4,059 research outputs found
Sulfhydryl oxidation: A potential strategy to achieve neuroprotection during severe hypoxia?
No full textPreviously we reported that sulfhydryl (SH) modulation affects the susceptibility of rat hippocampal slices to severe hypoxia. SH-oxidation by DTNB (5,5'-dithiobis 2-nitrobenzoic acid) or H2O2 postponed the onset of hypoxia-induced spreading depression (HSD), thereby delaying the loss of neuronal function, whereas SH-reduction by DTT (1,4-dithio-DL-threitol) hastened HSD onset. To judge the neuroprotective merit that might arise from a postponement of HSD by oxidants, we have extended our earlier observations by multiparametric recordings and screened for changes in the extracellular K+ accumulation, HSD propagation velocity, and its maximum spread. As parameters for neuronal network function, the failure of synapses during hypoxia and their posthypoxic recovery were analyzed. DTNB (2 mM) or H2O2 (5 mM) postponed HSD but did not attenuate the rise in extracellular K+ concentration ([K+](o)), HSD propagation velocity or its maximum spread. H2O2 slightly postponed the synaptic failure during hypoxia; the posthypoxic recovery of synapses was, however, incomplete. DTNB slowed the synaptic recovery upon reoxygenation. DTT (2 mM) hastened HSD onset, but HSD propagation velocity and tissue invasion were not affected. Upon reoxygenation, however, normalization of [K+](o) was disturbed and synaptic recovery failed. Therefore, SH-reducing conditions at the onset of HSD proved to be devastating for the hippocampal network. In conclusion, the only merit of DTNB or H2O2 treatment is a delayed HSD onset, i.e. some extra time before neuronal function is lost during severe hypoxia. Attenuation of the severe changes during HSD or an improved outcome was not observed. Nevertheless, combination of SH-oxidants with established neuroprotectants might be a potential therapeutic approach. (c) 2008 IBRO. Published by Elsevier Ltd. All rights reserved
CHAMBER MUSIC CONCERT featuring students of The Shepherd School of Music The Complete Brandenburg Concertos by Johann Sebastian Bach Tuesday, May 9, 2006 8:00 p.m. Lillian H. Duncan Recital Hall
No full textProgram: Concerto No. I in F Major, BWV 1046 / Johann Sebastian Bach (1685-1750) -- Concerto No. 2 in F Major, B WV 1047 / Johann Sebastian Bach -- Concerto No.3 in G Major, BWV 1048 / Johann Sebastian Bach -- Concerto No.4 in G Major, BWVJ049 / Johann Sebastian Bach -- Concerto No. 5 in D Major, BWV1050 / Johann Sebastian Bach -- Concerto No. 6 in B-flat Major, BWV 1051 / Johann Sebastian Bach
Bey der Grvft Des Hochwuerdigen Vnd Hochgelahrten Herrn Herrn Bernh. Sebastian Grosse Hochverordnet Gewesenen Wuerklichen Ober-Consistorial-Assessors Zv Weimar, Oberpfarrer, Svperintendenten Vnd Ephorvs Zv Ilmenav, Welcher Den XXV. Merz MDCCLXXII. Im Herrn Entschlief
No full textBEY DER GRVFT DES HOCHWUERDIGEN VND HOCHGELAHRTEN HERRN HERRN BERNH. SEBASTIAN GROSSE HOCHVERORDNET GEWESENEN WUERKLICHEN OBER-CONSISTORIAL-ASSESSORS ZV WEIMAR, OBERPFARRER, SVPERINTENDENTEN VND EPHORVS ZV ILMENAV, WELCHER DEN XXV. MERZ MDCCLXXII. IM HERRN ENTSCHLIEF
Bey der Grvft Des Hochwuerdigen Vnd Hochgelahrten Herrn Herrn Bernh. Sebastian Grosse Hochverordnet Gewesenen Wuerklichen Ober-Consistorial-Assessors Zv Weimar, Oberpfarrer, Svperintendenten Vnd Ephorvs Zv Ilmenav, Welcher Den XXV. Merz MDCCLXXII. Im Herrn Entschlief ([1])
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Sulfhydryl oxidation reduces hippocampal susceptibility to hypoxia-induced spreading depression by activating BK channels
No full textThe cytosolic redox status modulates ion channels and receptors by oxidizing/ reducing their sulfhydryl ( SH) groups. We therefore analyzed to what degree SH modulation affects hippocampal susceptibility to hypoxia. In rat hippocampal slices, severe hypoxia caused a massive depolarization of CA1 neurons and a negative shift of the extracellular DC potential, the characteristic sign of hypoxia- induced spreading depression ( HSD). Oxidizing SH groups by 5,5 '- dithiobis 2- nitrobenzoic acid ( DTNB, 2 mM) postponed HSD by 30%, whereas their reduction by 1,4- dithio- DL- threitol ( DTT, 2 mM) or alkylation by N- ethylmaleimide ( 500 mu M) hastened HSD onset. The DTNB- induced postponement of HSD was not affected by tolbutamide ( 200 mu M), DL- 2- amino- 5-phosphonovaleric acid ( 150 mu M), or 6- cyano- 7- nitroquinoxaline- 2,3-dione ( 25 mu M). It was abolished, however, by Ni2+ ( 2 mM), withdrawal of extracellular Ca2+, charybdotoxin ( 25 nM), and iberiotoxin ( 50 nM). In CA1 neurons DTNB induced a moderate hyperpolarization, blocked spontaneous spike discharges and postponed the massive hypoxic depolarization. DTT induced burst firing, depolarized glial cells, and hastened the onset of the massive hypoxic depolarization. Schaffer- collateral/ CA1 synapses were blocked by DTT but not by DTNB; axonal conduction remained intact. Mitochondria did not markedly respond to DTNB or DTT. While the targets of DTT are less clear, the postponement of HSD by DTNB indicates that sulfhydryl oxidation increases the tolerance of hippocampal tissue slices against hypoxia. We identified as the underlying mechanism the activation of BK channels in a Ca2+- sensitive manner. Accordingly, ionic disregulation and the loss of membrane potential occur later or might even be prevented during short- term insults. Therefore well- directed oxidation of SH groups could mediate neuroprotection
Materials from Webinar "Reproducibility and Transparency in Abortion Research"
No full textThis is a project with a variety of materials shared during the webinar "Reproducibility and Transparency in Abortion Research," presented by Lori Frohwirth, Isaac Maddow-Zimet, Sebastian Karcher, Jennifer Mueller and Rachel Jone
Materials from Webinar "Reproducibility and Transparency in Abortion Research"
No full textThis is a project with a variety of materials shared during the webinar "Reproducibility and Transparency in Abortion Research," presented by Lori Frohwirth, Isaac Maddow-Zimet, Sebastian Karcher, Jennifer Mueller and Rachel Jone
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