Intermixing during Epitaxial Growth of van der Waals Bonded Nominal GeTe/Sb₂Te₃ Superlattices

In the present work, GeTe and Sb₂Te₃ van der Waals bonded superlattices epitaxially grown by molecular beam epitaxy are investigated. These structures are grown on passivated Si substrates, resulting in one single epitaxial domain and its twinned domain, both sharing the same out-of-plane orientation. Supported by X-ray diffraction and Raman spectroscopy, attention is called to the thermodynamically driven tendency of GeTe and Sb₂Te₃ to intermix into a Ge–Sb–Te (GST) alloy at the interfaces. A growth model is proposed to explain how these GST structures are formed

Toward Truly Single Crystalline GeTe Films: The Relevance of the Substrate Surface

The growth of GeTe thin films on a Si(111)-(√3 × √3)­R30°-Sb surface is reported. At growth onset, the rapid formation of fully relaxed crystalline GeTe(0001)-(1 × 1) is observed. During growth, a GeTe(0001)-(√3 × √3)­R30° surface reconstruction is also detected. Indeed, density functional theory (DFT) simulations indicate that the reconstructed GeTe(0001)-(√3 × √3)­R30° structure is energetically competing with the GeTe(0001)-(1 × 1) reconstruction. The out-of-plane α-GeTe<0001>||Si<111> and in-plane α-GeTe<−1010>||Si<−211> epitaxial relationships are confirmed by X-ray diffraction (XRD). Suppression of rotational twist and reduction of twinned domains are achieved. The formation of rotational domains in GeTe grown on Si(111)-(7 × 7) is explained by domain matched coincidence lattice formation with the Si(111)-(1 × 1) surface. Atomic force microscopy (AFM) images show the coalescence of well-oriented islands with subnanometer roughness on their top part. van der Pauw measurements are performed to verify the electric properties of the films. The quality of epitaxial GeTe thin film is discussed and related to the crystalline structure of GeTe and its rhombohedrally distorted resonant bonds

Surface Reconstruction-Induced Coincidence Lattice Formation Between Two-Dimensionally Bonded Materials and a Three-Dimensionally Bonded Substrate

Sb₂Te₃ films are used for studying the epitaxial registry between two-dimensionally bonded (2D) materials and three-dimensional bonded (3D) substrates. In contrast to the growth of 3D materials, it is found that the formation of coincidence lattices between Sb₂Te₃ and Si(111) depends on the geometry and dangling bonds of the reconstructed substrate surface. Furthermore, we show that the epitaxial registry can be influenced by controlling the Si(111) surface reconstruction and confirm the results for ultrathin films

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<p>The mechanisms by which vitamins regulate immunity and their effect as an adjuvant treatment for tuberculosis have gradually become very important research topics. Studies have found that vitamin B5 (VB5) can promote epithelial cells to express inflammatory cytokines. We aimed to examine the proinflammatory and antibacterial effect of VB5 in macrophages infected with Mycobacterium tuberculosis (MTB) strain H37Rv and the therapeutic potential of VB5 in vivo with tuberculosis. We investigated the activation of inflammatory signal molecules (NF-κB, AKT, JNK, ERK, and p38), the expression of two primary inflammatory cytokines (tumor necrosis factor and interleukin-6) and the bacterial burdens in H37Rv-infected macrophages stimulated with VB5 to explore the effect of VB5 on the inflammatory and antibacterial responses of macrophages. We further treated the H37Rv-infected mice with VB5 to explore VB5’s promotion of the clearance of H37Rv in the lungs and the effect of VB5 on regulating the percentage of inflammatory cells. Our data showed that VB5 enhanced the phagocytosis and inflammatory response in macrophages infected with H37Rv. Oral administration of VB5 decreased the number of colony-forming units of H37Rv in lungs of mice at 1, 2, and 4 weeks after infection. In addition, VB5 regulated the percentage of macrophages and promoted CD4⁺ T cells to express interferon-γ and interleukin-17; however, it had no effect on the percentage of polymorphonuclear neutrophils, CD4⁺ and CD8⁺ T cells. In conclusion, VB5 significantly inhibits the growth of MTB by regulating innate immunity and adaptive immunity.</p