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Download Translational Stroke Research: From Target Selection to by Sara Morales Palomares PhD, Marilyn J. Cipolla PhD (auth.), PDF

By Sara Morales Palomares PhD, Marilyn J. Cipolla PhD (auth.), Paul A. Lapchak, John H. Zhang (eds.)

This quantity units a foundation for potent translational examine. Authored via specialists within the box of translational stroke learn, each one bankruptcy in particular addresses a number of parts of preclinical stroke examine. The emphasis is put on objective identity and drug improvement utilizing state of the art in vitro and in vivo assays, together with in vitro toxicology assays, AMDE and scientific design.

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Extra resources for Translational Stroke Research: From Target Selection to Clinical Trials

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A) Myogenic tone development in MCA exposed to different periods of ischemia, all with 24 h of reperfusion: sham-operated control (n = 6) and 15 (n = 6), 30 (n = 7), and 120 min (n = 8) of ischemia. 01 vs. control. (b) F-actin content in the same arteries shown in ( a ). Average F-actin content determined by fluorescence intensity of each group of ischemic arteries. 01 vs. control. From Cipolla et al. [61] 1 a Vascular Targets for Ischemic Stroke Treatment b 50 Ischemic Contralateral 45 ** 25 20 ** ** ** Diameter (µm) % Tone 30 280 260 40 35 13 - 22 hrs.

It is likely that the mechanism by which ischemia affects the cerebral circulation is different from that of reperfusion. For example, during ischemia there is a loss of ATP [73] and upregulation of endothelial NOS (eNOS) and neuronal NOS (nNOS) activity that increases NO production within 10 min after focal ischemia and returns to normal at 60 min [79]. These events may explain why F-actin appears to be more susceptible to ischemic injury. However, during reperfusion other mechanisms are prominent, including production of superoxide and hydrogen peroxide, that also dilate cerebral vasculature by activating ATP-sensitive K+ (KATP) and large-conductance Ca2+-activated K+ (BK) channels, respectively [80].

6 ** 0 15 30 ** 45 60 75 90 105 120 135 Time of Ischemia (minutes) Fig. 5 The effect of ischemic duration of myogenic responses and filamentous (F-) actin content of MCA. (a) Myogenic tone development in MCA exposed to different periods of ischemia, all with 24 h of reperfusion: sham-operated control (n = 6) and 15 (n = 6), 30 (n = 7), and 120 min (n = 8) of ischemia. 01 vs. control. (b) F-actin content in the same arteries shown in ( a ). Average F-actin content determined by fluorescence intensity of each group of ischemic arteries.

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