Optical Visualization of Radiative Recombination at Partial Dislocations in GaAs

Individual dislocations in an ultra-pure GaAs epilayer are investigated with spatially and spectrally resolved photoluminescence imaging at 5~K. We find that some dislocations act as strong non-radiative recombination centers, while others are efficient radiative recombination centers. We characterize luminescence bands in GaAs due to dislocations, stacking faults, and pairs of stacking faults. These results indicate that low-temperature, spatially-resolved photoluminescence imaging can be a powerful tool for identifying luminescence bands of extended defects. This mapping could then be used to identify extended defects in other GaAs samples solely based on low-temperature photoluminescence spectra.Comment: 4 pages, 4 figure

Control of InGaAs facets using metal modulation epitaxy (MME)

Control of faceting during epitaxy is critical for nanoscale devices. This work identifies the origins of gaps and different facets during regrowth of InGaAs adjacent to patterned features. Molecular beam epitaxy (MBE) near SiO2 or SiNx led to gaps, roughness, or polycrystalline growth, but metal modulated epitaxy (MME) produced smooth and gap-free "rising tide" (001) growth filling up to the mask. The resulting self-aligned FETs were dominated by FET channel resistance rather than source-drain access resistance. Higher As fluxes led first to conformal growth, then pronounced {111} facets sloping up away from the mask.Comment: 18 pages, 7 figure

α-MSH inhibits induction of C/EBPβ-DNA binding activity and NOS2 gene transcription in macrophages

α-MSH inhibits induction of C/EBPβ-DNA binding activity and NOS2 gene transcription in macrophages.Backgroundα-Melanocyte–stimulating hormone (α-MSH) is an endogenous tridecapeptide that exerts anti-inflammatory actions and abrogates postischemic renal injury in rodents. α-MSH inhibits lipopolysaccharide (LPS)-induced gene expression of several cytokines, chemokines, and nitric oxide synthase-2 (NOS2), but the molecular mechanisms underlying these effects have not been clearly defined. To test the hypothesis that α-MSH inhibits the expression of inducible trans-activating factors involved in NOS2 regulation, we used RAW 264.7 macrophage cells to examine the effects of α-MSH on the activation of nuclear factor-кB (NF-кB) and CCAAT/enhancer binding protein-β (C/EBPβ), trans-acting factors known to be involved in LPS + interferon (IFN)-γ induction of the NOS2 gene.MethodsGel shift assays were performed to identify NF-кB and C/EBP DNA binding activities in LPS + IFN-γ–treated RAW 264.7 cells in the presence and absence of α-MSH. NOS2 promoter assays were conducted to identify the effects of α-MSH on LPS + IFN-γ–mediated induction of NOS2 transcription.ResultsGel shift assays demonstrated LPS + IFN-γ induction of NF-кB and C/EBP family protein-DNA complexes in nuclei harvested from the cells. Supershift assays revealed that the C/EBP complexes were comprised of C/EBPβ, but not C/EBPα, C/EBPα, or C/EBPϵ. α-MSH (100 nmol/L) inhibited the LPS + IFN-γ–mediated induction of nuclear DNA binding activity of C/EBPβ, but not that of NF-кB (in contrast to reports in other cell types), as well as the activity of a murine NOS2 promoter-luciferase construct. In contrast, α-MSH (100 nmol/L) had no effect on the induction of NOS2 promoter-luciferase genes harboring deletion or mutation of the C/EBP box.ConclusionsThese data indicate that α-MSH inhibits the induction of C/EBPβ DNA binding activity and that this effect is a major mechanism by which α-MSH inhibits the transcription of the NOS2 gene. The inability of α-MSH to inhibit LPS + IFN-γ induction of NF-кB in murine macrophage cells, which contrasts with inhibitory effects of the neuropeptide in other cell types, suggests that cell-type–specific mechanisms are involved

Energy and Exergy Analysis on Si Engine by Blend of Ethanol with Petrol

Need to use renewable energy in the form of ethanol fuel derived using agriculture waste to reduce load on petrol derived from crude oil, which is available in limited quantity. This is mostly due to stock of petroleum product are depleting day by day, hence more use of renewable fuels gets attraction in developing country like India. In recent years, Considerable efforts made to develop and introduce alternative renewable fuel, to replace conventional petroleum-base fuels.The main objective of the current work id to investigate influences of blends of ethanol-petrol blend used in IC engine performance using energy and exergy analysis. Here, experimental work divided into mainly two parts. In first part, Engine performance carried out using E0, E25, E40 and E100 blends of ethanol-petrol blends. In other part, exergy analysis carried out. Experimental test set-up developed in laboratory. The stationary petrol engine was run in laboratory at a medium speed, variable load condition experienced in most urban driving conditions and various measurements like fuel flow, exhaust temperature, exhaust emission measurement and exhaust smoke test were carried out. The fuel properties of biodiesel such as kinematic viscosity, calorific value, flash point, carbon residue and specific gravity investigated. Heat balance sheet and availability calculated for different condition like E0, E25, E40 and E100 blends of ethanol-petrol blends

Measurement of the ground-state distributions in bistable mechanically interlocked molecules using slow scan rate cyclic voltammetry

In donor–acceptor mechanically interlocked molecules that exhibit bistability, the relative populations of the translational isomers—present, for example, in a bistable [2]rotaxane, as well as in a couple of bistable [2]catenanes of the donor–acceptor vintage—can be elucidated by slow scan rate cyclic voltammetry. The practice of transitioning from a fast scan rate regime to a slow one permits the measurement of an intermediate redox couple that is a function of the equilibrium that exists between the two translational isomers in the case of all three mechanically interlocked molecules investigated. These intermediate redox potentials can be used to calculate the ground-state distribution constants, K. Whereas, (i) in the case of the bistable [2]rotaxane, composed of a dumbbell component containing π-electron-rich tetrathiafulvalene and dioxynaphthalene recognition sites for the ring component (namely, a tetracationic cyclophane, containing two π-electron-deficient bipyridinium units), a value for K of 10 ± 2 is calculated, (ii) in the case of the two bistable [2]catenanes—one containing a crown ether with tetrathiafulvalene and dioxynaphthalene recognition sites for the tetracationic cyclophane, and the other, tetrathiafulvalene and butadiyne recognition sites—the values for K are orders (one and three, respectively) of magnitude greater. This observation, which has also been probed by theoretical calculations, supports the hypothesis that the extra stability of one translational isomer over the other is because of the influence of the enforced side-on donor–acceptor interactions brought about by both π-electron-rich recognition sites being part of a macrocyclic polyether

Role of Transforming Growth Factor Beta in Corneal Function, Biology and Pathology

Transforming growth factor-beta (TGFβ) is a pleiotropic multifunctional cytokine that regulates several essential cellular processes in many parts of the body including the cornea. Three isoforms of TGFβ are known in mammals and the human cornea expresses all of them. TGFβ1 has been shown to play a central role in scar formation in adult corneas whereas TGFβ2 and TGFβ3 have been implicated to play a critical role in corneal development and scarless wound healing during embryogenesis. The biological effects of TGFβ in the cornea have been shown to follow SMAD dependent as well as SMAD-independent signaling pathways depending upon cellular responses and microenvironment. Corneal TGFβ expression is necessary for maintaining corneal integrity and corneal wound healing. On the other hand, TGFβ is perhaps the most important cytokine in the pathogenesis of fibrotic disease in the cornea. Although the transformation of keratocytes to myofibroblasts induced by TGFβ is largely believed to cause corneal fibrosis or scarring, the precise molecular mechanism(s) involved in this process is still unknown. Currently no drugs are available to treat corneal scarring effectively without causing significant side effects. Many approaches to treat TGFβ-mediated corneal scarring are under investigation. These include blocking of TGFβ, TGFβ receptor, TGFβ function and/or TGFβ maturation. Other strategies such as modulating keratocyte proliferation, apoptosis, transcription and DNA condensation are also being investigated. The potential of gene therapy to neutralize the pathologic effects of TGFβ has also been demonstrated recently