Role of hydrogen in hydrogen-induced layer exfoliation of germanium

The role of hydrogen in the exfoliation of Ge is studied using cross-sectional transmission electron microscopy, atomic force microscopy, and multiple-internal transmission mode Fourier-transform infrared absorption spectroscopy and compared with the mechanism in silicon. A qualitative model for the physical and chemical action of hydrogen in the exfoliation of these materials is presented, in which H-implantation creates damage states that store hydrogen and create nucleation sites for the formation of micro-cracks. These micro-cracks are chemically stabilized by hydrogen passivation, and upon annealing serve as collection points for molecular hydrogen. Upon further heating, the molecular hydrogen trapped in these cracks exerts pressure on the internal surfaces causing the cracks to extend and coalesce. When this process occurs in the presence of a handle substrate that provides rigidity to the thin film, the coalescence of these cracks leads to cooperative thin film exfoliation. In addition to clarifying the mechanism of H-induced exfoliation of single-crystal thin Ge films, the vibrational study helps to identify the states of hydrogen in heavily damaged Ge. Such information has practical importance for the optimization of H-induced layer transfer as a technological tool for materials integration with these materials systems

Spectroscopic studies of the mechanism for hydrogen-induced exfoliation of InP

The motion and bonding configurations of hydrogen in InP are studied after proton implantation and subsequent annealing, using Fourier transform infrared (FTIR) spectroscopy. It is demonstrated that, as implanted, hydrogen is distributed predominantly in isolated pointlike configurations with a smaller concentration of extended defects with uncompensated dangling bonds. During annealing, the bonded hydrogen is released from point defects and is recaptured at the peak of the distribution by free internal surfaces in di-hydride configurations. At higher temperatures, immediately preceding exfoliation, rearrangement processes lead to the formation of hydrogen clusters and molecules. Reported results demonstrate that the exfoliation dynamics of hydrogen in InP and Si are markedly different, due to the higher mobility of hydrogen in InP and different implant-defect characteristics, leading to fundamental differences in the chemical mechanism for exfoliation

InGaAs/InP double heterostructures on InP/Si templates fabricated by wafer bonding and hydrogen-induced exfoliation

Hydrogen-induced exfoliation combined with wafer bonding has been used to transfer ~600-nm-thick films of (100) InP to Si substrates. Cross-section transmission electron microscopy (TEM) shows a transferred crystalline InP layer with no observable defects in the region near the bonded interface and an intimately bonded interface. InP and Si are covalently bonded as inferred by the fact that InP/Si pairs survived both TEM preparation and thermal cycles up to 620 °C necessary for metalorganic chemical vapor deposition growth. The InP transferred layers were used as epitaxial templates for the growth of InP/In0.53Ga0.47As/InP double heterostructures. Photoluminescence measurements of the In0.53Ga0.47As layer show that it is optically active and under tensile strain, due to differences in the thermal expansion between InP and Si. These are promising results in terms of a future integration of Si electronics with optical devices based on InP-lattice-matched materials

Design approaches and materials processes for ultrahigh efficiency lattice mismatched multi-junction solar cells

In this study, we report synthesis of large area (>2cm^2), crack-free GaAs and GaInP double heterostructures grown in a multi-junction solar cell-like structure by MOCVD. Initial solar cell data are also reported for GaInP top cells. These samples were grown on Ge/Si templates fabricated using wafer bonding and ion implantation induced layer transfer techniques. The double heterostructures exhibit radiative emission with uniform intensity and wavelength in regions not containing interfacial bubble defects. The minority carrier lifetime of ~1ns was estimated from photoluminescence decay measurements in both double heterostructures. We also report on the structural characteristics of heterostructures, determined via atomic force microscopy and transmission electron microscopy, and correlate these characteristics to the spatial variation of the minority carrier lifetime

Investigation of the marine compound spongistatin 1 links the inhibition of PKCα translocation to nonmitotic effects of tubulin antagonism in angiogenesis

The aims of the study were to meet the demand of new tubulin antagonists with fewer side effects by characterizing the antiangiogenic properties of the experimental compound spongistatin 1, and to elucidate nonmitotic mechanisms by which tubulin antagonists inhibit angiogenesis. Although tubulin-inhibiting drugs and their antiangiogenic properties have been investigated for a long time, surprisingly little is known about their underlying mechanisms of action. Antiangiogenic effects of spongistatin 1 were investigated in endothelial cells in vitro, including functional cell-based assays, live-cell imaging, and a kinome array, and in the mouse cornea pocket assay in vivo. Spongistatin 1 inhibited angiogenesis at nanomolar concentrations (IC50: cytotoxicity>50 nM, proliferation 100 pM, migration 1.0 nM, tube formation 1.0 nM, chemotaxis 1.0 nM, aortic ring sprouting 500 pM, neovascularization in vivo 10 μg/kg). Further, a kinome array and validating data showed that spongistatin 1 inhibits the phosphorylation activity of protein kinase Cα (PKCα), an essential kinase in angiogenesis, and its translocation to the membrane. Thus, we conclude that PKCα might be an important target for the antiangiogenic effects of tubulin antagonism. In addition, the data from the kinase array suggest that different tubulin antagonists might have individual intracellular actions.—Rothmeier, A. S., Ischenko, I., Joore, J., Garczarczyk, D., Fu¨rst, R., Bruns, C. J., Vollmar, A. M., Zahler, S. Investigation of the marine compound spongistatin 1 links the inhibition of PKCα translocation to nonmitotic effects of tubulin antagonism in angiogenesis

A novel technique for selective NF-kappa B inhibition in Kupffer cells: contrary effects in fulminant hepatitis and ischaemia-reperfusion.

Background and aims: The transcription factor nuclear factor kappa B (NF-kB) has risen as a promising target for anti-inflammatory therapeutics. In the liver, however, NFkB inhibition mediates both damaging and protective effects. The outcome is deemed to depend on the liver cell type addressed. Recent gene knock-out studies focused on the role of NF-kB in hepatocytes, whereas the role of NF-kB in Kupffer cells has not yet been investigated in vivo. Here we present a novel approach, which may be suitable for clinical application, to selectively target NF-kB in Kupffer cells and analyse the effects in experimental models of liver injury. Methods: NF-kB inhibiting decoy oligodeoxynucleotides were loaded upon gelatin nanoparticles (D-NPs) and their in vivo distribution was determined by confocal microscopy. Liver damage, NF-kB activity, cytokine levels and apoptotic protein expression were evaluated after lipopolysaccharide (LPS), D-galactosamine (GalN)/LPS, or concanavalin A (ConA) challenge and partial warm ischaemia and subsequent reperfusion, respectively. Results: D-NPs were selectively taken up by Kupffer cells and inhibited NF-kB activation. Inhibition of NF-kB in Kupffer cells improved survival and reduced liver injury after GalN/LPS as well as after ConA challenge. While anti-apoptotic protein expression in liver tissue was not reduced, pro-apoptotic players such as cJun N-terminal kinase (JNK) were inhibited. In contrast, selective inhibition of NF-kB augmented reperfusion injury. Conclusions: NF-kB inhibiting decoy oligodeoxynucleotide- loaded gelatin nanoparticles is a novel tool to selectively inhibit NF-kB activation in Kupffer cells in vivo. Thus, liver injury can be reduced in experimental fulminant hepatitis, but increased at ischaemia–reperfusion

Endothelial preconditioning by transient oxidative stress reduces inflammatory responses of cultured endothelial cells to TNF-α

Brief episodes of ischemia can render an organ resistant to subsequent severe ischemia. This ‘ischemic preconditioning’ is ascribed to various mechanisms, including oxidative stress. We investigated whether preconditioning exists on an endothelial level. Human umbilical vein endothelial cells (HUVECs) were transiently confronted with oxidative stress (1 mM H2O2, 5 min). Adhesion molecules ICAM-1 and E-selectin and release of cytokines IL-6 and IL-8 to subsequent stimulation with TNF-α (2.5 ng/ml, 4 h) were measured (flow cytometry and immunoassay), as were nuclear translocation of the transcription factor NFkB (Western blotting, confocal microscopy) and redox status of HUVECs (quantification of glutathione by HPLC). TNF-α elevated IL-6 in the cell supernatant from 8.8 ± 1 to 41 ± 3 pg/ml and IL-8 from 0.5 ± 0.03 to 3 ± 0.2 ng/ml. ICAM-1 was increased threefold and E-selectin rose eightfold. Oxidative stress (decrease of glutathione by 50%) reduced post-TNF-α levels of IL-6 to 14 ± 3 and IL-8 to 1 ± 0.2; the rise of ICAM-1 was completely blocked and E-selectin was only doubled. The anti-inflammatory effects of preconditioning via oxidative stress were paralleled by reduction of the translocation of NFkB on stimulation with TNF-α, and antagonized by the intracellular radical scavenger N-acetylcysteine. ‘Anti-inflammatory preconditioning’ of endothelial cells by oxidative stress may account for the inhibitory effects of preconditioning on leukocyte adhesion in vivo