16 research outputs found

    Edge Couplers with relaxed Alignment Tolerance for Pick-and-Place Hybrid Integration of III-V Lasers with SOI Waveguides

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    We report on two edge-coupling and power splitting devices for hybrid integration of III-V lasers with sub-micrometric silicon-on-insulator (SOI) waveguides. The proposed devices relax the horizontal alignment tolerances required to achieve high coupling efficiencies and are suitable for passively aligned assembly with pick-and-place tools. Light is coupled to two on-chip single mode SOI waveguides with almost identical power coupling efficiency, but with a varying relative phase accommodating the lateral misalignment between the laser diode and the coupling devices, and is suitable for the implementation of parallel optics transmitters. Experimental characterization with both a lensed fiber and a Fabry-P\'erot semiconductor laser diode has been performed. Excess insertion losses (in addition to the 3 dB splitting) taken as the worst case over both waveguides of respectively 2 dB and 3.1 dB, as well as excellent 1 dB horizontal loss misalignment ranges of respectively 2.8 um and 3.8 um (worst case over both in-plane axes) have been measured for the two devices. Back-reflections to the laser are below -20 dB for both devices within the 1 dB misalignment range. Devices were fabricated with 193 nm DUV optical lithography and are compatible with mass-manufacturing with mainstream CMOS technology

    Design of a waveguide-coupled GeSn disk laser

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    We report on the design of a waveguide coupled GeSn microdisk-laser cavity in which the germanium virtual substrate serving as a template for GeSn growth is repurposed for the definition of passive on-chip interconnection waveguides. A main challenge resides in transferring the optical power from the upper (Si)GeSn gain stack to the underlying virtual substrate layer and is solved with laser mode engineering. Designs are based on experimentally realized layer stacks and waveguide outcoupling efficiencies as high as 27% are shown in compact resonator geometries with a small, 7 μ\mum radius, with 42% of the power being recycled in the laser cavity

    Characterization of CD4+and CD8+T Cell Subsets and Interferon Regulatory Factor 4 (IRF4) in MS Patients Treated with Fingolimod (FTY-720): A Follow-up Study

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    Fingolimod is a novel immunomodulatory drug used in patients with relapsing multiple sclerosis (MS) which reversibly inhibits egress of lymphocytes from lymph nodes. In this longitudinal study, the frequency of Interferon- gamma (IFN-gamma)+, IL4+, IL17+ and IL10+ CD4+ and CD8+ T cell subsets were measured in Fingolimod treated patients before and after 12 months'(12M) therapy using flow cytometry and compared to those of naive, Betaferon treated MS patients and healthy individuals. Additionally, the level of transcription factor IRF4 and IL-6, IL-23, TGF-beta 1 cytokines, required for differentiation of IL-17+ T cells, were assessed by RT-PCR and ELISA, respectively. In Fingolimod treated MS patients, we observed a significant decrease in the percentage of IFN-gamma+/IL17+ CD4+ and CD8+ T cell subsets. In contrast, Fingolimod increased IL10+ CD4+ T cells. We also showed that IFN-gamma+IL17+ co-producing CD8+ T cells were reduced in patients under fingolimod therapy. furthermore, Fingolimod could reduce the expression level of IRF4 in patients while IL6 was increased in the supernatant of cultured peripheral blood mononuclear cells. Our data showed that Fingolimod treatment alters CD4+ and CD8+ T cell subsets and reduces expression of IRF-4, which affects the proportion of pathogenic memory T cells in peripheral blood

    Modulation by insulin-like growth factor I of the phosphatase PTEN in astrocytes

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    Characterization of intracellular pathways underlying the pleiotropic actions of insulin-like growth factor-I (IGF-I) on brain cells is incomplete. We analyzed IGF-I signalling on astrocytes through the canonical phosphatidylinositol 3-kinase (PI3K)/Akt pathway and focused on possible changes in PTEN, a phosphatase that modulates IGF-I signalling by inhibiting Akt activation and, in turn is positively regulated by PI3K. After exposure of astrocytes to IGF-I, PTEN mRNA and protein levels were reduced and its phosphatase activity diminished. Inhibition of PTEN involved activation of a PI3K/protein kinase C (PKC) pathway that decreased in a proteasome-dependent step the levels of the transcription factor Egr-1, a key regulator of PTEN levels in astrocytes, causing decreased binding of Egr-1 to the PTEN promoter. Enhanced mitogenesis in PTEN siRNA-transduced astrocytes after IGF-I suggested that reduced PTEN may be a permissive factor for the mitogenic activity of IGF-I. Subsequent recovery of reduced PTEN required also activation by IGF-I of PI3K to recruit in this case protein kinase A (PKA) which stimulated Egr-1 levels and, consequently PTEN synthesis. Because basal levels of PTEN in astrocytes are also governed by PI3K, IGF-I appears to modulate PTEN in astrocytes by redirecting its homeostasic control through PI3K in a timed fashion. © 2007 Elsevier B.V. All rights reserved.Peer Reviewe
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