Mechanism of Electrochemical Delamination of Two-Dimensional Materials from Their Native Substrates by Bubbling

A capacitor-based circuit model is proposed to explain the electrochemical delamination of two-dimensional materials from their native substrates where produced gas bubbles squeeze into the interface. The delamination is actually the electric breakdown of the capacitor formed between the solution and substrate. To facilitate the procedure, the backside of the ubstrate has to be shielded so that the capacitor breakdown voltage can be reached. The screening effect can be induced either by nonreactive ions around the electrode or, more effectively, by an undetachable insulator. This mechanism serves as a guideline for the surface science and applications involving the bubbling delamination

Uremia toxin helps to induce inflammation in intestines by activating the ATM/NEMO/ NF-B signalling pathway in human intestinal epithelial cells

638-642During progressive chronic kidney disease, toxic substances known as uremic toxins accumulate in body fluids. Uremia toxin has been documented to be involved in most inflammatory reactions, and indoxyl-sulfate (IS) a major serum metabolite of uremia is a key player in this. The mechanism by which uremia toxin establishes it inflammatory activity is scarcely known; however, researchers believes that a clear understanding of this process can serve as a guide to combat the situation. The study was designed to investigate the role played by uremia toxin in intestinal inflammation. SW480 was used as cell lines for this study. Luciferase assay was used to detect the cell viability of different concentrations of IS. RT-qPCR was used to detect the effect of IS on the expression of inflammatory factors. The comet assay was used as a tool to detect DNA damage. Western blot was used to detect the phosphorylation level of ATM/NEMO/NF-kB protein. The IS of 0.09 nM was determined to be the best experimental concentration by luciferase assay. Result showed that IS promotes the expression of inflammatory factors TNF-α and IL-6. In addition, IS led to enhanced DNA damage in cells. IS promoted ATM phosphorylation leading to phosphorylation of NEMO to activate the NF-kB signalling pathway. In conclusion, uremia toxin facilitates inflammation in intestines by activating the ATM/NEMO/ NF-kB signalling pathway in human intestinal epithelial cells

Uremia toxin helps to induce inflammation in intestines by activating the ATM/NEMO/NF-kB signalling pathway in human intestinal epithelial cells

During progressive chronic kidney disease, toxic substances known as uremic toxins accumulate in body fluids. Uremia toxin has been documented to be involved in most inflammatory reactions, and indoxyl-sulfate (IS) a major serum metabolite of uremia is a key player in this. The mechanism by which uremia toxin establishes it inflammatory activity is scarcely known; however, researchers believes that a clear understanding of this process can serve as a guide to combat the situation. The study was designed to investigate the role played by uremia toxin in intestinal inflammation. SW480 was used as cell lines for this study. Luciferase assay was used to detect the cell viability of different concentrations of IS. RT-qPCR was used to detect the effect of IS on the expression of inflammatory factors. The comet assay was used as a tool to detect DNA damage. Western blot was used to detect the phosphorylation level of ATM/NEMO/NF-kB protein. The IS of 0.09 nM was determined to be the best experimental concentration by luciferase assay. Result showed that IS promotes the expression of inflammatory factors TNF-α and IL-6. In addition, IS led to enhanced DNA damage in cells. IS promoted ATM phosphorylation leading to phosphorylation of NEMO to activate the NF-kB signalling pathway. In conclusion, uremia toxin facilitates inflammation in intestines by activating the ATM/NEMO/ NF-kB signalling pathway in human intestinal epithelial cells

Identification of predictors for the comprehensive clinical risk and severity of coronary lesions of acute coronary syndrome

BackgroundAcute coronary syndrome (ACS) is the most common cause of death in patients with coronary artery disease. The aim of the study was to identify the predictors of both comprehensive clinical risk and severity of coronary lesions by comprehensive use of GRACE and SYNTAX scores in patients with ACS.MethodsClinical data of 225 ACS patients who underwent coronary angiography between 2015 and 2016 were collected. Multiple logistic regression analysis (stepwise) was used to identify the predictors. The predictive ability of predictors and the model were determined using receiver operating characteristics analyses.ResultsMultivariable logistic regression analyses showed that high aspartate aminotransferase (AST) predicted the comprehensive clinical risk with odds ratios (ORs) and 95% confidence intervals (CIs) of 1.011 (1.002–1.021). High total cholesterol (TC) and red blood cell distribution width (RDW) predicted the severity of coronary lesions with ORs and 95% CIs of 1.517 (1.148–2.004) and 1.556 (1.195–2.028), respectively. Low prealbumin predicted both severity of coronary lesions and comprehensive clinical risk of ACS patients with ORs and 95% CIs of 0.743 (0.672–0.821) and 0.836 (0.769–0.909), respectively. The model with a combination of prealbumin and AST had the highest predictive efficacy for comprehensive clinical risk, and the combination of prealbumin, TC, and RDW had the highest predictive efficacy for the severity of coronary lesions. The sensitivity and specificity, and the optimal cut-off values of these four indexes were determined.ConclusionsFour predictors for the comprehensive clinical risk and severity of coronary lesions of ACS were identified, which provided important information for the early diagnosis and appropriate treatment of ACS

Predictors for unfavorable prognosis after stroke with perforator artery disease

Background and purposePerforator artery disease (PAD) is an important subtype of ischemic stroke. The risk factors affecting the prognosis of patients with PAD are unclear. This study aimed to investigate the risk factors affecting the unfavorable prognosis of PAD.MethodsPatients with PAD were enrolled from Dushu Lake Hospital Affiliated to Soochow University and diagnosed as stroke with PAD during the period from September 2021 to July 2023 and followed up with a modified Rankin Scale (mRS) after 90 days, defining the mRS of 0–2 as a group with favorable prognosis, and 3–6 as a group with unfavorable functional outcome. Logistic regression was used to identify predictors for PAD. Multiple logistic regression analysis and receiver operating characteristics (ROC) were used to identify predictors of unfavorable prognosis.ResultsOf the 181 enrolled patients, 48 (26.5%) were identified with unfavorable prognosis. On multivariate analysis, increased age (OR = 1.076, 95% CI: 1.012 ~ 1.144, p = 0.019), higher National Institutes of Health Stroke Scale (NIHSS) score at admission (OR = 2.930, 95% CI: 1. 905 ~ 4.508, p < 0.001), and increased neutrophil-to-lymphocyte ratio (NLR) (OR = 3.028, 95% CI: 1.615 ~ 5.675, p = 0.001) were independent risk factors for unfavorable prognosis in patients with PAD, and the area under the receiver operating characteristic curve was 0.590, 0.905, and 0.798, and the multi-factor diagnostic model (Model 2) showed reliable diagnostic specificity and sensitivity (area under the curve = 0.956, p < 0.001, specificity 0.805, sensitivity 0.958, accuracy 0.845).ConclusionIncreased baseline NLR and NIHSS score and aging may be independent risk factors for unfavorable prognosis of patients with PAD. NLR can be used as a potential biological indicator to predict the prognosis of stroke with PAD

Transcriptional and Functional Analysis of the Effects of Magnolol: Inhibition of Autolysis and Biofilms in Staphylococcus aureus

BACKGROUND: The targeting of Staphylococcus aureus biofilm structures are now gaining interest as an alternative strategy for developing new types of antimicrobial agents. Magnolol (MOL) shows inhibitory activity against S. aureus biofilms and Triton X-100-induced autolysis in vitro, although there are no data regarding the molecular mechanisms of MOL action in bacteria. METHODOLOGY/PRINCIPAL FINDINGS: The molecular basis of the markedly reduced autolytic phenotype and biofilm inhibition triggered by MOL were explored using transcriptomic analysis, and the transcription of important genes were verified by real-time RT-PCR. The inhibition of autolysis by MOL was evaluated using quantitative bacteriolytic assays and zymographic analysis, and antibiofilm activity assays and confocal laser scanning microscopy were used to elucidate the inhibition of biofilm formation caused by MOL in 20 clinical isolates or standard strains. The reduction in cidA, atl, sle1, and lytN transcript levels following MOL treatment was consistent with the induced expression of their autolytic repressors lrgA, lrgB, arlR, and sarA. MOL generally inhibited or reversed the expression of most of the genes involved in biofilm production. The growth of S. aureus strain ATCC 25923 in the presence of MOL dose-dependently led to decreases in Triton X-100-induced autolysis, extracellular murein hydrolase activity, and the amount of extracellular DNA (eDNA). MOL may impede biofilm formation by reducing the expression of cidA, a murein hydrolase regulator, to inhibit autolysis and eDNA release, or MOL may directly repress biofilm formation. CONCLUSIONS/SIGNIFICANCE: MOL shows in vitro antimicrobial activity against clinical and standard S. aureus strains grown in planktonic and biofilm cultures, suggesting that the structure of MOL may potentially be used as a basis for the development of drugs targeting biofilms