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001-es BibID:	BIBFORM033449
Első szerző:	Althausen, Sonja
Cím:	Changes in the phosphorylation of initiation factor eIF-2a,elongation factor eEF-2 and p70 S6 kinase after transient focal cerebral ischaemia in mice / Althausen S., Mengesdorf T., Mies G., Oláh L., Nairn A. C., Proud C. G., Paschen W.
Dátum:	2001
Megjegyzések:	Mice were subjected to 60 min occlusion of the left middle cerebral artery (MCA) followed by 1-6 h of reperfusion. Tissue samples were taken from the MCA territory of both hemispheres to analyse ischaemia-induced changes in the phosphorylation of the initiation factor eIF-2alpha, the elongation factor eEF-2 and p70 S6 kinase by western blot analysis. Tissue sections from additional animals were taken to evaluate ischaemia-induced changes in global protein synthesis by autoradiography and changes in eIF-2alpha phosphorylation by immunohistochemistry. Transient MCA occlusion induced a persistent suppression of protein synthesis. Phosphorylation of eIF-2alpha was slightly increased during ischaemia, it was markedly up-regulated after 1 h of reperfusion and it normalized after 6 h of recirculation despite ongoing suppression of protein synthesis. Similar changes in eIF-2alpha phosphorylation were induced in primary neuronal cell cultures by blocking of endoplasmic reticulum (ER) calcium pump, suggesting that disturbances of ER calcium homeostasis may play a role in ischaemia-induced changes in eIF-2alpha phosphorylation. Dephosphorylation of eIF-2alpha was not paralleled by a rise in levels of p67, a glycoprotein that protects eIF-2alpha from phosphorylation, even in the presence of active eIF-2alpha kinase. Phosphorylation of eEF-2 rose moderately during ischaemia, but returned to control levels after 1 h of reperfusion and declined markedly below control levels after 3 and 6 h of recirculation. In contrast to the only short-lasting phosphorylation of eIF-2a and eEF-2, transient focal ischaemia induced a long-lasting dephosphorylation of p70 S6 kinase. The results suggest that blocking of elongation does not play a major role in suppression of protein synthesis induced by transient focal cerebral ischaemia. Investigating the factors involved in ischaemia-induced suppression of the initiation step of protein synthesis and identifying the underlying mechanisms may help to further elucidate those disturbances directly related to the pathological process triggered by transient cerebral ischaemia and leading to neuronal cell injury.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Journal of Neurochemistry. - 78 : 4 (2001), p. 779-787. -
További szerzők:	Mengesdorf, Thorsten Mies, Günter Oláh László (1967-) (neurológus) Nairn, Angus C. Proud, Christopher G. Paschen, Wulf
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001-es BibID:	BIBFORM033457
Első szerző:	Mengesdorf, Thorsten
Cím:	Phosphorylation State, Solubility, and Activity of Calcium/Calmodulin-Dependent Protein Kinase IIa in Transient Focal Ischemia in Mouse Brain / Thorsten Mengesdorf, Sonja Althausen, Günter Mies, Laszlo Oláh, Wulf Paschen
Dátum:	2002
ISSN:	0364-3190
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Neurochemical Research. - 27 : 6 (2002), p. 477-484. -
További szerzők:	Althausen, Sonja Mies, Günter Oláh László (1967-) (neurológus) Paschen, Wulf
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001-es BibID:	BIBFORM033463
Első szerző:	Paschen, Wulf
Cím:	Effect of transient focal ischemia of mouse brain on energy state and NAD levels : no evidence that NAD depletion plays a major role in secondary disturbances of energy metabolism / Wulf Paschen, Laszlo Olah, Gunter Mies
Dátum:	2000
Megjegyzések:	It has been proposed that NAD depletion resulting from excessive activation of poly(ADP-ribose) polymerase is responsible for secondary energy failure after transient cerebral ischemia. However, this hypothesis has never been verified by measurement of ATP and NAD levels in the same tissue sample. In this study, we therefore investigated the effect of transient focal cerebral ischemia on the temporal profiles of changes in the levels of energy metabolites and NAD. Ischemia was induced in mice by occluding the left middle cerebral artery using the intraluminal filament technique. Animals were subjected to 1-h ischemia, followed by 0, 1, 3, 6, or 24 h of reperfusion. During ischemia, ATP levels, total adenylate pool, and adenylate energy charge dropped to approximately 20, 50, and 40% of control, respectively, whereas NAD levels remained close to control. Energy state recovered transiently, peaking at 3 h of recovery (ATP levels and total adenylate pool recovered to 78 and 81% of control). In animals subjected to reperfusion of varying duration, the extent of ATP depletion was clearly more pronounced than that of NAD. The results imply that depletion of NAD pools did not play a major role in secondary disturbances of energy-producing metabolism after transient focal cerebral ischemia. Changes in ATP levels were closely related to changes in total adenylate pool (p<0.001). The high energy charge after 6 h of reperfusion (0.90 versus a control value of 0.93) and the close relationship between the decline of ATP and total adenylate pool suggest that degradation or a washout of adenylates (owing to leaky membranes) rather than a mismatch between energy production and consumption is the main causative factor contributing to the secondary energy failure observed after prolonged recovery.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Journal of Neurochemistry. - 75 :4 (2000), p. 1675-1680. -
További szerzők:	Oláh László (1967-) (neurológus) Mies, Günter
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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