Multiscale simulations of growth-dominated Sb2_2Te phase-change material for non-volatile photonic applications

Chalcogenide phase-change materials (PCMs) are widely applied in electronic and photonic applications, such as non-volatile memory and neuro-inspired computing. Doped Sb$_2$Te alloys are now gaining increasing attention for on-chip photonic applications, due to their growth-driven crystallization features. However, it remains unknown whether Sb$_2$Te also forms a metastable crystalline phase upon nanoseconds crystallization in devices, similar to the case of nucleation-driven Ge-Sb-Te alloys. Here, we carry out ab initio simulations to understand the changes in optical properties of amorphous Sb$_2$Te upon crystallization and post annealing. During the continuous transformation process, changes in the dielectric function are highly wavelength-dependent from the visible-light range towards the telecommunication band. Our finite-difference time-domain simulations based on the ab initio input reveal key differences in device output for color display and photonic memory applications upon tellurium ordering. Our work serves as an example of how multiscale simulations of materials can guide practical photonic phase-change applications.Comment: 16 pages,8 figure

Study on the Effect of the Water Injection Rate on the Cavern Leaching Strings of Salt Cavern Gas Storages

In the early construction of cavern leaching in salt cavern gas storages, the inner leaching tubing is often blocked, frequently leading to the bending deformation phenomenon of the leaching strings, which can result in out-of-control cavity shapes. It is difficult to monitor the stress, vibration, and morphological changes of the inner tube during the construction of a cavity. There are few research results in this field at home and abroad, and they are limited only to preliminary explorations of the mechanism or summaries and speculation of the field operation. In this paper, an experimental device for testing the dynamic characteristics of salt cavern leaching strings is developed based on the similarity principle. The device is used to simulate two types of operation processes, i.e., the direct and reverse circulation leaching processes. The experimental data are processed using the modal analysis method to obtain the vibration characteristic parameters of the inner leaching tubing in the circulation process with identical flow rates inside the tubing and the annular region. The following main conclusions can be drawn: The circulation mode has no significant effect on the vibration frequency of cavern leaching strings. The deformation characteristics of cavern leaching strings during direct and reverse circulation are identical, featuring maximum deformation at the bottom and minimum deformation in the middle. The maximum deformation of cavern leaching strings during reverse circulation is about 1.5 times that during direct circulation. Through an experimental investigation and analysis, the effects of the water injection rate and the cavern leaching method on the vibration frequency and bending deformation of cavern leaching strings was determined, providing a reference for further solving the bending problem of cavern leaching strings in combination with engineering practice

SKF96365 and 2-APB reduce Ca2+ influx and HMGB1-induced permeability.

<p>EA.hy926 cells were preincubated with 1, 5, 10 μM SKF96365 (A), or 10, 30, 50 μM 2-APB(B) or vehicle (DMSO), then stimulated with 200 ng/ml HMGB1, followed by the addition of 2 mM CaCl2. Intracellular calcium transients were measured using an Olympus FV1000 confocal microscope. Peak intracellular Ca2+ was quantified during intracellular release or extracellular Ca2+ influx. EA.hy926 cells were plated in the upper part of transwell chambers until the formation of a tight monolayer. The cells were preincubated with 1, 5, 10, 20 μM SKF96365 (C), or 10, 30, 50, 70 μM 2-APB (D) for 1 h, respectively. HMGB1 200 ng/ml was then added and the cells were incubated for an additional 24 h. After incubation, the integrity of the tight junctions was assessed by measuring the TER. Data are presented as mean ± SD of three independent experiments. *Indicates significant difference compared with the control group (P<0.05).</p

STIM1 knockdown decreases Ca2+ influx, HMGB1-induced permeability and Src phosphorylation.

<p>A. STIM1 protein expression after RNA inference. EA.hy926 cells were transfected for 48 h with STIM1 siRNA-1, siRNA-2 or control (scrambled) siRNA. Cells were harvested and total protein was extracted and subjected to western blotting with anti-STIM1 antibodies, with anti-GAPDH antibodies as a loading control. STIM1 expression was quantified and analyzed statistically based on three independent experiments. Transfected cells were also stimulated with 200 ng/ml HMGB1 (B) or 1 μM TG (C), followed by the addition of 2 mM CaCl2. Intracellular calcium transients were measured using an Olympus FV1000 confocal microscope. Peak intracellular Ca2+ was quantified during intracellular release or extracellular Ca2+ influx. D. HMGB1-induced permeability was inhibited by STIM1 knockdown. EA.hy926 cells were plated in the upper part of transwell chambers until the formation of a tight monolayer, then transfected with STIM1 siRNA-1, siRNA-2 or control (scrambled) siRNA. HMGB1 200 ng/ml was added and cells were incubated for an additional 24 h. After incubation, endothelial permeability was assessed, as described above. E. Representative immunoblots showing that STIM1 knockdown inhibits Src activation. Transfected cells were treated with or without 200 ng/ml HMGB1 for 2 h. Cell lysates were analyzed by SDS-PAGE followed by western blotting using antibodies against phosphorylated Src and Src. Data are presented as mean ± SD of three independent experiments. *Indicates significant difference compared with the control group (P<0.05).</p

Disruption of VE-cadherin and intercellular gap formation in HMGB1-treated EA.hy926 cells.

<p>A. Representative immunoblots showing reduced expression of VE-cadherin protein by HMGB1. Total and cell membrane VE-cadherin protein levels were measured by western blotting in EA.hy926 cells treated with HMGB1 for 6, 12, 24 and 48 h, respectively. GAPDH and Na,K-ATPase α1 were used as loading controls for intact cells and plasma membranes, respectively. Western blots were quantified and analyzed statistically based on three independent experiments. *Indicates significant difference compared with wild-type group (P<0.05). B. HMGB1 increased intercellular gap formation. EA.hy926 cells were plated onto a Petri dish until the formation of a tight monolayer then treated with 200 ng/ml HMGB1 for 6, 12 and 24 h, respectively. The cells were fixed and distribution of VE-cadherin was detected using rabbit anti-human VE-cadherin antibody and FITC-labeled goat anti-rabbit antibody. Nuclei were stained with DAPI. Red arrows indicate intercellular gaps. A merged picture is shown for each condition. A representative field for each condition was captured using an Olympus FV1000 confocal microscope. Scale bar = 10 μm.</p

HMGB1 induces Src activation.

<p>A. Representative immunoblots showing HMGB1-induced Src activation. EA.hy926 cells were treated with 200 ng/ml HMGB1 for 1, 2, 3 and 4h, respectively. Cell lysates were analyzed by SDS-PAGE followed by western blotting using antibodies against phosphorylated Src and Src. B. PP2 and CGP77675 inhibit HMGB1-induced permeability. EA.hy926 cells were plated in the upper part of transwell chambers until the formation of a tight monolayer. The cells were preincubated with 1, 2.5, 5, 10 or 20μM PP2 (upper) or 0.5, 1, 2.5, 5 or 10 μM CGP77675 (lower) for 1 h, respectively. HMGB1 200 ng/ml was then added and the cells were incubated for an additional 24 h. After incubation, the integrity of the tight junctions was assessed by measuring the TER. Representative immunoblots showing that PP2 (C) and CGP77675 (D) decreased HMGB1-induced Src phosphorylation. Cells were preincubated with 1, 2.5, 5, or 10μM PP2 or 0.5, 1, 2.5 or 10 μM CGP77675 for 1 h, respectively. 200 ng/ml HMGB1 was then added and cells were incubated for an additional 24h. Cell lysates were analyzed by SDS-PAGE followed by western blotting using antibodies against phosphorylated Src and Src. GAPDH was used as a loading control. Western blots were quantified and analyzed statistically based on three independent experiments. Data are presented as mean ± SD of three independent experiments. *Indicates significant difference compared with the control group (P<0.05).</p

HMGB1 increases endothelial cell permeability.

<p>A. HMGB1-induced TEER decrease. EA.hy926 cells cultured on transwell filters were incubated for 3, 6, 12, 24, 36 and 48h, respectively, with or without 50, 100, 200 and 400 ng/ml HMGB1. The integrity of the tight junctions was assessed by measuring the TER. B. Cell viability in the cells treated by HMGB1. EA.hy926 cells were treated with 50, 100, 200, 400 and 800ng/ml HMGB1, respectively, for 24 h. The cell viability was measured by CCK-8 assay. Data are presented as mean ± SD of three independent experiments. *Indicates significant difference compared with the control group (P<0.05).</p

Variations in pleural microbiota and metabolic phenotype associated with malignant pleural effusion in human lung adenocarcinoma

Abstract Background Lung cancer is the most common cancer‐related death worldwide. In 2022, the number of daily deaths of lung cancer was estimated to reach around 350 in the United States. Lung adenocarcinoma is the main subtype of lung cancer and patients with malignant pleural effusion (MPE) suffer from poor prognosis. Microbiota and its metabolites are associated with cancer progression. However, the effect of pleural microbiota on pleural metabolic profile of MPE in lung adenocarcinoma patients remains largely unknown. Methods Pleural effusion samples collected from lung adenocarcinoma patients with MPE (n = 14) and tuberculosis pleurisy patients with benign pleural effusion (BPE group, n = 10) were subjected to microbiome (16S rRNA gene sequencing) and metabolome (liquid chromatography tandem mass spectrometry [LC‐MS/MS]) analyses. The datasets were analyzed individually and integrated for combined analysis using various bioinformatic approaches. Results The metabolic profile of MPE in lung adenocarcinoma patients were clearly distinguished from BPE with 121 differential metabolites across six significantly enriched pathways identified. Glycerophospholipids, fatty and carboxylic acids, and derivatives were the most common differential metabolites. Sequencing of microbial data revealed nine significantly enriched genera (i.e., Staphylococcus, Streptococcus, Lactobacillus) and 26 enriched ASVs (i.e., species Lactobacillus_delbrueckii) in MPE. Integrated analysis correlated MPE‐associated microbes with metabolites, such as phosphatidylcholine and metabolites involved in the citrate cycle pathway. Conclusion Our results provide substantial evidence of a novel interplay between the pleural microbiota and metabolome, which was drastically perturbed in MPE in lung adenocarcinoma patients. Microbe‐associated metabolites can be used for further therapeutic explorations