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Major discovery raises prospect of better patient care by improving platelet life span
March 23, 2007The research team led by Drs Benjamin Kile and David Huang has discovered that platelet life span is controlled by two key molecules. The discovery raises the prospect of developing a new drug to prolong the life span of platelets stored in blood banks, effectively increasing the availability of this life-saving blood product.
An undesirable side effect of cancer chemotherapy is extensive bruising and potentially life-threatening bleeding. This is caused by the unintended depletion of platelets, tiny circulating blood cells that are essential for blood clotting and wound healing. Consequently, the well being of some patients depends upon platelet transfusions, particularly during the vulnerable periods that follow anti-cancer treatment. The significant demand for high quality platelets, coupled with their short shelf life of only five days, presents major logistical challenges in clinical practice.
The scientific team has found that two specialised molecules act in opposition to each other to control platelet life span by regulating the process known as "apoptosis." This term refers to the normal and healthy self destruction of old, damaged and surplus cells. One protein (known as Bcl-xL) acts to preserve the life of the platelet, while the other protein (Bak) prepares the cell to self-destruct after its usual life span within the body-about a week.
WEHI's Dr David Huang said, "Apoptosis is an essential process, common in other cells, but the central role it plays in controlling the life span of the highly specialised platelet has not been previously appreciated. With this new knowledge, we are in a much stronger position to devise better therapies for the management of platelet-related diseases."
Dr Kile added, "For fifty years doctors have speculated about what controls platelet life span. We now know the identity of the precise molecular switch responsible. The team is now actively pursuing a drug development program aimed at manipulating this switch in order to prolong the life span of blood bank platelets, increasing their availability to patients receiving cancer treatment and others in danger of serious bleeding".
At the opposite end of the scale, shortening platelet life span may be useful in the treatment of other diseases. For instance, too many platelets can trigger dangerous blood clots leading to strokes or heart attacks. Reducing platelet life span may therefore prove valuable in the prevention and management of these life-threatening conditions.
Research Australia
WEHI's Dr David Huang said, "Apoptosis is an essential process, common in other cells, but the central role it plays in controlling the life span of the highly specialised platelet has not been previously appreciated. With this new knowledge, we are in a much stronger position to devise better therapies for the management of platelet-related diseases."
Dr Kile added, "For fifty years doctors have speculated about what controls platelet life span. We now know the identity of the precise molecular switch responsible. The team is now actively pursuing a drug development program aimed at manipulating this switch in order to prolong the life span of blood bank platelets, increasing their availability to patients receiving cancer treatment and others in danger of serious bleeding".
At the opposite end of the scale, shortening platelet life span may be useful in the treatment of other diseases. For instance, too many platelets can trigger dangerous blood clots leading to strokes or heart attacks. Reducing platelet life span may therefore prove valuable in the prevention and management of these life-threatening conditions.
Research Australia
Platelet Current Events and Platelet News RSSNew mechanism explains how the body prevents formation of blood vessels
Researchers at Uppsala University, in collaboration with colleagues in Sweden and abroad, have identified an entirely new mechanism by which a specific protein in the body inhibits formation of new blood vessels.
How to identify early graft dysfunction preoperatively?
Small-for-size graft dysfunction (SFSGD) following living-related liver transplantation (LRLT) is characterized by early graft dysfunction (EGD) when the graft-to-recipient body weight ratio (GRBWR) is below 0.8%.
Blood counts are clues to human disease
A new genome-wide association study published today in Nature Genetics begins to uncover the basis of genetic variations in eight blood measurements and the impact those variants can have on common human diseases.
Platelet-rich plasma: Does it work?
Platelet -rich plasma (PRP) is currently used as an alternative treatment method for several common orthopaedic-related sports medicine conditions.
Are the monoamines involved in shaping conduct disorders?
Antisocial and aggressive behaviours represent a widespread and expensive social problem. Recent research has convincingly shown that there is a strong interaction between genetic inheritance and environment for development of personality and behaviour.
Green tea component may help preserve stored platelets, tissues
In two separate studies, a major component in green tea, epigallocatechin-3-O-gallate (EGCG), has been found to help prolong the preservation of both stored blood platelets and cryopreserved skin tissues.
New research confirms potential deadly nature of emerging new monkey malaria species in humans
Researchers in Malaysia have identified key laboratory and clinical features of an emerging new form of malaria infection.
Otamixaban for the treatment of patients with non-ST-elevation acute coronary syndromes
Data from a phase II trial of an investigational intravenous drug designed to block the formation of blood clots shows potential to reduce the risk of death, a second heart attack, or other coronary complications compared with the current standard of care in patients presenting with acute coronary syndromes (heart attacks or unstable angina).
University of Maryland researchers identify gene variant linked to effectiveness of plavix
Researchers at the University of Maryland School of Medicine have identified a common gene variant carried by as many as a third of the general population that is believed to play a major role in determining why people do not respond to a popular anti-clotting medication, Plavix.
Genetic variation associated with poorer response, cardiovascular outcomes with use of clopidogrel
Patients with a certain genetic variation who received the antiplatelet drug clopidogrel had a decreased platelet response to treatment and among those who had percutaneous coronary intervention (procedures such as balloon angioplasty or stent placement used to open narrowed coronary arteries) had an increased risk of having a cardiovascular event in the following year than patients who did not have this variant, according to a study in the August 26 issue of JAMA.
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