Abstract: A method for diagnosing a malignant proliferative disease or disorder in a subject, and/or for following up, monitoring or prognosticating the therapy of a malignant proliferative disease or disorder in a subject is disclosed. The method is based on measurement of platelet-mediated fibrinogen-like protein 2 (FGL2) activity in a sample essentially comprising platelets obtained from the subject. In accordance with the disclosed method, platelet-mediated FGL2 activity level higher than control is indicative of the presence of a malignant proliferative disease or disorder in a subject.

Abstract: The present invention reveals a strong correlation between FGL-2 prothrombinase activity levels and the presence of a malignant proliferative disorder in a subject. Thus, the present invention provides FGL-2 prothrombinase activity as a diagnostic tool for malignancy.

Abstract: The present: invention reveals a strong correlation between FGL-2 prothrombinase activity levels and the presence of a malignant proliferative disorder in a subject. Thus, the present invention provides FGL-2 prothrombinase activity as a diagnostic tool for malignancy.

Abstract: Subject of the present invention is the use of a Factor XIII-preparation preferably in injectable form for the treatment of diseases which are associated with disturbed blood perfusion of the tissue following transient or permanent ischemia.

Abstract: This invention combines the unique antiplatelet effects of S-nitrosothiols and the antiadhesive properties of fragments of von Willebrand (vWF) in the A1 domain to provide unique molecules that exploit both of these properties. Preferred molecules comprise a fragment of A1 (Ala 444-Asn 730) in which arginine at position 545 is replaced by cysteine (the most frequent von Willebrand disease type 2b mutation) that has been discovered to impair platelet adhesion, and to inhibit an antithrombotic activity in vivo. This cysteine residue may be S-nitrosated to produce a novel molecule that has the potential for impairing platelet adhesion as well as activation/aggregation, and such molecules form the basis of a novel therapeutic method for impairing platelet responses following vascular injury or in other thrombotic disorders according to this invention.

Abstract: This invention combines the unique antiplatelet effects of S-nitrosothiols and the antiadhesive properties of fragments of vWF in the A1 domain to provide unique molecules that exploit both of these properties. Preferred molecules comprise a fragment of A1 (ala444-asp73O) in which arginine at position 545 is replaced by cysteine (the most frequent von Willebrand disease type 2b mutation) that has been discovered to impair platelet adhesion, and to exhibit antithrombotic activity in vivo. This cysteine residue may be S-nitrosated to produce a novel molecule that has the potential for impairing platelet adhesion as well as activation/aggregation, and such molecules form the basis of a novel therapeutic method for impairing platelet responses following vascular injury or in other thrombotic disorders according to this invention.