Apo A-I binding to platelets detected by flow cytometry.

Lipoprotein-platelet interactions are very important in atherosclerosis and thrombosis. Several studies have been carried out on specific binding of various lipoproteins to platelets. But there is considerable disagreement about the details of these binding sites.

The importance of Lp(a)-fibronectin interaction in atherogenesis.

An elevated concentration of lipoprotein (a) (Lp(a)) in serum has been considered a risk factor for coronary heart disease by various investigators. The apo(a) portion of Lp(a) binds to the carboxyterminal heparin binding domain of fibronectin. Lp(a) bound to fibronectin is internalized through the fibronectin receptor pathway and thereby causes increased accumulation of lipid and foam cell formation.

Effect of defibrotide on platelet function.

Defibrotide, a polydeoxyribonucleotide, has been found to modulate endothelial cell function, causing an increase in tissue plasminogen activator (t-PA) levels, a decrease in plasminogen activator inhibitor (PAI) levels, and an increase in prostaglandin I2 (PGI2) formation in humans. Defibrotide has no direct anticoagulant effect but has a synergistic action with heparin. A strong antithrombotic effect has been observed in animal models.

Persistent vacuoles in leukocytes: familial Jordans anomaly.

Multiple persistent vacuoles were seen in the neutrophils, monocytes and eosinophils of a 9 year old boy and his 10 year old sister. The siblings were both asymptomatic. In the bone marrow, the cytoplasmic vacuoles were also present in the promyelocytes, myelocytes and metamyelocytes, but not in the myeloblasts and they tended to be single and large in immature cells.

The effect of endothelin-1 on vena jugularis thrombus model in rabbits.

Endothelins (ET) are the most important vasoconstrictors known, and administration results in contraction of vascular strips in man and experimental animals in vitro. We examined the effects of ET-1 on thrombus formation in rabbits. We used vasoconstrictor and thrombus forming agents and we selected an animal model, the vena jugularis thrombus model.

The pharmacology and clinical pharmacology of defibrotide: a new profibrinolytic, antithrombotic and anti-platelet substance.

Defibrotide, a deoxypolyribonuclide, has been found to modulate endothelial cell function causing increase in t-PA and decrease in PAI levels and also increase in PGI2 production. In addition, it increases platelet c-AMP levels and decreases MDA and TXB2 formation in human. Defibrotide inhibits platelet aggregate formation in vitro experiments as well as end-to-end anostomosis in rats.

Clinical pharmacology and mode of action of a new antithrombotic compound: Defibrotide.

Defibrotide is a derivative of polydeoxyribonucleotide extracted from bovine lung. Defibrotide has been found to modulate endothelial cell function causing increase in t-PA production and release with correction the defect in Cuff test in vascular disorders. Defibrotide causes a significant elevation in the PGI2 formation.

Alteration of platelet glucose transport system in atherosclerosis.

Functional and biochemical alterations of platelets in patients suffering from atherosclerosis were studied in our laboratory. One of the most striking alterations observed is in the platelet active glucose transport system. The Na+/K+ gradient dependent active transport system of glucose is found to be absent in the platelets of atherosclerotics.

Effect of defibrotide in electrically induced thrombosis in dogs.

Thrombi were electrically induced in dogs. The alterations of the vessel wall were studied in samples obtained on the 8th day from control and treated animals. Changes in coagulation parameters were monitored daily.

Effects of defibrotide on peripheral obliterative vascular diseases.

Twenty-nine patients with atherosclerotic obliterative vascular disorder and 9 cases of Buerger's disease were treated with 600 mg defibrotide daily for 10 days and then three times weekly for 3 months. The response to therapy was evaluated from hemostatic parameters, venostasis test (cuff test), treadmill testing, and radionuclide arteriography. We observed increased pain-free intervals in daily life and during treadmill testing.

Alteration of prostanoids in atherosclerosis.

We have briefly summarized only the data obtained in our own laboratory without including an extensive literature review. We have evaluated the changes in platelet membrane phospholipids and prostanoid formation in platelets. In atherosclerosis platelets show an activated prostanoid formation, whereas the plasma PGI2 levels are decreased.

Palmitic acid transport in platelets of normal subjects and of patients with liver cirrhosis.

Bovine serum albumin bound 14C-palmitic acid (BSA-14C-PA) is transported into platelets of normal and cirrhotic subjects by simple diffusion. Initial uptake increases linearly with the concentration of BSA-14C-PA in the medium. The time course accumulation of BSA-14C-PA is found to be higher in the platelets of patients with cirrhosis compared to that of normals.