Investigation of degradation caused by charge trapping at etching-stop layer under AC gate-bias stress for InGaZnO thin film transistors

A great amount of literatures has been focusing on bias-induced instability issues including threshold voltage shift (ΔVt ) and subthreshold swing (S.S) degradations [1]. However, in practical TFT operation circuits, very limited knowledge could be applied since operation modes are mostly applied with alternative current (AC). Based on these backgrounds, in this work, Indium-Gallium-Zinc-Oxide Thin Film Transistors (IGZO TFTs) are applied with AC PBS degradations. Compared with previous work, this work observed a structure dependent degradation. An etch-stop structure IGZO TFT observed a serious threshold voltage shift after AC stress but shown great stability after direct current (DC) stress. The device structure and transfer characteristic curves are demonstrated in Figure 1(a) and (b) respectively. From results of DC PBS/NBS, a favorable stability indicating a great quality of gate insulator. Therefore, the positive threshold voltage shift is believed to be origin from electron trapping at the etching stop layer (ESL), since ESL possesses a relatively poor quality compared to the gate insulator. The charge trapping at etching stop layer could be confirmed by results of asymmetric source/drain metal under AC stress, illustrated in Figure 1(c). Please click Additional Files below to see the full abstract

Effect of different a-InGaZnO TFTs channel thickness upon self-heating stress

In this work, Indium-Galium-Zinc-Oxide Thin Film Transistors (IGZO TFTs) with different channel thickness has been compared after self-heating stress (SHS). In previous literatures, self-heating of TFTs has been widely discussed and Joule Heat caused during driving TFTs has been compared with different channel length and width [1]. However, different channel thickness hasn’t been investigated. Although TFTs with a larger channel thickness possess a greater drain current, a less degradation is observed when comparing with small channel thickness structures, demonstrated in Figure 1(a). The ΔVt shift in the transfer characteristics are well described by the stretched-exponential equation. The Eτ value, which is the average effective barrier height for electron transport, is extracted in Figure (b). Results has shown that in the thick IGZO TFTs, the value is almost twice of that in the thin IGZO TFTs. From COMSOL simulations demonstrated in Figure 1(c), in could be noticed that different channel thickness effects the electrical field locating at the gate insulator. Therefore, a model is proposed to explain the degradation difference, illustrated in Figure (4). Please click Additional Files below to see the full abstract

Wearable multi-channel microelectrode membranes for elucidating electrophysiological phenotypes of injured myocardium

Understanding the regenerative capacity of small vertebrate models has provided new insights into the plasticity of injured myocardium. Here, we demonstrate the application of flexible microelectrode arrays (MEAs) in elucidating electrophysiological phenotypes of zebrafish and neonatal mouse models of heart regeneration. The 4-electrode MEA membranes were designed to detect electrical signals in the aquatic environment. They were micro-fabricated to adhere to the non-planar body surface of zebrafish and neonatal mice. The acquired signals were processed to display an electrocardiogram (ECG) with high signal-to-noise-ratios, and were validated via the use of conventional micro-needle electrodes. The 4-channel MEA provided signal stability and spatial resolution, revealing the site-specific electrical injury currents such as ST-depression in response to ventricular cryo-injury. Thus, our polymer-based and wearable MEA membranes provided electrophysiological insights into long-term conduction phenotypes for small vertebral models of heart injury and regeneration with a translational implication for monitoring cardiac patients

Cytokine Profile in Plasma Extracellular Vesicles of Parkinson's Disease and the Association with Cognitive Function

Plasma extracellular vesicles (EVs) containing various molecules, including cytokines, can reflect the intracellular condition and participate in cell-to-cell signaling, thus emerging as biomarkers for Parkinson’s disease (PD). Inflammation may be a crucial risk factor for PD development and progression. The present study investigated the role of plasma EV cytokines as the biomarkers of PD. This cross-sectional study recruited 113 patients with PD, with mild to moderate stage disease, and 48 controls. Plasma EVs were isolated, and the levels of cytokines, including pro-interleukin (IL)-1β, IL-6, IL-10, tumor necrosis factor (TNF)-α, and transforming growth factor (TGF)-β1, were evaluated. Patients with PD had significantly increased plasma EV pro-IL-1β and TNF-α levels compared with controls after adjustment for age and sex. Despite the lack of a significant association between plasma EV cytokines and motor symptom severity in patients with PD, cognitive dysfunction severity, assessed using the Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment, was significantly associated with plasma EV pro-IL-1β, IL-6, IL-10, and TNF-α levels. This association was PD specific and not found in controls. Furthermore, patients with PD cognitive deficit (MMSE < 26) exhibited a distinguished EV cytokine profile compared to those without cognitive deficit. The findings support the concept of inflammatory pathogenesis in the development and progression of PD and indicate that plasma EV cytokines may serve as PD biomarkers in future

Fucosyltransferase 1 and 2 play pivotal roles in breast cancer cells.

FUT1 and FUT2 encode alpha 1, 2-fucosyltransferases which catalyze the addition of alpha 1, 2-linked fucose to glycans. Glycan products of FUT1 and FUT2, such as Globo H and Lewis Y, are highly expressed on malignant tissues, including breast cancer. Herein, we investigated the roles of FUT1 and FUT2 in breast cancer. Silencing of FUT1 or FUT2 by shRNAs inhibited cell proliferation in vitro and tumorigenicity in mice. This was associated with diminished properties of cancer stem cell (CSC), including mammosphere formation and CSC marker both in vitro and in xenografts. Silencing of FUT2, but not FUT1, significantly changed the cuboidal morphology to dense clusters of small and round cells with reduced adhesion to polystyrene and extracellular matrix, including laminin, fibronectin and collagen. Silencing of FUT1 or FUT2 suppressed cell migration in wound healing assay, whereas FUT1 and FUT2 overexpression increased cell migration and invasion in vitro and metastasis of breast cancer in vivo. A decrease in mesenchymal like markers such as fibronectin, vimentin, and twist, along with increased epithelial like marker, E-cadherin, was observed upon FUT1/2 knockdown, while the opposite was noted by overexpression of FUT1 or FUT2. As expected, FUT1 or FUT2 knockdown reduced Globo H, whereas FUT1 or FUT2 overexpression showed contrary effects. Exogenous addition of Globo H-ceramide reversed the suppression of cell migration by FUT1 knockdown but not the inhibition of cell adhesion by FUT2 silencing, suggesting that at least part of the effects of FUT1/2 knockdown were mediated by Globo H. Our results imply that FUT1 and FUT2 play important roles in regulating growth, adhesion, migration and CSC properties of breast cancer, and may serve as therapeutic targets for breast cancer

The nucleolar protein NIFK promotes cancer progression via CK1α/β-catenin in metastasis and Ki-67-dependent cell proliferation.

Nucleolar protein interacting with the FHA domain of pKi-67 (NIFK) is a Ki-67-interacting protein. However, its precise function in cancer remains largely uninvestigated. Here we show the clinical significance and metastatic mechanism of NIFK in lung cancer. NIFK expression is clinically associated with poor prognosis and metastasis. Furthermore, NIFK enhances Ki-67-dependent proliferation, and promotes migration, invasion in vitro and metastasis in vivo via downregulation of casein kinase 1α (CK1α), a suppressor of pro-metastatic TCF4/β-catenin signaling. Inversely, CK1α is upregulated upon NIFK knockdown. The silencing of CK1α expression in NIFK-silenced cells restores TCF4/β-catenin transcriptional activity, cell migration, and metastasis. Furthermore, RUNX1 is identified as a transcription factor of CSNK1A1 (CK1α) that is negatively regulated by NIFK. Our results demonstrate the prognostic value of NIFK, and suggest that NIFK is required for lung cancer progression via the RUNX1-dependent CK1α repression, which activates TCF4/β-catenin signaling in metastasis and the Ki-67-dependent regulation in cell proliferation

Plasma lipoprotein subfraction concentrations are associated with lipid metabolism and age-related macular degeneration

10.1194/jlr.M073684Journal of Lipid Research5891785-179

INFLUENCE OF APPROACH SPEED AND DISTANCE ON BIOMECHANICS DURING SINGLE-LEGGED RUNNING VERTICAL JUMP

The purpose of this study was to look into the kinematics, kinetics and EMG of the single legged running vertical jumps in different approach speed and distance. 12 basketball player performed single-legged running vertical jumps with 2 approach speed and 3 distance randomly. Kinematic and Kinetic data were collected by a force and 11 infrared high speed cameras. EMG data were recorded by Delsys surface EMG system. Two-way repeated measures AMOVA (2 speeds x 3 distance) was used for establishing differences (significance level p< .05). The jump height, jumt moment of lower extremity, knee power and the activation of tibialis anterior and gastrocnemius were found significantly larger in fast approach speed. We suggested using fast approach speed and 9m approach distance to enhance the single-legged running vertical jump ability

Small-Size Humanoid Soccer Robot Design for FIRA HuroSot

Non

Relatively preserved functional immune capacity with standard COVID-19 vaccine regimen in people living with HIV

IntroductionPeople living with HIV (PLWH) are at a higher risk of severe disease with SARS-CoV-2 virus infection. COVID-19 vaccines are effective in most PLWH. However, suboptimal immune responses to the standard two-shot regimen are a concern, especially for those with moderate to severe immunodeficiency. An additional dose is recommended as part of the extended primary series in Taiwan. Herein, we study the efficacy of this additional shot in PLWH with mild immunodeficiency compared to that in healthy non-HIV people.MethodsIn total, 72 PLWH that were asymptomatic or with mild immunodeficiency (CD4 counts ≥200/mm3) and suppressed virology, and 362 healthcare workers of our hospital were enrolled. None of the participants had a history of SARS-CoV-2 infection. They received mRNA-1273 and ChAdOx1 vaccines. Anti-SARS-CoV-2 neutralizing and anti-Spike IgG antibodies, and SARS-CoV-2-specific T cell responses were evaluated.ResultsThe standard two-shot regimen elicited lower responses in PLWH than the healthcare workers without HIV infection, although the difference was statistically insignificant. They had comparable levels of neutralizing and anti-Spike antibodies and comparable effector CD4+ and CD8+ T cell responses. The third shot boosted the SARS-CoV-2 immunity significantly more with better antibody responses and higher IFN-γ and IL-2 responses of the CD4+ and CD8+ T cells in PLWH compared to those without HIV. Upon in vitro stimulation with extracted Wuhan strain SARS-CoV-2 proteins, CD8+ T cells from PLWH after 3 shots had more durable effector responses than the non-HIV controls with extended time of stimulation.ConclusionThis subtle difference between PLWH and non-HIV people implied immune exhaustion with two shots in non-HIV people. Slightly compromised immunity in PLWH indeed preserved the functional capacity for further response to the third shot or natural infection