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Of cerebral tissue

Griffin, J.L. and Corcoran, O., High-resolution magic-angle spinning 13C NMR spectroscopy of cerebral tissue, Magn. Reson. Mater. Phys. Biol. Med., 18,1352, 2005. [Pg.198]

The TET-induced inhibitory influence on cyclic 3 ,5 -AMP phosphodiesterase (PDE) activities precedes edema formation in the rat brain [74]. lb clarify the mechanism of the protective action of EGb against TET-toxidty in rats, in vitro and ex vivo effects of EGb on PDE activities of cerebral tissue were investigated [75]. Higher concentrations of EGb (5-250 mg/L) inhibited the PDE activity in the brain in normal rats, whereas lower concentrations (0.25-4.0 mg/L) of EGb enhanced the activity of the enzyme. The inhbitory effect of TET on the high affinity PDE activity (measured with 0.25 ftM cyclic AMP) of the brain was diminished in the presence of low EGb concentrations. Furthermore, preventive and curative treatment of 1 El-poisoned rats with EGb (100 mg/kg, p.o., for 7 days) prevented both the formation of edema and the fall of PDE activity induced by TET alone. These results suggested the antiedema action of EGb might be partly associated with its modulating influences on cellular cyclic AMP levels via activation of membrane-bound PDE. [Pg.174]

Dijkhuizen RM, Knollema S, van der Worp HB, Ter Horst GJ, De Wildt DJ, Berkelbach van der Sprenkel JW, Tulleken KA, Nicolay K (1998) Dynamics of cerebral tissue injury and perfusion after temporary hypoxia-ischemia in the rat evidence for region-specific sensitivity and delayed damage. Stroke 29 695-704... [Pg.146]

Primary cultures of astrocytes are made from newborn rat cerebral cortex according to Dehouck et al. (1990). The meninges is cleaned off and the brain tissue is forced gently through a nylon sieve. DMEM supplemented with 10 % fetal calf serum, 2 mM glutamine, and 50 pg/ml of gentamicin is used for the dissociation of cerebral tissue and development of astrocytes. [Pg.526]

On a similar level, Z. X. Jiang et al. presented a device that allowed noninvasive measurement of cerebral tissue oxygenation to be performed [30]. Again based on fiber optics,... [Pg.148]

Z. X. Jiang et al., Novel NIR Instrument for Non-Invasive Monitoring and Quantification of Cerebral Tissue Oxygenation, paper 44, Proc. SPIE, 3257 (Photonics West), San Francisco, January, 1998. [Pg.173]

Studies of Cerebral Tissue Oxygenation and Related Autoregulation... [Pg.298]

With MRI, there is often a volume mismatch between tissue showing reduced water molecule diffusion (a signature for cell swelling and ischemic tissue) and a larger area of compromised tissue perfusion early after stroke onset - the so-called diffusion/perfusion mismatch. The difference, at least for all practical purposes, is believed to reflect the ischemic penumbra [138, 148-151]. Perfusion MRI currently affords a relative, rather than absolute, quantitative measure of cerebral tissue perfusion. Many studies have shown that the MRI-documented mismatch volume shrinks over time. However, mismatch may persist, for example those who present beyond 3 h and still have substantial mismatch [152], suggesting a longer window of therapeutic opportunity in select patients. [Pg.11]

Metabolic regulators of cerebral tissue PtO are complex and involve both vascular and metabolic adaptations. For the brain, the pattern of adaptation includes sequential responses that raise brain PtO (Xu and LaManna, 2006). The initial response is to increase blood flow, followed by an increase in hematocrit and then microvessel density as a result of angiogenesis (vascular adaptations) (Brown et al., 1985 Beck and Krieglstein, 1987 LaManna et al., 1992 LaManna and Harik, 1997 Dunn et al., 2000 LaManna et al., 2004)... [Pg.18]

The brain was fixed in situ by perfusion with 10% buffered formalin and removed 1 week later. After weighing, thin pieces of cerebral tissue (0.5mm or less in thickness) were taken from certain regions of the frontal lobes and fixed again in 10% buffered formalin for 24 hours. Specimens were subsequently embedded in celloidin. All sections were stained with fast cresyl violet and Weil s methods for myelin. Blocks from similar areas were treated with Golgi s silver impregnation. [Pg.250]

The oxygen transporting capacity of SNO-PEG-Hb was evaluated using a hemorrhagic shock model in rats by monitoring the redox state of cytochrome oxidase reduction of cerebral tissues, in which a near-infrared spectroscopy... [Pg.210]

On the other hand, aluminum staining was absent in cytoplasmic clearings themselves which were devoid of the neurofibrillaiy material. Interestingly, some of the neurons which demonstrated aluminum in the cytoplasm also showed positive blue staining of the nucleolus (p. 190). Galle et al. used an electron microprobe to examine for aluminum in their sections of cerebral tissue from aluminum-treated rats. They observed aluminum in lysosomes and lipofuscin granules containing crystals. Aluminum was not observed in any other part of the brain. [Pg.245]

The role of sialic acid residues in the brain tissue was illustrated by the restoration of excitability to applied electrical pulses of cerebral tissue that had lost its reactivity by exposure to cold. This restoration was obtained by addition of sialic-acid-containing glycoproteins or gangliosides (Mcllwain, 1960). [Pg.224]

Evans, W. H., and Mcllwain, H., 1%7, Excitability and ion content of cerebral tissues treated with alkylating agents, tetanus toxin, or a neuraminidase, J. Neurochem. 14 35-44. [Pg.345]


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