Novel neuroprotective effect of cisternal and intra-cerebral magnesium sulfate solution infusion on delayed cerebral death in rat hippocampal neurons after transient global ischemia

2012 ◽  
Vol 1480 ◽  
pp. 72-80 ◽  
Author(s):  
Kentaro Mori ◽  
Takuji Yamamoto ◽  
Yasuaki Nakao ◽  
Masahiro Miyazaki ◽  
Junko Iwata ◽  
...  
Keyword(s):  
Magnesium Sulfate ◽  
Hippocampal Neurons ◽  
Neuroprotective Effect ◽  
Sulfate Solution ◽  
Global Ischemia ◽  
Transient Global Ischemia ◽  
Magnesium Sulfate Solution

Experimental Investigation of the Corrosion Mechanism of Cemented Soils in Magnesium Sulfate Solution

2014 ◽  
Vol 56 (9) ◽  
pp. 675-680 ◽  
Author(s):  
Pengju Han ◽  
Y. Frank Chen ◽  
Bozhu Shen ◽  
David Y. Du
Keyword(s):  
Experimental Investigation ◽  
Magnesium Sulfate ◽  
Sulfate Solution ◽  
Corrosion Mechanism ◽  
Cemented Soils ◽  
Magnesium Sulfate Solution

scholarly journals Importance of Cation Species during Sulfate Resistance Tests for Alkali-Activated FA/GGBFS Blended Mortars

Materials ◽  
2019 ◽  
Vol 12 (21) ◽  
pp. 3547
Author(s):  
Youngkeun Cho ◽  
Joo Hyung Kim ◽  
Sanghwa Jung ◽  
Yoonseok Chung ◽  
Yeonung Jeong
Keyword(s):  
Compressive Strength ◽  
Magnesium Sulfate ◽  
Sulfate Solution ◽  
Magnesium Ions ◽  
Sulfate Resistance ◽  
Granulated Blast Furnace Slag ◽  
Significant Difference ◽  
Furnace Slag ◽  
Alkali Activated ◽  
Magnesium Sulfate Solution

In this study, the changes in mass, compressive strength, and length of blended mortars were analyzed to investigate their sulfate resistance according to the ground granulated blast furnace slag (GGBFS) blending ratio and type of sulfate solution applied. All alkali-activated mortars showed an excellent sulfate resistance when immersed in a sodium sulfate (Na2SO4) solution. However, when immersed in a magnesium sulfate (MgSO4) solution, different sulfate resistance results were obtained depending on the presence of GGBFS. The alkali-activated GGBFS blended mortars showed a tendency to increase in mass and length and decrease in compressive strength when immersed in a magnesium sulfate solution, whereas the alkali-activated FA mortars did not show any significant difference depending on the types of sulfate solution applied. The deterioration of alkali-activated GGBFS blended mortars in the immersion of a magnesium sulfate solution was confirmed through the decomposition of C–S–H, which is the reaction product from magnesium ions, and the formation of gypsum (CaSO4·2H2O) and brucite (Mg(OH)2).

scholarly journals Cloning and Characterization of Rat Caspase-9: Implications for a Role in Mediating Caspase-3 Activation and Hippocampal Cell Death after Transient Cerebral Ischemia

2002 ◽  
Vol 22 (5) ◽  
pp. 534-546 ◽  
Author(s):  
Guodong Cao ◽  
Yumin Luo ◽  
Tetsuya Nagayama ◽  
Wei Pei ◽  
R. Anne Stetler ◽  
...  
Keyword(s):  
Neuronal Death ◽  
Hippocampal Neurons ◽  
Caspase 3 ◽  
Neuronal Survival ◽  
Global Ischemia ◽  
Adult Brain ◽  
Caspase 8 ◽  
Intrinsic Pathway ◽  
Caspase 9 ◽  
Transient Global Ischemia

Delayed hippocampal neurodegeneration after transient global ischemia is mediated, at least in part, through the activation of terminal caspases, particularly caspase-3, and the subsequent proteolytic degradation of critical cellular proteins. Caspase-3 may be activated by the membrane receptor-initiated caspase-8–dependent extrinsic pathway and the mitochondria-initiated caspase-9–dependent intrinsic pathway; however, the precise role of these deduced apoptosis-signaling pathways in activating caspase-3 in ischemic neurons remains elusive. The authors cloned the caspase-9 gene from the rat brain and investigated its potential role in mediating ischemic neuronal death in a rat model of transient global ischemia. Caspase-9 gene expression and protease activity were extremely low in the adult brain, whereas they were developmentally upregulated in newborn rats, especially at postnatal 12 weeks, a finding consistent with the theory of an essential role for caspase-9 in neuronal apoptosis during brain development. After 15-minute transient global ischemia, caspase-9 was overexpressed and proteolytically activated in the hippocampal CA1 neurons at 8 to 72 hours of reperfusion. The temporal profile of caspase-9 activation coincided with that of cytochrome c release and caspase-3 activation, but preceded CA1 neuronal death. Immunoprecipitation experiments revealed that there was enhanced formation of Apaf-1/caspase-9 complex in the hippocampus 8 and 24 hours after ischemia. Furthermore, intracerebral ventricular infusion of the relatively specific caspase-9 inhibitor N-benzyloxycarbonyl-Leu-Glu-His-Asp-fluoro-methylketone before ischemia attenuated caspase-3–like activity and significantly enhanced neuronal survival in the CA1 sector. In contrast, inhibition of caspase-8 activity had no significant effect on caspase-3 activation or neuronal survival. These results suggest that the caspase-9–dependent intrinsic pathway may be the primary mechanism responsible for the activation of caspase-3 in ischemic hippocampal neurons.

TGF-β1 Protects Hippocampal Neurons Against Degeneration Caused by Transient Global Ischemia

Stroke ◽  
1996 ◽  
Vol 27 (9) ◽  
pp. 1609-1615 ◽  
Author(s):  
P. Henrich-Noack ◽  
J.H.M. Prehn ◽  
J. Krieglstein
Keyword(s):  
Hippocampal Neurons ◽  
Global Ischemia ◽  
Transient Global Ischemia ◽  
Tgf Β1

scholarly journals Neuroprotective effect of FK506, an immunosuppressant, on transient global ischemia in gerbil

1996 ◽  
Vol 206 (2-3) ◽  
pp. 81-84 ◽  
Author(s):  
Tomoo Tokime ◽  
Kazuhiko Nozaki ◽  
Haruhiko Kikuchi
Keyword(s):  
Neuroprotective Effect ◽  
Global Ischemia ◽  
Transient Global Ischemia
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