Data_Sheet_1_A general dual-pathway network for EEG denoising.docx

IntroductionScalp electroencephalogram (EEG) analysis and interpretation are crucial for tracking and analyzing brain activity. The collected scalp EEG signals, however, are weak and frequently tainted with various sorts of artifacts. The models based on deep learning provide comparable performance with that of traditional techniques. However, current deep learning networks applied to scalp EEG noise reduction are large in scale and suffer from overfitting.MethodsHere, we propose a dual-pathway autoencoder modeling framework named DPAE for scalp EEG signal denoising and demonstrate the superiority of the model on multi-layer perceptron (MLP), convolutional neural network (CNN) and recurrent neural network (RNN), respectively. We validate the denoising performance on benchmark scalp EEG artifact datasets.ResultsThe experimental results show that our model architecture not only significantly reduces the computational effort but also outperforms existing deep learning denoising algorithms in root relative mean square error (RRMSE)metrics, both in the time and frequency domains.DiscussionThe DPAE architecture does not require a priori knowledge of the noise distribution nor is it limited by the network layer structure, which is a general network model oriented toward blind source separation.</p

Representative plasma cytokine/chemokine expression levels in TB patients (<i>n</i> = 151) and no-TB donors (<i>n</i> = 107).

<p>(A) TNF-α, (B) IFN-γ, (C) IP-10/CXCL-10, (D) MIP-1β, and (E) IL-6 levels. *<i>P</i> < 0.05, **<i>P</i> < 0.001. <i>P</i>: <i>P</i> value. Independent-sample T testing was performed to compare the results from TB patients with those of no-TB cases.</p

Patient characteristics.

<p>Patient characteristics.</p

Classification of detective cytokines and chemokines.

<p>Classification of detective cytokines and chemokines.</p

Association of patient cytokine expression profiles and disease.

<p>Association of patient cytokine expression profiles and disease.</p

Cytokine/chemokine levels in PBMCs from BCG-vaccinated healthy donors (BHD), with or without ESAT-6 stimulation.

<p>The levels of (A) TNF-α, (B) IL-1β, (C) MIP-1β, (D) GM-CSF, (E) IL-12p40, (F) IL-12p70, (G) IL-10, (H) IL-1α, and (I) CX3CL1 are shown. *<i>P</i> < 0.05, **<i>P</i> < 0.001. <i>P</i>: <i>P</i> value. An independent-sample T test was performed.</p

data_sheet_1.docx

<p>The mechanisms by which vitamins regulate immunity and their effect as an adjuvant treatment for tuberculosis have gradually become very important research topics. Studies have found that vitamin B5 (VB5) can promote epithelial cells to express inflammatory cytokines. We aimed to examine the proinflammatory and antibacterial effect of VB5 in macrophages infected with Mycobacterium tuberculosis (MTB) strain H37Rv and the therapeutic potential of VB5 in vivo with tuberculosis. We investigated the activation of inflammatory signal molecules (NF-κB, AKT, JNK, ERK, and p38), the expression of two primary inflammatory cytokines (tumor necrosis factor and interleukin-6) and the bacterial burdens in H37Rv-infected macrophages stimulated with VB5 to explore the effect of VB5 on the inflammatory and antibacterial responses of macrophages. We further treated the H37Rv-infected mice with VB5 to explore VB5’s promotion of the clearance of H37Rv in the lungs and the effect of VB5 on regulating the percentage of inflammatory cells. Our data showed that VB5 enhanced the phagocytosis and inflammatory response in macrophages infected with H37Rv. Oral administration of VB5 decreased the number of colony-forming units of H37Rv in lungs of mice at 1, 2, and 4 weeks after infection. In addition, VB5 regulated the percentage of macrophages and promoted CD4⁺ T cells to express interferon-γ and interleukin-17; however, it had no effect on the percentage of polymorphonuclear neutrophils, CD4⁺ and CD8⁺ T cells. In conclusion, VB5 significantly inhibits the growth of MTB by regulating innate immunity and adaptive immunity.</p