sj-pdf-2-nnr-10.1177_15459683211062895 – Supplemental Material for Brain–Computer Interface Training Based on Brain Activity Can Induce Motor Recovery in Patients With Stroke: A Meta-Analysis

Supplemental Material, sj-pdf-2-nnr-10.1177_15459683211062895 for Brain–Computer Interface Training Based on Brain Activity Can Induce Motor Recovery in Patients With Stroke: A Meta-Analysis by Ippei Nojima, Hisato Sugata, Hiroki Takeuchi and Tatsuya Mima in Neurorehabilitation and Neural Repair</p

sj-pdf-1-nnr-10.1177_15459683211062895 – Supplemental Material for Brain–Computer Interface Training Based on Brain Activity Can Induce Motor Recovery in Patients With Stroke: A Meta-Analysis

Supplemental Material, sj-pdf-1-nnr-10.1177_15459683211062895 for Brain–Computer Interface Training Based on Brain Activity Can Induce Motor Recovery in Patients With Stroke: A Meta-Analysis by Ippei Nojima, Hisato Sugata, Hiroki Takeuchi and Tatsuya Mima in Neurorehabilitation and Neural Repair</p

Plasmon Dephasing and Near-Field Enhancement of Periodical Arrays of Au Nanogap Dimers

The manipulation of near-field enhancements in plasmonic nanostructures is essentially significant in boosting the performance of plasmon-enhanced near-fields in various applications. Far-field coupling induced in the periodically arrayed plasmonic nanostructures offers a promising platform for manipulating not only the near-field enhancements but also the dephasing dynamics in plasmonic nanostructures. In this study, we fabricated periodic arrays of Au nanoblock dimers with various pitch sizes and systematically investigated the far-field coupling effect on the plasmon dephasing time. Ultrafast time-resolved measurements revealed that the pitch size of the arrays crucially influences the plasmon dephasing of the Au nanoblock dimers. The observed pitch-size dependency of the dephasing time was qualitatively reproduced by electromagnetic simulations. We also simulated near-field distributions on the arrays and found that the far-field coupling enables us to manipulate the near-field enhancement without impairing the mode volume of the plasmonic nanostructures. Our study provides a deeper understanding of the plasmon dephasing of the periodically arrayed nanostructures and gives fruitful information for optimizing plasmonic near-field enhancements in various applications

Exploring Hybrid States and Their Ultrafast Dynamics in Exciton–Plasmon Strong Coupling Systems

To enhance the interaction between light and matter, it is crucial to confine light into minute spaces while simultaneously slowing it down. Plasmon resonance has been a principle used to amplify the interaction between light and matter by acting as a nanoscale optical resonator. However, their light confinement capability is limited, indicating a short phase relaxation time. Here, we explored the possibility of extending this phase relaxation time through strong coupling to long-lived excitons. Initially, estimation from the width of the far-field spectrum suggested that the spectral width of the exciton–plasmon strong coupling system narrowed compared to the plasmon bandwidth, hinting at an extension of the phase relaxation time. In the excitation spectrum measurements, we not only demonstrated the extended phase relaxation time similar to the analysis results from the far-field spectrum but also successfully highlighted the clear formation of hybrid states based on strong coupling. Ultrafast time-resolved measurements and electromagnetic simulations employing the finite-difference time-domain method further revealed the extended lifetime of the exciton–plasmon hybrid structure compared to the precoupled plasmon, foreseeing applications in nonlinear photochemical reaction fields based on enhanced electromagnetic field derived from the extension of phase relaxation time

<i>P</i>. <i>gingivalis</i> gingipains degrade JAM1 in IHGE cells.

(A) IHGE cells were infected for 1 h with P. gingivalis WT or the Δkgp ΔrgpA ΔrgpB mutant at an MOI of 100. The cells were then analyzed by immunoblotting with the indicated antibodies. (B–E) IHGE cells were transiently transfected with plasmid encoding Myc-mCherry-CLDN1 (B), Myc-mCherry-CLDN4 (C), Myc-mCherry-OCLN (D), or HA-TJP1 (E). After 48 h of incubation, cells were infected with P. gingivalis at an MOI of 100 for 1 or 3 h. The cells were then analyzed by immunoblotting with the indicated antibodies. β-actin was used as a loading control. IB, immunoblot.</p

The K134 and R234 residues are involved in degradation of JAM1 by <i>P</i>. <i>gingivalis</i> in IHGE cells.

(A) Schematic view of the JAM1 structure and derivatives. SP, IG-LIKE, or TMD domains are indicated by gray boxes. HA-tag is shown in green. The point mutations K134H and R234H are shown in magenta. (B) IHGE cells were transiently transfected with plasmid encoding HA-inserted JAM1 or the indicated JAM1 mutants. Following 48 h of incubation, the cells were infected with P. gingivalis at an MOI of 100 for 1 h, and then analyzed by immunoblotting using the indicated antibodies. (C) IHGE cells stably expressing HA-tagged JAM1 Δ (1–133) or HA-tagged JAM1 Δ (1–133) K134H R234H were infected for 1 h with P. gingivalis WT or the Δkgp ΔrgpA ΔrgpB mutant at an MOI of 100. The cells were then fixed, stained with DAPI (cyan) and anti-HA (yellow), and analyzed by immunofluorescence microscopy. Scale bars, 10 μm.</p

Confocal microscopic images of JAM1 in IHGE cells infected with <i>P</i>. <i>gingivalis</i> WT or the Δ<i>kgp</i> Δ<i>rgpA</i> Δ<i>rgpB</i> mutant.

(A) IHGE cells were infected with P. gingivalis WT or the Δkgp ΔrgpA ΔrgpB mutant at an MOI of 100 for 1.5 h. The cells were then fixed, stained with DAPI (cyan) and anti-JAM1 (yellow), and analyzed by confocal microscopy. Scale bars, 10 μm. (B, C) Schematic illustration (B) and confocal microscopic cross-sectional images (C) of the 3D-tissue model of IHGE cells. Gingival epithelial tissues on coverslips were infected with P. gingivalis WT or the Δkgp ΔrgpA ΔrgpB mutant for 2 h. The tissues were then fixed, stained with anti-JAM1 (white) and Alexa Fluor 568–conjugated phalloidin (magenta), and analyzed by confocal microscopy. Scale bars, 30 μm.</p

JAM1 is required for epithelial barrier function of IHGE cells.

(A) Schematic image of the culture insert system. Monolayer of IHGE cells stably expressing shLuc, shJAM1 #110, or shJAM1 #508 were cultured in culture inserts. FITC-labeled tracer was added to culture media in the upper compartment. Following 30 min of incubation, the transmission of tracer from the upper compartment to the lower compartment was analyzed by spectrometry. (B) JAM1 expression in IHGE cells stably expressing shLuc, shJAM1 #110, or shJAM1 #508 was analyzed by immunoblotting with the indicated antibodies. (C–I) Permeability to 40 kDa FITC-dextran (C), 3–5 kDa FITC-dextran (D), 0.5 kDa Lucifer Yellow (E), FITC–P. gingivalis LPS (F), FITC–P. gingivalis PGN (G), FITC–E. coli LPS (H), or FITC–S. aureus PGN (I) in IHGE cells expressing shLuc and shJAM1. Results are expressed as fold change relative to cells expressing shLuc and are the means ± SD of eight technical replicates. *, pt test (H, I).</p

SerB inhibits nuclear translocation of NF-κB p65 but not p105/p50.

<p>(<b>A</b>) Confocal microscopy of TIGKs transiently co-transfected with Myc (Vector) or Myc-SerB along with GFP-NF-κB p65 or GFP-NF-κB p65 S536D and left unstimulated or stimulated with TNF-α (5 ng/ml) for 30 min. Cells were fixed and stained with DAPI and anti-Myc. Bars = 5 µm. Result is representative of 3 biological replicates. (<b>B</b>) Quantification of nuclear translocation in cells in A). Results are expressed as percentage of Myc positive cells with nuclear GFP- NF-κB p65 and are the mean with SEM of three independent experiments. At least 90 Myc/GFP positive cells were counted per test. *, p<0.05. (<b>C</b>) Confocal microscopy of TIGKs transiently co-transfected with Myc (Vector) or Myc-SerB along with GFP-NF-κB p105 and left unstimulated or stimulated with TNF-α (5 ng/ml) for 30 min. Cells were fixed and stained with DAPI and anti-Myc. Bars = 5 µm. Result is representative of 3 biological replicates. (<b>D</b>) Confocal microscopy of TIGKs transiently co-transfected with Myc (Vector) or Myc-SerB along with GFP-NF-κB p50 and left unstimulated or stimulated with TNF-α (5 ng/ml) for 30 min. Cells were fixed and stained with DAPI and anti-Myc. Bars = 5 µm. Result is representative of 3 biological replicates.</p

Proposed model of how <i>P</i>. <i>gingivalis</i> gingipains send bacterial virulence factors through the gingival epithelium.

P. gingivalis gingipains degrade JAM1, which increases the permeability of gingival epithelium to gingipains and other factors. Subsequently, gingipains are transferred to the deeper epithelium to further degrade JAM1, which allows LPS and PGN to penetrate the gingival epithelium and reach subepithelial tissues. Finally, gingipains, LPS, and PGN induce inflammation in gingival tissues.</p