Michael T. Lin

TL;DR: The data suggest that it is rare for any one particular acquired mtDNA mutation to reach levels in the brain that are functionally significant, and does not exclude the possibility that the cumulative burden of multiple, individually rare, acquired mutations impairs mitochondrial function.

TL;DR: HR-3D volumetric image analysis allows for better visualization of intraneuronal Aβ pathology and provides new insights into plaque formation in AD, supporting that Aβ fibrillization begins within AD vulnerable neurons, leading to disruption of cytoarchitecture and degeneration of spines and neurites.

TL;DR: It is concluded that the Ca0 and Kd values of the BK channel can be modulated by differential channel phosphorylation, which can be explained by a greater extent of channelosphorylation of fetal than adult myocytes.

TL;DR: It is observed that at voltage-clamped membrane potentials of +60 mV in perforated whole cell studies, the normalized outward current densities in fetal myocytes were >30% higher than in those of the adult (P < 0.05) and that these were predominantly due to iberiotoxin-sensitive currents from BKCa channels.

TL;DR: It is shown that BK channel activity is modulated during development by differential phosphorylation and that the activities of CAPAKs change substantially during development, and it is suggested that the functional stoichiometry ofCAPAKs varies significantly during development and that such variation may be a hitherto unrecognized mechanism of ion channel regulation.