Robust Heteroepitaxial Growth of GaN Formulated on Porous TiN Buffer Layers

Gallium nitride (GaN) heteroepitaxial growth is widely studied as a semiconductor material due to its various benefits. Especially, development of a buffer layer between GaN and the substrate verifies to be an effective strategy to reduce high threading dislocation density. However, the buffer layer often impedes strong adhesion between the epilayer and foreign substrate because thermally induced residual stress often causes delamination of the epilayer during fabrication. Here, we developed a robust GaN heteroepitaxy employing a porous buffer layer formulated by hydride vapor phase epitaxy. A sufficiently low but completely coated thin Ti layer was deposited on the sapphire substrate, which led to a rough and porous TiN layer after nitridation. This porous structure enables the penetration of the GaN source into the porous structure, allowing GaN epitaxy initiation throughout the TiN layer. As a result, GaN crystal growth can fill the porous area during the GaN heteroepitaxy. Integrated visualization demonstrated that the voids were successfully removed by GaN infiltration, enabling the heteroepitaxial structure to show little deformation, confirmed by multiple indentations. Last, the void-free GaN heteroepitaxy with the porous TiN buffer layer displayed robust adhesion after delamination tests

Robust Heteroepitaxial Growth of GaN Formulated on Porous TiN Buffer Layers

Gallium nitride (GaN) heteroepitaxial growth is widely studied as a semiconductor material due to its various benefits. Especially, development of a buffer layer between GaN and the substrate verifies to be an effective strategy to reduce high threading dislocation density. However, the buffer layer often impedes strong adhesion between the epilayer and foreign substrate because thermally induced residual stress often causes delamination of the epilayer during fabrication. Here, we developed a robust GaN heteroepitaxy employing a porous buffer layer formulated by hydride vapor phase epitaxy. A sufficiently low but completely coated thin Ti layer was deposited on the sapphire substrate, which led to a rough and porous TiN layer after nitridation. This porous structure enables the penetration of the GaN source into the porous structure, allowing GaN epitaxy initiation throughout the TiN layer. As a result, GaN crystal growth can fill the porous area during the GaN heteroepitaxy. Integrated visualization demonstrated that the voids were successfully removed by GaN infiltration, enabling the heteroepitaxial structure to show little deformation, confirmed by multiple indentations. Last, the void-free GaN heteroepitaxy with the porous TiN buffer layer displayed robust adhesion after delamination tests

Robust Heteroepitaxial Growth of GaN Formulated on Porous TiN Buffer Layers

Gallium nitride (GaN) heteroepitaxial growth is widely studied as a semiconductor material due to its various benefits. Especially, development of a buffer layer between GaN and the substrate verifies to be an effective strategy to reduce high threading dislocation density. However, the buffer layer often impedes strong adhesion between the epilayer and foreign substrate because thermally induced residual stress often causes delamination of the epilayer during fabrication. Here, we developed a robust GaN heteroepitaxy employing a porous buffer layer formulated by hydride vapor phase epitaxy. A sufficiently low but completely coated thin Ti layer was deposited on the sapphire substrate, which led to a rough and porous TiN layer after nitridation. This porous structure enables the penetration of the GaN source into the porous structure, allowing GaN epitaxy initiation throughout the TiN layer. As a result, GaN crystal growth can fill the porous area during the GaN heteroepitaxy. Integrated visualization demonstrated that the voids were successfully removed by GaN infiltration, enabling the heteroepitaxial structure to show little deformation, confirmed by multiple indentations. Last, the void-free GaN heteroepitaxy with the porous TiN buffer layer displayed robust adhesion after delamination tests

Robust Heteroepitaxial Growth of GaN Formulated on Porous TiN Buffer Layers

Gallium nitride (GaN) heteroepitaxial growth is widely studied as a semiconductor material due to its various benefits. Especially, development of a buffer layer between GaN and the substrate verifies to be an effective strategy to reduce high threading dislocation density. However, the buffer layer often impedes strong adhesion between the epilayer and foreign substrate because thermally induced residual stress often causes delamination of the epilayer during fabrication. Here, we developed a robust GaN heteroepitaxy employing a porous buffer layer formulated by hydride vapor phase epitaxy. A sufficiently low but completely coated thin Ti layer was deposited on the sapphire substrate, which led to a rough and porous TiN layer after nitridation. This porous structure enables the penetration of the GaN source into the porous structure, allowing GaN epitaxy initiation throughout the TiN layer. As a result, GaN crystal growth can fill the porous area during the GaN heteroepitaxy. Integrated visualization demonstrated that the voids were successfully removed by GaN infiltration, enabling the heteroepitaxial structure to show little deformation, confirmed by multiple indentations. Last, the void-free GaN heteroepitaxy with the porous TiN buffer layer displayed robust adhesion after delamination tests

Discovery and Biosynthesis of Imidazolium Antibiotics from the Probiotic <i>Bacillus licheniformis</i>

Antibiotic resistance is one of the world’s most urgent public health problems, and novel antibiotics to kill drug-resistant bacteria are needed. Natural product-derived small molecules have been the major source of new antibiotics. Here we describe a family of antibacterial metabolites isolated from a probiotic bacterium, Bacillus licheniformis. A cross-streaking assay followed by activity-guided isolation yielded a novel antibacterial metabolite, bacillimidazole G, which possesses a rare imidazolium ring in the structure, showing MIC values of 0.7–2.6 μg/mL against human pathogenic Gram-positive and Gram-negative bacteria including methicillin-resistant Staphylococcus aureus (MRSA) and a lipopolysaccharide (LPS)-lacking Acinetobacter baumannii ΔlpxC. Bacillimidazole G also lowered MICs of colistin, a Gram-negative antibiotic, up to 8-fold against wild-type Escherichia coli MG1655 and A. baumannii. We propose a biosynthetic pathway to the characterized metabolites based on precursor-feeding studies, a chemical biological approach, biomimetic total synthesis, and a biosynthetic gene knockout method

Ordered Arrays of ZnO Nanorods Grown on Periodically Polarity-Inverted Surfaces

Periodically polarity inverted (PPI) ZnO templates were fabricated using molecular beam epitaxy by employing MgO buffer layers. The polarity of ZnO film was controlled by the transformation of crystal structure from hexagonal to rocksalt due to the thickness of the MgO buffer layers. The polarity of ZnO in the PPI template was confirmed by AFM and PRM measurement. Higher growth rate and lower current value under positive supplied voltage in the region of Zn-polar were measured with comparing to that of O-polar. Holographic lithographic technique was employed for the realization of submicron pattern of periodical inverted polar ZnO over large area. After reaction using a carbothermal reduction, spatially well-separated ZnO nanorods with pitch of submicron were only observed in the Zn-polar regions. The possible reason for the difference of surface characteristics was considered as being due to the configuration of dangling bonds according to polarity

Additional file 1 of Ninjurin1 drives lung tumor formation and progression by potentiating Wnt/β-Catenin signaling through Frizzled2-LRP6 assembly

Additional file 1

AKAP12 KO mice showed leakage from the lesion with abnormal morphology of the fibrotic scar.

<p>(A) Evans blue extravasation assay. Significant differences between the WT and AKAP12 KO mice were observed from day 14 after injury. Scale bar: 2 mm (LC: lesion core, PL: peri-lesion) (B) Evans blue was extracted from the brain tissue, and the amount of Evans blue was quantitatively analyzed by measuring the OD (mean ± S.D.; n = 4 mice per WT and KO at each time point; P**<0.01, P#<0.001). (C) The lesion site of the WT mouse was tightly separated with the normal tissue on day 14 and 21 after injury without any leakage. However, the AKAP12 KO mice showed an unclear boundary between the lesion site and normal tissue with a dispersion of Evans blue. Scale bar: 1 mm.</p

AKAP12 is highly expressed in the fibrotic scar surrounding the lesion in the process of CNS repair.

<p>(A) Brain sections were stained with antibody against AKAP12. AKAP12 was highly expressed in the normal meninges, and the number of AKAP12-positive cells in the scar tissue increased over time. Yellow boxes were magnified in right panels. Scale bar: 500 µm (large panels), 50 µm (magnified panels) (B) The AKAP12-positive area of three representative sections per mouse was analyzed using Image J. (Mean ± S.D.; n = 4 mice per each time; P*<0.05, P#<0.001) (C) Mouse brains were harvested at 21 days after photothrombotic injury. Brain sections were stained with antibody against AKAP12, GFAP (a marker for the glial scar) and fibronectin (a marker for the fibrotic scar). Yellow box was magnified in lower panels. Scale bar: 500 µm (largest panel), 200 µm (magnified panels) (D) AKAP12 gene KO was confirmed through genomic PCR and tissue western blotting. PCR analysis of mouse brain DNA showing the AKAP12 WT and KO alleles in the WT or AKAP12 KO mice and immunoblotting analysis of the brain lysates from the WT and KO mice using two different AKAP12 antibodies. (E) Mouse brains were harvested at 21 days after photothrombotic injury. The specificity of the AKAP12 signal was supported by lack of AKAP12 staining in the fibrotic scar in the AKAP12 KO mice. Scale bar: 200 um [LC: lesion core, FS: fibrotic scar, GS: glial scar].</p

Supplementary Figures from Essential Role of DNA Methyltransferase 1–mediated Transcription of Insulin-like Growth Factor 2 in Resistance to Histone Deacetylase Inhibitors

Supplementary Figure S1. The involvement of the IGF-1R activation in acquired resistance to vorinostat. Supplementary Figure S2. Differential regulation of the CTCF binding to the CTCF6 site in the H19/IGF2 ICR according to vorinostat sensitivity. Supplementary Figure S3. Enhanced apoptosis by combinatorial treatment with vorinostat and Stattic. Supplementary Figure S4. The association of DNMT1 expression with vorinostat sensitivity in lymphoma cell lines.</p