The fronto-central N2 but not parietal P3 reflects response inhibition in the count/no-count task.

This study aimed to investigate whether the N2 or P3 component in the count/no-count task reflects response inhibition. The participants were asked to count/withhold counting the number of O/X letters in the count/no-count task, and to calculate the sum of all digits (i.e., 1/0) in the digital accumulation task. Therefore, four conditions were obtained in this study: count, no-count, Add 1, and Add 0. In the count and Add 1 conditions, the counting/calculation number need to be updated. In both no-count and Add 0 conditions, the memory of counting/calculation number need not to be updated; a No-go (withhold) instruction was given in the no-count condition, but a Go instruction was given in the Add 0 condition. Results showed that an enhanced fronto-central N2 was evoked in the no-count than in the Add 0 condition, indicating that a stronger response conflict or stronger inhibition might be triggered in the No-count condition. The frontocentral P3 showed no differences between no-count and Add 0 conditions, however, an enhanced centro-parietal P3 component was observed for the count relative to the no-count condition and for the Add 1 relative to the Add 0 condition, indicating that a greater amount of attentional resources might be consumed during memory updating process. Taken together, in the count/no-count task, the fronto-central N2 might reflect response inhibition or conflict and the parietal P3 might reflect attentional resource allocation but not response inhibition.

Response inhibition and memory updating in the count/nocount task: an ERP study.

The present study aimed to separate the neural activities between response inhibition and memory updating processes in the Count/Nocount task. Memory load was manipulated to investigate the memory updating process. Within each trial, participants were asked to count/withhold counting the number of O/X letters in the Count/Nocount task. The participants were asked to silently add 1 if a Count letter was presented in the low load condition, and add 2 in the high load condition. Data from 28 healthy participants showed that: (1) in both high load and low load conditions, the latencies of P2 and N2 components were shorter for the Nocount than Count trials, indicating faster attentional orienting and conflict monitoring processes for the Nocount stimuli (i.e., inhibition processes triggered by the Nocount stimuli against those response execution processes triggered by Count stimuli); (2) more positive frontal P3 amplitudes were evoked for the Nocount relative to the Count stimuli, indicating a more intensive response inhibition process for the Nocount trials; (3) a more positive parietal P3 component was evoked for the low load relative to high load condition, indicating a more intensive working memory updating process for the high load condition. This load effect was absent for the frontal P3 component, suggesting that the frontal P3 might not be associated with the memory updating process. In sum, both the cognitive inhibition process (reflected by the frontal P3 component) and working memory updating process (reflected by the parietal P3 component) appear to be involved in the Count/Nocount task.

A functional near-infrared spectroscopy investigation of item-method directed forgetting.

Whether directed forgetting is passive or active remains debated. Using functional near-infrared spectroscopy (fNIRS), blood-oxygen level-dependent responses of intentional forgetting were investigated in the item-method directed forgetting (DF) paradigm. During the study phase, each word was followed by a random remembering or forgetting cue indicating whether the word is to be remembered (TBR) or to be forgotten (TBF). A recognition test was used in the test phase and four cue-response conditions were obtained: remembering/forgetting cues associated with the subsequently remembered (TBR-r/TBF-r) or forgotten (TBR-f/TBF-f) words. Data from 16 healthy adult participants showed a DF effect. The fNIRS data revealed that, during the 5-9 s time window, the oxygenate hemoglobin (oxy-Hb) levels were higher during intentional forgetting compared to intentional remembering in the left inferior frontal (TBF-f vs. TBR-f) and right superior frontal gyrus (TBF-r vs. TBR-r), indicating more frontal inhibition involved during intentional forgetting. During the 9-11 s time window, the oxy-Hb level in the frontal and parietal gyrus was higher for forgetting than remembering cues, indicating that the TBF words might be automatically encoded. In sum, the TBF words might receive inhibition control triggered by forgetting cues and then be automatically encoded with the increase of the post-cue interval.

The role of forgetting cues in directed forgetting: Ceasing maintenance rehearsal.

The effect of forgetting cues on maintenance rehearsal in item-method directed forgetting (DF) paradigm was explored from behavioral and electrophysiological evidence. In Experiment 1, maintenance rehearsal was induced by a maintenance cue. Specifically, after the studied word, a maintenance (M) cue was presented before the presentation of a remembering/forgetting cue. When an M cue appeared, participants were required to wait for the following remembering (M-R) or forgetting (M-F) cue to determine whether the word needs to be remembered or not, and words were kept in short-term memory with maintenance rehearsal until the presentation of M-R/M-F cues. Four conditions were utilized: maintain-remembering (M-R), maintain-forgetting (M-F), maintenance (M), and forgetting (F). The results showed that, 1) superior recognition was found for the M-R relative to the M-F words, revealing a typical DF effect; 2) No recognition difference was found between M and M-F words, indicating that M-F cues showed little effect in promoting forgetting; 3) Inferior recognition was found for F than M words, indicating that the maintenance rehearsal might cease or be reduced by the presentation of F cues. In Experiment 2, event related potentials time-locked to cue (M-R, M-F, M, and F cues) onset during study phase. An enhanced fronto-central P3a component was evoked for F relative to M cues, indicating a more intensive attention orienting or attentional inhibition process triggered by F cues. These results demonstrated that forgetting cues might trigger an inhibition process to terminate the maintenance rehearsal process.

Complete sequence analysis of mitochondrial DNA and telomere length in aplastic anemia.

The present study was primarily undertaken to examine the hypothesis that mitochondrial DNA (mtDNA) mutations and telomere length may be associated with aplastic anemia (AA). Our study included a single institution analysis of 40 patients presenting with AA first diagnosed at the Affiliated Hospital of Shandong, University of Traditional Chinese Medicine between 2010 and 2013. Bone marrow and oral epithelial samples were collected from patients with AA (n=40) for mtDNA mutation and telomere length determinations. Bone marrow specimens were collected from 40 healthy volunteers as controls for the examination of telomere length. The mitochondrial genome was amplified by polymerase chain reaction (PCR), and the products were used for sequencing and analysis. We detected 146 heteroplasmic mutations in 18 genes from 40 patients with AA, including 39 silent mutations and 28 frameshift mutations. We used the gamma globin gene (HBG) as the control gene in real-time PCR to survey the relative telomere length measurements of the patients with AA and the healthy volunteers. Telomere length was expressed as the relative T/S value. We observed a negative correlation between the mtDNA non-silent mutation and the white blood cell (WBC) count, hemoglobin and platelet count. Of note, there was a positive correlation between the relative T/S value and WBC count, hemoglobin and platelet count, and a negative correlation between the non-silent mutation and the relative T/S value. We conclude that the functional impairment of the mitochondrial respiratory chain induced by mutation and telomere length shortening may play an important role in the process of hematopoietic failure in patients with AA. Additionally, mtDNA mutations and telomere length shortening influenced each other.