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Platelets, deficiency

Moroi M, Jung SM, Okuma M, Shinmyozu K A patient with platelets deficient in glycoprotein VI that lack both collagen-induced aggregation and adhesion. J Clin Invest 84 1440-1445,1989... [Pg.92]

Weiss HJ, Turitto VT, Baumgartner HR Platdet adhesion and thrombus formation on subendotfadium in platelets deficient in glycoproteins Ilb-IHa, Ib, and storage granules. Blood 67 322-330,1986. [Pg.355]

The development of platelets or thrombocytes takes place chiefly in the bone marrow from primitive totipotential reticulum or stem cells. The normal concentration of thrombocytes in the peripheral circulation of the adult is approximately 250,000-355,000/mm . Thrombocyte activity is necessary in the process of coagulation. Quantitative platelet deficiency or thrombocytopenia is one of the most common causes of hemorrhagic diathesis, and it may be due either to decreased platelet production or to increased platelet destruction. [Pg.119]

As a stimulator of megakaryopoiesis, IL-12 may be of therapeutic benefit in patients with platelet deficiencies. Ex vivo expansion witli stem cell factor and IL-11 augments both short-term recovery posttransplant and tlie ability to transplant bone marrow seriaUy. ... [Pg.682]

A 2B 2M 2N Type 3 vWD Decreased platelet-dependent vWF function owing to lack of larger multime rs Increased platelet-dependent vWF function owing to lack of larger multime rs Defective platelet-dependent vWF functions not associated with multimer defects Defective vWF binding to factor VIII Severe quantitative deficiency of vWF 1 %-5% Autosomal recessive... [Pg.992]

Since erythrocytes, platelets, and leukocytes have received the greatest attention, the discussion that follows will be limited to these carriers. Fibroblasts [180] and hepatocytes [181] have been specifically used as viable sources to deliver missing enzymes in the management of enzyme-deficiency diseases, whereas islets are useful as a cellular transplant to produce insulin [182,183],... [Pg.562]

IL-6 participates in both atherogenesis and inflammatory processes. In one interesting mouse model that was double deficient at the apoE and IL-6 loci, animals displayed similar hypercholesterolemia compared to apoE-null mice, but disclosed larger and more calcified lesions at 1 year of age (Klinge 2001). Thus, IL-6 appears to be involved at the fibrous plaque stage of the atherosclerotic process. Moreover, IL-6 is a key factor in the generation of the hepatic acute-phase response and so increases the levels of CRP, fibrinogen, platelet... [Pg.231]

In sensitive individuals G-6-PDH activity of platelets was also found to be deficient (R7, W22). A reduced activity of saliva has been reported (R5). The results of these investigations led to the suggestion... [Pg.272]

R7. Ramot, B., Szeinberg, A., Adam. A., Sheba, C., and Gafni, D., A study of subjects with erythrocyte glucose-6-phosphate dehydrogenase deficiency Investigations of platelet enzymes. J. Clin. Invest. 38, 1659-1661 (1959). [Pg.305]

Further plaque enlargement with platelet and fibrin deposition causes severe reduction in blood flow and cells down stream become oxygen-deficient (hypoxia)... [Pg.166]

The von Willebrandt s factor plays a key role in thrombogenesis. Lack of this factor causes thrombasthenia, a pathologically decreased platelet aggregation. Relative deficiency of the von Wille-Liillmann, Color Atlas of Pharmacology... [Pg.148]

The 1960 s and 1970 s saw several other hypotheses proposed and dis-proven. The monoamine oxidase (MAO) deficiency hypothesis was based on the observation of diminished activity of platelet MAO-B in schizophrenia, although this was likely to be an artifact of drug treatment and the small deficits could not, in any case, account for changes in monoamine transmitters. Other hypotheses relating to, among other transmitter molecules, noradrenaline and enkephalin/endorphin have also been proposed. Each of these have had propo-... [Pg.281]


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See also in sourсe #XX -- [ Pg.26 ]




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