82 research outputs found

    Critical process temperatures for resistive InGaAsP/InP heterostructures heavily implanted by Fe or Ga ions

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    We report on critical ion implantation and rapid thermal annealing (RTA) process temperatures that produce resistive Fe- or Ga-implanted InGaAsP/InP heterostructures. Two InGaAsP/InP heterostructure compositions, with band gap wavelengths of 1.3 μm and 1.57 μm, were processed by ion implantation sequences done at multiple MeV energies and high fluence (1015 cm−2). The optimization of the fabrication process was closely related to the implantation temperature which influences the type of implant-induced defect structures. With hot implantation temperatures, at 373 K and 473 K, X-ray diffraction (XRD) revealed that dynamic defect annealing was strong and prevented the amorphization of the InGaAsP layers. These hot-implanted layers were less resistive and RTA could not optimize them systematically in favor of high resistivity. With cold implantation temperatures, at 83 K and even at 300 K, dynamic annealing was minimized. Damage clusters could form and accumulate to produce resistive amorphous-like structures. After recrystallization by RTA, polycrystalline signatures were found on every low-temperature Fe- and Ga-implanted structures. For both ion species, electrical parameters evolved similarly against annealing temperatures, and resistive structures were produced near 500 °C. However, better isolation was obtained with Fe implantation. Differences in sheet resistivities between the two alloy compositions were less than band gap-related effects. These observations, related to damage accumulation and recovery mechanisms, have important implications for the realization ion-implanted resistive layers that can be triggered with near infrared laser pulses and suitable for ultrafast optoelectronics

    Clinical utilization of genomics data produced by the international Pseudomonas aeruginosa consortium

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    The International Pseudomonas aeruginosa Consortium is sequencing over 1000 genomes and building an analysis pipeline for the study of Pseudomonas genome evolution, antibiotic resistance and virulence genes. Metadata, including genomic and phenotypic data for each isolate of the collection, are available through the International Pseudomonas Consortium Database (http://ipcd.ibis.ulaval.ca/). Here, we present our strategy and the results that emerged from the analysis of the first 389 genomes. With as yet unmatched resolution, our results confirm that P. aeruginosa strains can be divided into three major groups that are further divided into subgroups, some not previously reported in the literature. We also provide the first snapshot of P. aeruginosa strain diversity with respect to antibiotic resistance. Our approach will allow us to draw potential links between environmental strains and those implicated in human and animal infections, understand how patients become infected and how the infection evolves over time as well as identify prognostic markers for better evidence-based decisions on patient care

    Defects in death-inducing signalling complex formation prevent JNK activation and Fas-mediated apoptosis in DU 145 prostate carcinoma cells

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    Androgen-independent prostate carcinomas are resistant to chemotherapy and cell lines derived from androgen-independent prostate carcinomas such as DU 145 cells are highly resistant to Fas-mediated apoptosis. The incubation of DU 145 cells with anti-Fas IgM agonistic antibody of Fas receptor fails to activate JNK, a stress kinase involved in regulating apoptosis. We have previously shown that JNK activation is sufficient and necessary to promote Fas-mediated apoptosis in DU 145 cells. We investigate the mechanisms by which JNK activation and apoptosis are abrogated. HSP27 is overexpressed in DU 145 cells and has previously been reported to sequester DAXX and prevent JNK activation in cells treated with anti-Fas IgM. However, we find no evidence that HSP27 interacts with DAXX in DU 145 cells. Instead, we find that FADD does not interact with caspase-8 and this results in defective death-inducing signalling complex formation following Fas receptor activation

    Irradiation leads to apoptosis of Kupffer cells by a Hsp27-dependant pathway followed by release of TNF-α

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    In a previous publication, we were able to show that irradiation of Kupffer cells, the liver resident macrophages, leads to an increased TNF-α concentration in the culture medium. The pathomechanisms underlying this phenomenon, however, remained to be elucidated. Here, we show that following irradiation of Kupffer cells, the apoptosis rate increased drastically within 48 h. At the same time, the total TNF-α concentration in cell lysates of Kupffer cells attached to the culture plate decreased. However, normalization of the TNF-α concentration with respect to cell number revealed that TNF-α concentration per attached cell remained constant during the observation period. Western blot analysis showed that heat shock protein 27 (Hsp27) is strongly downregulated and bax is upregulated in irradiated Kupffer cells as compared to sham-irradiated cells. Overexpression of Hsp27 in Kupffer cells was shown to prevent the effect of irradiation on bax expression, apoptosis and, at the same time, on increase of TNF-α concentration in the Kupffer cell medium. We conclude that irradiation of Kupffer cells leads to apoptosis because of downregulation of Hsp27 and consecutive upregulation of bax expression. Furthermore, we suggest that apoptosis of Kupffer cells leads to an increase of TNF-α concentration in the culture medium which may be due to cell death rather than active release or synthesis

    BQJ Photodetector Signal Processing

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