Mechanically bone fragments

Blood platelets are key players in the blood-clotting mechanism. These tiny fragments of cytoplasm are shed into the circulation from the surface of megakaryocytes located in the bone marrow. When the lining of a blood vessel is injured, activated platelets release clotting factors, adhere to each other and to damaged surfaces, and send out numerous filopodia. The shape changes that occur in activated platelets are the result of actin polymerization. Before activation, there are no microfilaments because profilin binds to G-actin and prevents its polymerization. After activation, profilin dissociates from G-actin, and bundles and networks of F-actin filaments rapidly appear within the platelet. 

Bone tissue has a rather unique capability among human tissues in response to injury or other changes that alter its mechanical requirements it can continuously remodel itself to meet those mechanical needs best [51, 52], For example, when a bone fractures, the body creates new bone to connect the broken fragments together, and then remodels the new bone to optimize its mechanical function in the particular region of the skeleton that the fracture has occurred. Human skeletal tissue has several functions, but, when a bone is fractured by trauma, or removed surgically due to disease or tumor formation, we only seek solutions so that its mechanical function can be carried out [53, 54],... 

Pyrolysis of acetylene to a mixture of aromatic hydrocarbons has been the subject of many studies, commencing with the work of Berthelot in 1866 (1866a, 1866b). The proposed mechanisms have ranged from formation of CH fragments by fission of acetylene (Bone and Coward, 1908) to free-radical chain reactions initiated by excitation of acetylene to its lowest-lying triplet state (Palmer and Dormisch, 1964 Palmer et al., 1966) and polymerization of monomeric or dimeric acetylene biradicals (Minkoff, 1959 see also Cullis et al., 1962). Photosensitized polymerization of acetylene and acetylene-d2 and isotopic analysis of the benzene produced indicated involvement of both free-radical and excited state mechanisms (Tsukuda and Shida, 1966). 

B-cell lymphopoiesis in mouse bone marrow has been shown to be inhibited by incubation with fluoranthene In vitro at concentrations of >5 ig/mL (25 pmol). This effect on B- cell precursors may be mediated in part by a stimulation of programmed cell death, as demonstrated by the increase in DNA fragmentation induced by fluoranthene 15-17 hours after addition to the incubation medium. Furthermore, fluoranthene-induced DNA fragmentation always preceded fluoranthene-induced B-cell precursor death. Another mechanism for fluoranthene-induced inhibition of B-cell lymphopoiesis may be alterations in cell growth rates (fluoranthene was shown to slow the rate of B-cell precursor growth at concentrations <5 ig/mL) and/or altered cell survival (Hinoshita et al. 1992). 

Nature provides different types of mechanisms to repair fractures in order to be able to cope with different mechanical environments about a fracture [Hulth, 1989 Schenk, 1992]. For example, incomplete fractures (cracks), which only allow micromotion between the fracture fragments, heal with a small amount of fracture-line callus, known as primary healing. In contrast, complete fractures which are unstable, and therefore generate macromotion, heal with a voluminous callus stemming from the sides of the bone, known as secondary healing [Brighton, 1984 Hulth, 1989]. 

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