Platelets, also called thrombocytes (from Greek θρÏŒμβος, "clot" and κύτος, "cell"), are a component of blood whose function (along with the coagulation factors) is to react to bleeding from blood vessel injury by clumping, thereby initiating a blood clot. Platelets have no cell nucleus; they are fragments of cytoplasm that are derived from the megakaryocytes of the bone marrow, which then enter the circulation. Circulating unactivated platelets are biconvex discoid (lens-shaped) structures, 2–3 µm in greatest diameter. Activated platelets have cell membrane projections covering their surface. Platelets are found only in mammals, whereas in other vertebrates (e.g. birds, amphibians), thrombocytes circulate as intact mononuclear cells.

The ligands, denoted by letter L, signal for platelets (P) to migrate towards the wound (Site A). As more platelets gather around the opening, they produce more ligands to amplify the response. The platelets congregate around the wound in order to create a cap to stop blood flow out of the tissue.

On a stained blood smear, platelets appear as dark purple spots, about 20% the diameter of red blood cells. The smear is used to examine platelets for size, shape, qualitative number, and clumping. A healthy adult typically has 10 to 20 times more red blood cells than platelets. One major function of platelets is to contribute to hemostasis: the process of stopping bleeding at the site of interrupted endothelium. They gather at the site and, unless the interruption is physically too large, they plug the hole. First, platelets attach to substances outside the interrupted endothelium: adhesion. Second, they change shape, turn on receptors and secrete chemical messengers: activation.

The blood tests will come from a huge gathering of individuals who recently took part in the Johns Hopkins GeneSTAR study, a hereditary exploration drive with a data set of 4,000 individuals who have relatives with early coronary illness. That review, which was the biggest platelet work concentrate on the planet, revealed a significant hereditary area identified with platelet work and the impact of anti-inflamatory medicine on blood coagulating.

"From GeneSTAR, we definitely realize that these people have acquired hereditary variations that influence their platelet work. We will request some from them to return to give a little blood test to assist us with this new examination," says Diane Becker, Sc.D, M.P.H, teacher of medication and overseer of the GeneSTAR hereditary exploration program in the Division of General Internal Medicine, who is likewise a specialist on the investigation.

The five-year study is one of nine new undeveloped cell projects financed by the NIH to look at how quality variations cause sickness. "These examinations will enlighten how explicit qualities carry on in various tissues and ought to explain the components by which a quality related with a sickness

influences the science of various tissues," says Susan B. Shurin, M.D., acting head of the NIH's National Heart, Lung and Blood Institute.