11 research outputs found

    Investigation of the Effect of Substrate Orientation on the Structural, Electrical and Optical Properties of n-type GaAs1-xBix Layers Grown by Molecular Beam Epitaxy

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    Current-Voltage (I-V), Capacitance-Voltage (C-V), Deep Level Transient Spectroscopy (DLTS), Laplace DLTS, Photoluminescence (PL) and Micro-Raman techniques have been employed to investigate the effect of the orientation of the substrates on the structural, electrically and optically active defects in dilute GaAs1−xBix epilayers structures having a Bi composition x = ~5.4%, grown by Molecular Beam Epitaxy (MBE) on (100) and (311)B GaAs planes. X-ray diffraction results revealed that the in-plane strain in the Ga(As,Bi) layer of the samples grown on (100)-oriented substrate (−0.0484) is significantly larger than that of the samples grown on (311)B-oriented substrate. The substrate orientation is found to have a noticeable impact on the Bi incorporation and the electrical properties of dilute GaAsBi Schottky diodes. The I-V characteristics showed that (100) Schottky diodes exhibited a larger ideality factor and higher barrier height compared with (311)B samples. The DLTS measurements showed that the number of electrically active traps were different for the two GaAs substrate orientations. In particular, three and two electron traps are detected in samples grown on (100) and (311)B GaAs substrates, respectively, with activation energies ranging from 0.12 to 0.41 eV. Additionally, one hole trap was observed only in sample grown on (100) substrates with activation energy 0.24 eV. The observed traps with small activation energies are attributed to Bi pair defects. The photoluminescence (PL) and Raman spectra have evidenced different compressive strain which affects considerably the optical properties. Furthermore, the PL spectra were also affected by different contributions of Bi- related traps which are different for different substrate orientation in agreement with DLTS results

    Biallelic loss of LDB3 leads to a lethal pediatric dilated cardiomyopathy.

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    Autosomal dominant variants in LDB3 (also known as ZASP), encoding the PDZ-LIM domain-binding factor, have been linked to a late onset phenotype of cardiomyopathy and myofibrillar myopathy in humans. However, despite knockout mice displaying a much more severe phenotype with premature death, bi-allelic variants in LDB3 have not yet been reported. Here we identify biallelic loss-of-function variants in five unrelated cardiomyopathy families by next-generation sequencing. In the first family, we identified compound heterozygous LOF variants in LDB3 in a fetus with bilateral talipes and mild left cardiac ventricular enlargement. Ultra-structural examination revealed highly irregular Z-disc formation, and RNA analysis demonstrated little/no expression of LDB3 protein with a functional C-terminal LIM domain in muscle tissue from the affected fetus. In a second family, a homozygous LDB3 nonsense variant was identified in a young girl with severe early-onset dilated cardiomyopathy with left ventricular non-compaction; the same homozygous nonsense variant was identified in a third unrelated female infant with dilated cardiomyopathy. We further identified homozygous LDB3 frameshift variants in two unrelated probands diagnosed with cardiomegaly and severely reduced left ventricular ejection fraction. Our findings demonstrate that recessive LDB3 variants can lead to an early-onset severe human phenotype of cardiomyopathy and myopathy, reminiscent of the knockout mouse phenotype, and supporting a loss of function mechanism

    Oxone activated TiO2 in presence of UV-LED light for the degradation of moxifloxacin : a mechanistic study

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    202309 bcvcVersion of RecordOthersPrincess Nourah Bint Abdulrahman UniversityPublishe

    Calorimetric and Spectroscopic Studies of the Effects of the Cell Penetrating Peptide Pep‑1 and the Antimicrobial Peptide Combi‑2 on Vesicles Mimicking <i>Escherichia coli</i> Membrane

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    The objective of this study is to measure and compare the effects of the cell penetrating peptide (CPP) Pep-1 and the antimicrobial peptide (AMP) combi-2 on vesicles of membranes mimicking <i>Escherichia coli</i> (<i>E. coli</i>). To characterize the effects of Pep-1 and combi-2 on <i>E. coli</i> membrane vesicles, a combination of five biophysical techniques was employed: fluorescence, infrared, scanning electron microscopy (SEM), thermogravimetric analysis (TGA), and differential scanning calorimetry (DSC) techniques. Upon addition of <i>E. coli</i> membranes, tryptophan fluorescence intensity of Pep-1 showed a sudden blue-shift and decreased in a nonconcentration-dependent manner while the intensity of combi-2 decreased in a concentration-dependent manner, most significantly for a very low peptide-to-lipid ratio of 1:40. Complexes of Pep-1 and combi-2 with <i>E. coli</i> membrane mimicking vesicles having shown a significant blue-shift in fluorescence intensity were then prepared and studied in freeze-dried states. IR results indicate that Pep-1 and combi-2 adopt a major 3<sub>10</sub>-helix structure in the presence of <i>E. coli</i> membrane mimicking vesicles at low peptide concentration. Pep-1 and combi-2 have a similar effect on <i>E. coli</i> membrane mimicking vesicles at low concentration even though combi-2 is in the interfacial region of the bilayer while Pep-1 is located between the interfacial region and the hydrophobic region. Combi-2 at low concentration acts as a CPP. TGA and DSC results reveal that combi-2 has a stabilizing effect on <i>E. coli</i> at any concentration while Pep-1 stabilizes the <i>E. coli</i> membrane only at high concentration. Both peptides show a preferential interaction with one of the anionic lipids leading to clustering in <i>E. coli</i> membrane. SEM images reveal that Pep-1 and combi-2 form superstructures including fibrils in the presence of <i>E. coli</i> membrane mimicking vesicles. Calorimetric and spectroscopic techniques may be used in a complementary way with imaging techniques to gain more insights into peptide–lipid interactions

    Biallelic loss of LDB3 leads to a lethal pediatric dilated cardiomyopathy

    No full text
    Autosomal dominant variants in LDB3 (also known as ZASP), encoding the PDZ-LIM domain-binding factor, have been linked to a late onset phenotype of cardiomyopathy and myofibrillar myopathy in humans. However, despite knockout mice displaying a much more severe phenotype with premature death, bi-allelic variants in LDB3 have not yet been reported. Here we identify biallelic loss-of-function variants in five unrelated cardiomyopathy families by next-generation sequencing. In the first family, we identified compound heterozygous LOF variants in LDB3 in a fetus with bilateral talipes and mild left cardiac ventricular enlargement. Ultra-structural examination revealed highly irregular Z-disc formation, and RNA analysis demonstrated little/no expression of LDB3 protein with a functional C-terminal LIM domain in muscle tissue from the affected fetus. In a second family, a homozygous LDB3 nonsense variant was identified in a young girl with severe early-onset dilated cardiomyopathy with left ventricular non-compaction; the same homozygous nonsense variant was identified in a third unrelated female infant with dilated cardiomyopathy. We further identified homozygous LDB3 frameshift variants in two unrelated probands diagnosed with cardiomegaly and severely reduced left ventricular ejection fraction. Our findings demonstrate that recessive LDB3 variants can lead to an early-onset severe human phenotype of cardiomyopathy and myopathy, reminiscent of the knockout mouse phenotype, and supporting a loss of function mechanism.Developmen

    Long-term outcomes of patients with COVID-19 treated with helmet noninvasive ventilation or usual respiratory support: follow-up study of the Helmet-COVID randomized clinical trial

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    To evaluate whether helmet noninvasive ventilation compared to usual respiratory support reduces 180-day mortality and improves health-related quality of life (HRQoL) in patients with acute hypoxemic respiratory failure due to COVID-19 pneumonia. Methods: This is a pre-planned follow-up study of the Helmet-COVID trial. In this multicenter, randomized clinical trial, adults with acute hypoxemic respiratory failure (n = 320) due to coronavirus disease 2019 (COVID-19) were randomized to receive helmet noninvasive ventilation or usual respiratory support
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