Induction, Resonance, and Secondary Electrostatic Interaction on Hydrogen Bonding in the Association of Amides and Imides

Both computations and experiments have confirmed that amides have stronger self-associations than imides. While this intriguing phenomenon is usually explained in the term of secondary electrostatic repulsion from the additional spectator carbonyl groups in imides, recently it was proposed that the π resonance effect from the spectator carbonyl which alters the balance between the acidity of the hydrogen-bond (H-bond) donor and the basicity of the H-bond acceptor is the major cause. In this work, we examined the roles of π resonance and the secondary electrostatic interaction in the formation of amide and imide dimers by deactivating the π conjugation from the spectator carbonyl and flipping the spectator carbonyl using the block-localized wave function method which is the simplest variant of valence bond theory. Energetic, geometrical, and spectral results show that three major forces, namely the σ induction effect (IE), π resonance effect (RE), and secondary electrostatic interaction (SEI), contribute to the different binding energies in the dimers of amides and imides. Whereas IE favors stronger binding among imides, both RE and SEI diminish the self-association of imides. Obviously, the negative force from RE and SEI exceeds the positive force from IE. Relatively, SEI plays a little bigger role than RE

Mean±95%CI distributions for 60 normal subjects (A,B) and 16 ESMs (C,D) for correct antisaccades (A,C) and error prosaccades (B,D).

<p>The grey region shows the express saccade latency range (80 ms to 130 ms). The intersubject mean of the individual subject median latencies (±SD), and the intersubject percentage of express saccades is also shown.</p

Data from antisaccade tasks.

<p>Comparison of mean±95%CI between 60 normal (non-ESM) subjects and 16 ESMs. A. Antisaccade directional error rate. B. Mean error pro-saccade latency. C. Mean correct antisaccade latency. Note different y-axis scales in B and C.</p

Percentage frequency distribution histograms of saccade latency in the prosaccade overlap task.

<p>A. Example from an individual “normal” subject; B. individual ESM. In A. and B. the median saccade latency, and the percentage of express saccades is shown. C. Mean±95%CI distribution for 60 “normal” subjects. D. Mean±95%CI distribution for 16 ESMs. In C. and D. the intersubject mean (±SD) of the individual median latencies and the intersubject mean (±SD) percentage of express saccades is shown. The vertical grey region shows the range of express saccade latency (80 ms to 130 ms) and the dotted vertical line is at 100 ms. The three horizontal grey bars in C. show the three latency ranges (1 to 3) over which latency was compared between ESMs and normal subjects.</p

Influence of target direction (Left vs Right) on the antisaccade directional error rate (%) for A.

<p>Normal participants; B ESMs. Solid line is the line of equality (x = y).</p

Data from prosaccade task.

<p>A. Plot of the percentage of express saccades against median prosaccade latency. B. Distribution of percentage of express saccades in the prosaccade task. Vertical dashed line shows the criterion used to define an ESM (30% ES in the prosaccade task). Columns to the right of this line show counts of ESMs.</p

Relationship between prosaccade (PS) and antisaccade (AS) performance.

<p>A. Median prosaccade latency and AS directional error rate. B. Percentage of express saccades in the PS task and AS directional error rate. C. Median PS latency and median AS prosaccade error latency. D. Percentage of express saccades in the PS task and median AS error prosaccade latency (AS). E. Percentage of express saccades in the PS task and percentage of ES in AS prosaccade errors. F. The difference between correct AS latency and PS latency calculated for each subject, and AS directional error rate. On each plot the solid black line is the least-squares linear regression line calculated for the whole dataset. Data from ESMs: grey symbols; data from normal subjects: black symbols.</p

Table_1_The Counterproductive Effect of Right Anodal/Left Cathodal Transcranial Direct Current Stimulation Over the Dorsolateral Prefrontal Cortex on Impulsivity in Methamphetamine Addicts.XLSX

The current study aimed to evaluate the effect of transcranial direct current stimulation (tDCS) over the dorsolateral prefrontal cortex (DLPFC) on behavioral impulsivity in methamphetamine addicts. Forty-five methamphetamine addicts were recruited and randomly divided into active tDCS and sham tDCS groups to receive a daily tDCS intervention for 5 days, with the intensity set to 2 mA for the active group and 0 mA for the sham group. Anodal and cathodal electrodes were, respectively, placed over the right and left DLPFC. Behavioral impulsivity in methamphetamine addicts was examined by the 2-choice oddball task at 3-time points: before tDCS intervention (baseline), after the first intervention (day 1), and after 5 repeated interventions (day 5). Besides, twenty-four healthy male participants were recruited as the healthy controls who completed a 2-choice oddball task. Analysis of accuracy for the 2-choice oddball task showed that behavioral impulsivity was counterproductively increased in the active group, which was shown by the decreased accuracy for the deviant stimulus. The results suggested that the present protocol may not be optimal and other protocols should be considered for the intervention of methamphetamine addicts in the future.</p

MSHF: A Multi-Source Heterogeneous Fundus (MSHF) Dataset for Image Quality Assessment

   MSHF: A Multi-Source Heterogeneous Fundus (MSHF) Dataset for Image Quality Assessment</p

Data_Sheet_1_Dosage consideration for transcranial direct current stimulation in post-stroke dysphagia: A systematic review and network meta-analysis.DOCX

ObjectiveThis systematic review and network meta-analysis sought to determine the efficacy of different intensities of transcranial direct current stimulation (tDCS) in patients with dysphagia after stroke to improve swallowing function.MethodsRandomized-controlled trials (RCTs) of tDCS in post-stroke dysphagia were searched from Pubmed, EMBASE, Cochrane Library, Web of Science, China National Knowledge Infrastructure (CNKI), Chinese Biomedical Literature Service System (SinoMed), Wanfang database, and Chinese Scientific Journals Database (VIP) from databases' inception to June 22, 2022. Article screening, data extraction, and article quality evaluation were completed by 2 independent researchers. Network meta-analysis was performed using Stata.ResultsA final total of 20 studies involving 838 stroke patients were included. The included control interventions were sham tDCS and conventional therapy (CT). Network meta-analysis showed that 20 min of 1.2, 1.4, 1.5, 1.6, and 2 mA anodal tDCS and 30 min of 2 mA anodal tDCS significantly improved post-stroke dysphagia compared with CT (all P ConclusionDifferent durations and intensities of anodal tDCS are effective in improving post-stroke dysphagia. However, 20 min of tDCS at 1.4 mA may be the optimal regimen.Systematic review registrationhttps://www.crd.york.ac.uk/PROSPERO/#recordDetails, identifier CRD42022342506.</p