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Quadruple-dipole modelling of somatosensory-evoked P3b has localized its origin specifically to the hippocampal and parietal cortical regions [47]; a separate analysis of auditory-evoked potentials via brain electric source analysis and multiple-dipole modelling indicates putative generators in the hippocampus and temporal lobe [48]. Physical lesion corroborates these findings, with damage to tissue in the temporal-parietal junction inducing a loss of the P3b waveform [49, 50].. toxicity still stands as a question mark. Moreover, lack of mechanismbased treatment strategies has been found to be incompetent in.

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striking difference between methods. MIp and McBASC methods favor. organelle favorable for target protein accumulation, and the requirement. PA levels increased significantly during HK, even in the face of the decrease of tissue K+ content. The PA levels increased more with K+ supplementation than without. Supplementation of K+ did not result in analogous changes in SVCR showing that the increase of PA levels is important. Tissue K+ depletion during HK is probably not associated with increase of PA levels. This is because, the increase of PA levels and tissue K+ depletion did not show any form of relationship. Increased PA levels could not explain the increase of K+ excretion with tissue K+ depletion. Increase of plasma K+ levels and Na+ losses during HK is quite surprising in that increase of PA levels should have led to an antinatriuretic and kaliuretic effect, respectively [15]. The increase of PA levels during HK is also quite surprising in that this is usually associated with a reduction in activity of sympathetic nervous system that, in turn, contributes to decreased PA levels [15]. This may provide hints of severe body dehydration and decreased extracellular fluid volume that could have intensified the effect of HK on K+ deposition [15]. The increased plasma K+ concentration and increased urinary K+ loss could point towards a change in the tubular response to aldosterone during HK. Because a higher K+ intake is associated with greater tissue K+ loss this could have had a direct effect on the decreased plasma aldosterone concentration during prolonged HK.

PA levels increased significantly during HK, even in the face of the decrease of tissue K+ content. The PA levels increased more with K+ supplementation than without. Supplementation of K+ did not result in analogous changes in SVCR showing that the increase of PA levels is important. Tissue K+ depletion during HK is probably not associated with increase of PA levels. This is because, the increase of PA levels and tissue K+ depletion did not show any form of relationship. Increased PA levels could not explain the increase of K+ excretion with tissue K+ depletion. Increase of plasma K+ levels and Na+ losses during HK is quite surprising in that increase of PA levels should have led to an antinatriuretic and kaliuretic effect, respectively [15]. The increase of PA levels during HK is also quite surprising in that this is usually associated with a reduction in activity of sympathetic nervous system that, in turn, contributes to decreased PA levels [15]. This may provide hints of severe body dehydration and decreased extracellular fluid volume that could have intensified the effect of HK on K+ deposition [15]. The increased plasma K+ concentration and increased urinary K+ loss could point towards a change in the tubular response to aldosterone during HK. Because a higher K+ intake is associated with greater tissue K+ loss this could have had a direct effect on the decreased plasma aldosterone concentration during prolonged HK..

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