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Infarct maturation

Fig.4.3a-f. The phenomenon of infarct maturation is shown as macroscopic appearance on hematoxylin-eosin stained coronal brain sections. Right permanent middle cerebral artery occlusion was performed in rats and histology obtained between 3 h and 7 days. Note the sparse changes at 3 h and lesion shrinkage at 7 days. [Reproduced with permission from Garcia et al. (1993)]... [Pg.45]

The GP Ilb-IIIa complex inhibitor Tirofiban has been used as an adjunct to thrombolysis in a number of small case series reports." A small transcranial Doppler (TCD) study suggests that it reduces microembolization from unstable carotid plaque." In an open pilot smdy, Tirohban administered within 9 hours after stroke onset blocked the conversion of ischemic penumbra to mature infarction." A phase III study (SETIS) has started recruiting patients to investigate its efficacy versus aspirin within the 6-hour window. [Pg.102]

The transdifferentiation of HSCs into a mature hematopoietic fate (e.g., endothelium) in the heart is less controversial [148]. In animal models of stem cell therapy in ischemic heart disease, the evidence points toward increased neovascularization (with reduced myocardial ischemia) and consequent improvement in cardiac function [149-151]. Bone marrow stem cells may directly contribute to an increase in contractility or, more likely, may passively limit infarct expansion and remodeling. Unfortunately, the limitations of the present animal models leave this question unanswered. [Pg.118]

Alemtuzumab is a recombinant DNA-derived humanized monoclonal antibody used in the treatment of chronic lymphocytic leukemia and T-cell lymphoma. It targets CD52, a protein present on the surface of mature lymphocytes. Alemtuzumab has been associated with infusion-related events including hypotension, rigors, fever, shortness of breath, bron-chospasm, chills, and/or rash. Also reported were syncope, pulmonary infiltrates, cardiac arrhythmias, myocardial infarction and cardiac arrest. [Pg.461]

Urate infarcts in the neonatal kidney and increased amounts of uric acid crystals in a newborn s urine are well known normal findings to neonatalogists. We were therefore prompted to undertake this study to investigate the normal excretion by the kidney of the newborn of uric acid and the progressive maturation of this function during the first year of life. [Pg.368]


See other pages where Infarct maturation is mentioned: [Pg.41]    [Pg.42]    [Pg.43]    [Pg.43]    [Pg.45]    [Pg.54]    [Pg.55]    [Pg.36]    [Pg.6]    [Pg.41]    [Pg.42]    [Pg.43]    [Pg.43]    [Pg.45]    [Pg.54]    [Pg.55]    [Pg.36]    [Pg.6]    [Pg.200]    [Pg.348]    [Pg.383]    [Pg.720]    [Pg.405]    [Pg.63]    [Pg.88]    [Pg.163]    [Pg.286]    [Pg.79]    [Pg.160]    [Pg.160]    [Pg.90]    [Pg.260]    [Pg.42]    [Pg.56]    [Pg.244]    [Pg.594]    [Pg.642]    [Pg.168]    [Pg.203]    [Pg.191]    [Pg.346]    [Pg.468]    [Pg.523]    [Pg.684]    [Pg.692]    [Pg.694]    [Pg.694]   
See also in sourсe #XX -- [ Pg.42 , Pg.43 , Pg.54 , Pg.55 ]




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