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1 presence of glucose and fell rapidly during aglycemia.
2 s failure after energetic stress like anoxia/aglycemia.
3 s or the rate of ATP depletion during anoxia/aglycemia.
4 iameter unmyelinated axons (C fibers) during aglycemia.
5 e neuronal metabolism and response to anoxia/aglycemia.
6 whether it supported axon conduction during aglycemia.
7 -diameter, myelinated axon conduction during aglycemia.
8 lasm, and these diminished after exposure to aglycemia.
9 peripheral nerve glycogen breaks down during aglycemia and is passed, probably as lactate, to myelina
11 B is sensitive to short exposures of hypoxia/aglycemia and that changes in endothelial cell calcium f
12 ne can each prevent the damage due to anoxia/aglycemia and to higher concentrations of N-methyl-D-asp
13 rotein synthesis inhibition following anoxia/aglycemia, and significantly reduced basal ATP levels (t
15 ve minutes of anoxia without glucose (anoxia-aglycemia) caused a dramatic depletion of ATP to less th
17 te acidification of the medium during anoxia/aglycemia did not reduce the damage to protein synthesis
20 otein synthesis failure after 7.5 min anoxia/aglycemia in the rat hippocampal slice can be prevented
22 inhibition and energy failure due to anoxia/aglycemia or exposure to N-methyl-D-aspartate in the rat
23 g the acidification and following the anoxia/aglycemia, protein synthesis was almost completely prote
24 e protein synthesis inhibition due to anoxia/aglycemia (to 55.6% of normoxic controls), but the prote
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