distance. The system also includes a first source configured to selectively introduce into the first channel a first biological composition at a first channel flow rate and a second source configured to selectively introduce into the second channel a second biological composition at a second channel flow rate. The sources are configured to create a differential between the first and second channel flow rates to generate physiological shear rates along the second channel that are bounded within a predetermined range.

An integrative pharmacokinetic/pharmacodynamics (PK/PD) ESA-EpoR mathematical model calculates the binding behavior of erythropoiesis stimulating agents (ESA). The invention provides methods for the determining of ESA binding sites in cells or patients suffering from anemia. Knowing the amount of ESA binding sites enables the clinical practitioner to optimize the dosage regimen during a treatment of anemia, in particular in patients suffering from a cancerous disease. Further provided are methods for screening ESAs which have a higher specificity for cells strongly expressing the EPO receptor such as colony forming units-erythroid (CFU-E) cells, and not to cells with a low level of EPO receptor cell surface expression, which is the case in cancer cells. Also provided is a computer implemented method, comprising the use of the mathematical model of the invention.

The invention relates to a method for determining, diagnosis, prognosis, treatment guidance, treatment monitoring, risk assessment and/or risk stratification of patients with abnormal platelet levels comprising providing a sample of said patient, determining a level of proadrenomedullin (proADM) or fragment(s) thereof in said sample, wherein said level of proADM or fragment(s) thereof correlates with the abnormal platelet levels in said patient. In embodiments of the invention, a level of proADM or fragment(s) thereof of high severity indicates low platelet levels in the subject and subsequent initiating or modifying a treatment of the patient to improve said condition. In some embodiments of the invention the method comprises determining a level of one or more additional markers in a sample isolated from the patient, such as the level of platelets, the level of PCT or fragment(s) thereof, one or more markers of thrombocytopenia and/or one or more markers of an inflammatory response.

A system and method are provided for harvesting target biological substances. The system includes a substrate and a first and second channel formed in the substrate. The channels longitudinally extending substantially parallel to each other. A series of gaps extend from the first channel to the second channel to create a fluid communication path passing between a series of columns with the columns being longitudinally separated by a predetermined separation distance. The system also includes a first source configured to selectively introduce into the first channel a first biological composition at a first channel flow rate and a second source configured to selectively introduce into the second channel a second biological composition at a second channel flow rate. The sources are configured to create a differential between the first and second channel flow rates to generate physiological shear rates along the second channel that are bounded within a predetermined range.

Compositions and methods are provided for determining platelet reactivity where the levels of FcRIIa on the surface of platelets is measured and if the levels of FcRIIa are greater than a reference value, the platelets have enhanced reactivity.

Described herein are method(s), kit(s), reagent(s) and the like for determining von Willebrand factor (VWF) activity in a sample in the absence of ristocetin.

The present invention provides a humanized antibody or antibody fragment comprising (a) a humanized light chain comprising 1) Complementarity Determining Region (CDR)-L1, the sequence of which is identical to the sequence of SEQ ID NO: 3; 2) CDR-L2, the sequence of which is identical to the sequence of SEQ ID NO: 4; and 3) CDR-L3, the sequence of which is identical to the sequence of SEQ ID NO: 5, and (b) a humanized heavy chain comprising 1) CDR-H1, the sequence of which is identical to the sequence of SEQ ID NO: 6; 2) CDR-H2, the sequence of which is identical to the sequence of SEQ ID NO: 7; and 3) CDR-H3, the sequence of which is identical to the sequence of SEQ ID NO: 8, as well as methods for treating, diagnosing, and monitoring the progression of HIT. The present invention also provides methods for assessing the antigenicity and ability to cause HIT of anionic anticoagulants. The present invention also provides a mutant protein which has the same amino acid sequence of a wild type PF4 monomer except that (i) at least one amino acid of the wild type PF4 monomer has been deleted, (ii) at least one amino acid of the wild type PF4 monomer has been replaced by another amino acid, or (iii) a combination of such changes has been made. The present invention also provides methods of treating or reducing the likelihood of HIT, treating angiogenesis, treating abnormal cell growth, or affecting coagulation pathologies that lead to thrombus formation, by administering such mutant proteins to a patient.

The present invention relates to a method for diagnosing a predisposition of a living being to develop thrombocytopenia, and uses associated therewith.