Standardization of platelet function tests

Roper-Drewinko, Pamela R.; Drewinko, Benjamin; Corrigan, Gail; Johnston, Dennis A.; McCredie, Kenneth B.; Freireich, Emil J.

doi:10.1002/ajh.2830110210

Cited by 22 publications

(8 citation statements)

References 81 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In a recent study, 9 aggregation of platelet count‐adjusted PRP (250/nl) did not differ from native PRP (348/nl to 711/nl), but higher platelet concentrations (1258 × 10 3 to 1535/nl) increased the aggregation response. Conversely, LTA was shown to be correlated to the platelet count in adjusted samples below 200/nl 10,11 . These findings implicate platelet count as an important topic in aggregation studies.…”

Section: Discussionmentioning

confidence: 77%

THIS ARTICLE HAS BEEN RETRACTED: Whole‐blood aggregometry: are there any limits with regard to platelet counts?

Mengistu

Mayer

Boldt

et al. 2008

Acta Anaesthesiol Scand

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 77%

THIS ARTICLE HAS BEEN RETRACTED: Whole‐blood aggregometry: are there any limits with regard to platelet counts?

Mengistu

Mayer

Boldt

et al. 2008

Acta Anaesthesiol Scand

View full text Add to dashboard Cite

show abstract

“…These parameters are now readily available on many automated platelet particle counters. [209][210][211] With the current trend of using antiplatelet agents as prophylaxis for thrombotic events, modalities to assess the efficacy of antiplatelet therapy are needed; platelet indices and platelet size distributions may give a reasonable clinical indication of response to antiplatelet therapy. [212][213][214] As platelets become activated, there is release of platelet factor 4 (PF4), beta-thromboglobulin (BTG), and thromboxane A 2 and as platelets are consumed, subsequent to activation, large young platelets are anticipated in the peripheral blood.…”

Section: Hyperactive Prethrombotic Plateletsmentioning

confidence: 99%

Platelet Function Defects: A Clinical Review

Bick¹

1992

Semin Thromb Hemost

View full text Add to dashboard Cite

Platelet dysfunction, especially acquired forms, are common causes of hemorrhage, especially in association with trauma and surgery. Although the hereditary platelet function defects are generally quite rare, hereditary storage pool disease is common enough to be suspected in an individual, usually a child, with characteristic historical and clinical findings. The acquired platelet function defects, especially those resulting from drugs, are very common and should promptly be suspected in patients developing easy and spontaneous bruising, mild to moderate mucosal membrane hemorrhage, or unexplained bleeding associated with trauma or surgery. The template bleeding time is generally useful as a screening test of platelet function, but a normal template bleeding time, in the presence of a suggestive history, suggestive clinical findings, or in the patient frankly bleeding, is not reliable and platelet aggregation or lumi-aggregation should be done in appropriate clinical situations. The mainstay of therapy for essentially all these defects, if bleeding is significant, is the liberal infusion of appropriate numbers of platelet concentrates. The acquired platelet function defects, of course, should also be managed by attempts to treat or control the underlying disease, if possible, and offending drugs or potentially offending drugs should promptly be discontinued.

show abstract

“…CPT induces a reversible breakage of DNA in vivo (24,25) and in vitro (28). CPT is also reported to inhibit DNA synthesis in L5178Y and HeLa cells (38) and to be more cytotoxic to the cells in S phase than in G1 or G2 phase (39,40). In vitro studies have demonstrated that topoisomerase I is required for the elongation step of adenovirus DNA replication (41).…”

mentioning

confidence: 99%

Characterization of a mammalian mutant with a camptothecin-resistant DNA topoisomerase I.

Andoh¹,

Ishii²,

Suzuki³

et al. 1987

Proc. Natl. Acad. Sci. U.S.A.

246

110

View full text Add to dashboard Cite

DNA topoisomerase I was purified to near homogeneity from a clonal line of human lymphoblastic leukemia cells, RPMI 8402, that is resistant to camptothecin, a cytotoxic alkaloid from Camptotheca acuminata, and compared with that of the parent wild-type cells. As assayed by relaxation of the supercoiled plasmid DNA and by formation of enzymelinked DNA breaks, the purified enzyme from the resistant cells was shown to be >125-fold as resistant to camptothecin as the wild-type enzyme, comparable to a cellular resistance index of about 300. Therefore, the cellular resistance appears to be due to the resistance of the enzyme. The amount of the immunoreactive enzyme protein in whole extract appeared to be reduced to less than half that of the wild-type enzyme. These results establish that DNA topoisomerase I is the cellular target of camptothecin and that DNA topoisomerase I is essential for the survival of mammalian cells.The DNA topoisomerases are enzymes that catalyze the concerted breakage and rejoining of the DNA backbone and thereby are presumed to participate in various genetic processes (1-5). The type I topoisomerases transiently cut and reseal one DNA strand so that the linking number changes by steps of one. Genetic and functional studies of the enzymes have been largely limited to prokaryotes and the lower eukaryote yeast. Viable mutants ofEscherichia coli defective in the topA gene encoding topoisomerase I were isolated (6, 7), but these proved to have mutations in DNA gyrase genes that compensated for the mutation in topA (8-10). This finding suggested an essential role for the enzyme in regulating the degree of supercoiling of DNA by counteracting the activity of the type II enzyme. In contrast, however, topoisomerase I-deficient mutants of yeast were isolated and shown to be viable, although they possessed the wild-type allele of topoisomerase II (11,12). The effect of the topoisomerase I mutation, however, was manifested by an additional mutation in topoisomerase II, implicating the complementary role of the latter (12).Topoisomerase I was previously found associated with transcriptionally active chromatin in mammalian cells (13,14). It also appears to be catalytically active on transcriptionally active genes in Drosophila polytene chromosomes (15) as well as on nucleolus-associated ribosomal genes (16-19). These experiments suggest a functional role for the enzyme in transcriptional events involving either RNA polymerase I or II.The availability of mutants and specific inhibitors of this enzyme as was the case in prokaryotes might help dissect and establish the role of this enzyme in DNA metabolism. We previously reported that heparin is a potent inhibitor of a mammalian DNA topoisomerase I (20, 21), but its broad specificity limits its usefulness for this purpose. Camptothecin (CPT) is a cytotoxic alkaloid isolated from Camptotheca acuminata (22, 23), which has a strong antitumor activity against a wide range of experimental tumors. CPT inhibits RNA and DNA synthesis and causes rapid and rev...

show abstract

Standardization of platelet function tests

Cited by 22 publications

References 81 publications

THIS ARTICLE HAS BEEN RETRACTED: Whole‐blood aggregometry: are there any limits with regard to platelet counts?

THIS ARTICLE HAS BEEN RETRACTED: Whole‐blood aggregometry: are there any limits with regard to platelet counts?

Platelet Function Defects: A Clinical Review

Characterization of a mammalian mutant with a camptothecin-resistant DNA topoisomerase I.

Contact Info

Product

Resources

About