Effect of Live-Fire Training Drills on Firefighters’ Platelet Number and Function

2011 ◽  
Vol 15 (2) ◽  
pp. 233-239 ◽  
Author(s):  
Denise L. Smith ◽  
Steven J. Petruzzello ◽  
Eric Goldstein ◽  
Uzma Ahmad ◽  
Krishnarao Tangella ◽  
...  
Keyword(s):  
1982 ◽  
Vol 48 (01) ◽  
pp. 108-111 ◽  
Author(s):  
Elisabetta Dejana ◽  
Silvia Villa ◽  
Giovanni de Gaetano

SummaryThe tail bleeding time (BT) in rats definitely varies according to the method applied. Of the various variables that may influence BT, we have evaluated the position (horizontal or vertical) of the tail, the environment (air or saline), the temperature (4°, 23° or 37° C) and the type of anaesthesia. Transection of the tail tip cannot be used to screen drugs active on platelet function since it is sensitive to coagulation defects. Template BT in contrast is not modified by heparin and is sensitive to defects of platelet number and function (“storage pool disease”, dipyridamole-like drugs, exogenous prostacyclin). In contrast the test fails to detect aspirin-induced platelet dysfunction. The evidence reported indicates that thromboxane A2-prostacyclin balance is not a factor regulating BT. Aspirin treatment however may be a precipitating factor when associated with other abnormalities of platelet function.Template BT is a valid screening test for platelet disorders and for antiplatelet drugs.


1983 ◽  
Vol 19 (11) ◽  
pp. 1593-1599 ◽  
Author(s):  
Tiziano Barbui ◽  
Sergio Cortelazzo ◽  
Piera Viero ◽  
Renato Bassan ◽  
Enrico Dini ◽  
...  

1989 ◽  
Vol 61 (01) ◽  
pp. 117-121 ◽  
Author(s):  
Chris van Geet ◽  
Didier Hauglustaine ◽  
Luc Verresen ◽  
Marleen Vanrusselt ◽  
Jos Vermylen

SummaryRecombinant human erythropoietin was administered for up to 40 weeks to nine patients on chronic haemodialysis. From the third week of administration onwards, not only haemoglobin and haematocrit but also the platelet count rose, the latter, however, transiently. Subnormal platelet aggregation before therapy also improved transiently and in parallel with the erythropoietin dosage. The bleeding time normalized in almost all patients. There were no major side-effects. We conclude that recombinant erythropoietin improves haemostasis in chronic haemodialysis patients by increasing the haematocrit and in addition transiently enhances platelet number and function.


2011 ◽  
Vol 11 ◽  
pp. 1131-1137 ◽  
Author(s):  
Fabrizio Vianello ◽  
Anna Battisti ◽  
Giuseppe Cella ◽  
Marina Marchetti ◽  
Anna Falanga

Polycythemia vera (PV) and essential thrombocythemia (ET) are two Philadelphia-negative myeloproliferative neoplasms (MPN) associated with an acquired mutation in theJAK2tyrosine kinase gene. There is a rare incidence of progression to myelofibrosis and myeloid metaplasia in both disorders, which may or may not precede transformation to acute myeloid leukemia, but thrombosis is the main cause of morbidity and mortality. The pathophysiology of thrombosis in patients with MPN is complex. Traditionally, abnormalities of platelet number and function have been claimed as the main players, but increased dynamic interactions between platelets, leukocytes, and the endothelium do probably represent a fundamental interplay in generating a thrombophilic state. In addition, endothelial dysfunction, a well-known risk factor for vascular disease, may play a role in the thrombotic risk of patients with PV and ET. The identification of plasma markers translating the hemostatic imbalance in patients with PV and ET would be extremely helpful in order to define the subgroup of patients with a significant clinical risk of thrombosis.


2010 ◽  
pp. 4506-4518
Author(s):  
Kathryn E. Webert ◽  
John G. Kelton

Platelets are released from megakaryocytes in the bone marrow and circulate for 5 to 10 days before being cleared by the cells of the reticuloendothelial system. They play a critical role in haemostasis, with key features being (1) adhesion—when the wall of a blood vessel is damaged, platelets adhere to exposed collagen and other components of the subendothelium via the glycoprotein Ib receptor and other adhesive receptors; followed by (2) activation—release of thrombin, adenosine diphosphate, and arachidonic acid, which is converted by a cascade of enzymes into platelet activating agents including thromboxane A...


2019 ◽  
Vol 45 (07) ◽  
pp. 685-694 ◽  
Author(s):  
Andrew D. Mumford ◽  
Sarah K. Westbury

AbstractRecent advances in genetic analysis are bringing huge benefits to patients with rare genetic disorders, including those with inherited disorders of platelet number and function. Modern clinical hematological practice now has a range of genetic techniques available to enable the precision diagnosis of inherited platelet disorders (IPDs). There are some features of this disparate group of inherited disorders that present specific challenges to establishing an accurate genetic diagnosis. This review aims to introduce the techniques that are relevant for the genetic diagnosis of IPDs and will discuss the key considerations necessary for their application to the clinic.


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