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Barium titanate (BaTiO3) is a promising material for silicon-integrated photonics due to its large electro-optical coefficients, low loss, high refractive index, and fast response speed. Several deposition methods have been employed to synthesize BaTiO3 films. Magnetron sputtering is one of these methods, which offers specific advantages for growing large-scale films. However, there is a scarcity of studies investigating the effect of sputtering target density on the quality of BaTiO3 films. Therefore, this study aims to uncover the effect of sputtering targets on the crystal and electronic structures of epitaxial BaTiO3 thin films. Two BaTiO3 ceramic targets were sintered at different densities by altering the sintering temperatures. The crystal structure and chemical composition of the targets were then characterized using X-ray diffraction, Raman spectroscopy, and scanning electron microscopy with energy-dispersive X-ray spectroscopy. Subsequently, BaTiO3 epitaxial films were grown by magnetron sputtering using these two targets. The crystal and electronic structures of the BaTiO3 films were analyzed using high-resolution X-ray diffraction, X-ray photoemission spectroscopy, atomic force microscopy, and spectroscopic ellipsometry. Notably, the BaTiO3 films grown with high-density targets show superior quality but contain oxygen vacancies, whereas those films synthesized with low-density targets display high surface roughness. These findings provide insights into the effect of sputtering target density on the crystal and electronic structures of epitaxial BaTiO3 thin films. [ABSTRACT FROM AUTHOR]

Compressive stress in glass‐to‐metal seals is crucial to ensure sealing quality and service reliability. Photoluminescence spectroscopy (PS), which relies on the piezospectroscopic effect of Cr‐doped α‐Al2O3, shows promise for stress detection owing to its rapid detection, non‐destruction, and high resolution. The premise of the PS technique is to fill a glass matrix with alumina particles and detect signals from the alumina. In this study, the interaction between alumina particles and the glass matrix was analyzed to calibrate the measured stresses and investigate the stress state in the glass. Test results for glass‐to‐metal seals are believed to consist of simultaneous internal residual stress and external applied stress. The internal residual stress is formed due to the coefficient of thermal expansion mismatch between glass and alumina and is assumed to transfer by radial compression. In the experiment, it was detected by the PS technique and verified by X‐ray diffraction using an unstressed sample without metal housing. The external applied stress is formed due to metal housing compaction and possibly transferred by the shear effect. The stress distribution within the pre‐stressed sample containing metal housing was also measured by the PS technique. Then, calibrations were conducted on the measured stresses based on the deduced stress transfer relationships. Finally, finite element models were established to simulate the internal residual stress and external applied stress respectively to prove the validity of the calibration method, and mutually anastomotic results were obtained within the target margin of error. [ABSTRACT FROM AUTHOR]

Tregs restrain both the innate and adaptive immune systems to maintain homeostasis. Allergic airway inflammation, characterized by a Th2 response that results from a breakdown of tolerance to innocuous environmental antigens, is negatively regulated by Tregs. We previously reported that prostaglandin I2 ([PGI.sub.2]) promoted immune tolerance in models of allergic inflammation; however, the effect of [PGI.sub.2] on Treg function was not investigated. Tregs from mice deficient in the [PGI.sub.2] receptor IP (IP KO) had impaired suppressive capabilities during allergic airway inflammatory responses compared with mice in which [PGI.sub.2] signaling was intact. IP KO Tregs had significantly enhanced expression of immunoglobulin-like transcript 3 (ILT3) compared with WT Tregs, which may contribute to the impairment of the IP KO Treg's ability to suppress Th2 responses. Using fate-mapping mice, we reported that [PGI.sub.2] signaling prevents Treg reprogramming toward a pathogenic phenotype. [PGI.sub.2] analogs promoted the differentiation of naive T cells to Tregs in both mice and humans via repression of [beta]-catenin signaling. Finally, a missense variant in IP in humans was strongly associated with chronic obstructive asthma. Together, these data support that [PGI.sub.2] signaling licenses Treg suppressive function and that [PGI.sub.2] is a therapeutic target for enhancing Treg function., Introduction Tregs are important components of the adaptive immune system that promote tolerance, prevent the development of autoimmune diseases, and suppress inflammation (1, 2). Tregs are characterized by their expression [...]

Background: Group 2 innate lymphoid cells (ILC2) are stimulated by IL‐33 to increase IL‐5 and IL‐13 production and airway inflammation. While sex hormones regulate airway inflammation, it remained unclear whether estrogen signaling through estrogen receptor‐α (ER‐α, Esr1) or ER‐β (Esr2) increased ILC2‐mediated airway inflammation. We hypothesize that estrogen signaling increases allergen‐induced IL‐33 release, ILC2 cytokine production, and airway inflammation. Methods: Female Esr1‐/‐, Esr2‐/‐, wild‐type (WT), and IL33fl/fleGFP mice were challenged with Alternaria extract (Alt Ext) or vehicle for 4 days. In select experiments, mice were administered tamoxifen or vehicle pellets for 21 days prior to challenge. Lung ILC2, IL‐5 and IL‐13 production, and BAL inflammatory cells were measured on day 5 of Alt Ext challenge model. Bone marrow from WT and Esr1‐/‐ female mice was transferred (1:1 ratio) into WT female recipients for 6 weeks followed by Alt Ext challenge. hBE33 cells and normal human bronchial epithelial cells (NHBE) were pretreated with 17β‐estradiol (E2), propyl‐pyrazole‐triol (PPT, ER‐α agonist), or diarylpropionitrile (DPN, ER‐β agonist) before allergen challenge to determine IL‐33 gene expression and release, extracellular ATP release, DUOX‐1 production, and necrosis. Results: Alt Ext challenged Esr1‐/‐, but not Esr2‐/‐, mice had decreased IL‐5 and IL‐13 production, BAL eosinophils, and IL‐33 release compared to WT mice. Tamoxifen decreased IL‐5 and IL‐13 production and BAL eosinophils. IL‐33eGFP + epithelial cells were decreased in Alt Ext challenged Esr1‐/‐ mice compared to WT mice. 17β‐E2 or PPT, but not DPN, increased IL‐33 gene expression, release, and DUOX‐1 production in hBE33 or NHBE cells. Conclusion: Estrogen receptor ‐α signaling increased IL‐33 release and ILC2‐mediated airway inflammation. [ABSTRACT FROM AUTHOR]

In this paper, we investigate the exponentially incremental dissipativity for nonlinear stochastic switched systems by using the designed state-dependent switching law and multiple Lyapunov functions approach. Specifically, using incremental supply rate as well as a state dissipation inequality in expectation, a stochastic version of exponentially incremental dissipativity is presented. The sufficient conditions for nonlinear stochastic switched systems to be exponentially incrementally dissipative are given by the designed state-dependent switching law. Furthermore, the extended Kalman–Yakubovich–Popov conditions are derived by using two times continuously differentiable storage functions. Moreover, the incremental stability conditions in probability for nonlinear stochastic switched systems are derived based on exponentially incremental dissipativity. The exponentially incremental dissipativity is preserved for the feedback-interconnected nonlinear stochastic switched systems with the composite state-dependent switching law; meanwhile, the incremental stability in probability is preserved under some certain conditions. A numerical example is given to illustrate the validity of our results. [ABSTRACT FROM AUTHOR]