33 research outputs found
Grand-averaged ERP waveforms and ERP scalp distribution results elicited by the Down shift of the F0.
<p>Left panel represents ERPs elicited in predictable and unpredictable experimental conditions measured a two electrode sites that were submitted for statistical analyses. Blue vertical bar depicted time window at which the mean amplitude of the ERP difference wave was measured for the statistical analyses. Right panel represents scalp distribution of N1 response in predictable (top) and unpredictable (middle) experimental conditions as well as the scalp distribution of the ERP difference wave (bottom).</p
Grand-averaged ERP waveforms and ERP scalp distribution results elicited by the Up shift of the F0.
<p>Left panel represents ERPs elicited in predictable and unpredictable experimental conditions measured at two electrode sites that were submitted for statistical analyses. Blue vertical bar depicts time window at which the mean amplitude of the ERP difference wave was measured for the statistical analyses. Right panel represents scalp distribution of N1 response in predictable (top) and unpredictable (middle) experimental conditions as well as the scalp distribution of the ERP difference wave (bottom).</p
Voice perturbation paradigm and behavioral study results.
<p>(A) Schematic illustration of voice output and perturbation stimuli. (B) Schematic representation of experimental conditions showing upward and downward pitch shifts in the unpredictable (top) and predictable conditions (bottom 2 rows). (C) Behavioral (voice) results. Grand-averaged F0 traces across all subjects separately for “Up” and “Down” stimuli with unpredictable and predictable experimental conditions. Thick lines show opposing and thin lines “following” responses. Vertical bars illustrate standard deviations of the averaged F0 traces. Vertical dashed lines represent pitch shift stimuli onset.</p
Long Patch Base Excision Repair Proceeds via Coordinated Stimulation of the Multienzyme DNA Repair Complex*
Base excision repair, a major repair pathway in mammalian cells, is
responsible for correcting DNA base damage and maintaining genomic integrity.
Recent reports show that the Rad9-Rad1-Hus1 complex (9-1-1) stimulates enzymes
proposed to perform a long patch-base excision repair sub-pathway (LP-BER),
including DNA glycosylases, apurinic/apyrimidinic endonuclease 1 (APE1), DNA
polymerase β (pol β), flap endonuclease 1 (FEN1), and DNA ligase I
(LigI). However, 9-1-1 was found to produce minimal stimulation of FEN1 and
LigI in the context of a complete reconstitution of LP-BER. We show here that
pol β is a robust stimulator of FEN1 and a moderate stimulator of LigI.
Apparently, there is a maximum possible stimulation of these two proteins such
that after responding to pol β or another protein in the repair complex,
only a small additional response to 9-1-1 is allowed. The 9-1-1 sliding clamp
structure must serve primarily to coordinate enzyme actions rather than
enhancing rate. Significantly, stimulation by the polymerase involves
interaction of primer terminus-bound pol β with FEN1 and LigI. This
observation provides compelling evidence that the proposed LP-BER pathway is
actually employed in cells. Moreover, this pathway has been proposed to
function by sequential enzyme actions in a “hit and run”
mechanism. Our results imply that this mechanism is still carried out, but in
the context of a multienzyme complex that remains structurally intact during
the repair process