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- Streubel, K., et al.
(författare)
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Long wavelength vertical cavity lasers
- 1999
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Ingår i: Proceedings of SPIE - The International Society for Optical Engineering. - San Jose, CA, USA. ; 3625:Bellingham, WA, United States, s. 304-314
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Tidskriftsartikel (refereegranskat)abstract
- We report on three novel vertical cavity laser (VCL) structures for 1.55 Όm operation. Two of the VCL structures utilize an n-type GaInAsP/InP Bragg mirror combined with an Al(Ga)As/GaAs mirror using either wafer-fusion or metamorphic epitaxial growth. The third VCL employs two wafer fused AlGaAs/GaAs mirrors, in which lateral current confinement is obtained by localized fusion of the p-mirror. All three VCLs use strained GaInAsP quantum wells as active material and achieve continuous-wave (CW) operation at room-temperature or above. The single fused VCL operates up to 17 °C and 101 °C in continuous-wave and pulsed mode, respectively. The monolithic VCL-structure with a metamorphic GaAs/AlAs n-type mirror uses a reversed biased tunnel junction for current injection. This laser achieves record high output power (1mW) at room temperature and operates CW up to 45 °C. The double fused VCLs with a 10×10 Όm2 active area operate CW up to 30 °C with threshold current as low as 2.5 mA and series resistance of 30 Ohms. The emission spectra exhibit a single lasing mode polarized with 30 dB extinction ratio and a spectral linewidth of 150 MHz.
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| 2. |
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| 3. |
- Stenman, U H, et al.
(författare)
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Summary report of the TD-3 workshop: characterization of 83 antibodies against prostate-specific antigen
- 1999
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Ingår i: Tumor Biology. - : Springer Science and Business Media LLC. - 1423-0380 .- 1010-4283. ; 20:Suppl. 1, s. 1-12
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Tidskriftsartikel (refereegranskat)abstract
- Twelve research groups participated in the ISOBM TD-3 Workshop in which the reactivity and specificity of 83 antibodies against prostate-specific antigen (PSA) were investigated. Using a variety of techniques including cross-inhibition assays, Western blotting, BIAcore, immunoradiometric assays and immunohistochemistry, the antibodies were categorized into six major groups which formed the basis for mapping onto two- and three-dimensional (2-D and 3-D) models of PSA. The overall findings of the TD-3 Workshop are summarized in this report. In agreement with all participating groups, three main antigenic domains were identified: free PSA-specific epitopes located in or close to amino acids 86-91; discontinuous epitopes specific for PSA without human kallikrein (hK2) cross-reactivity located at or close to amino acids 158-163; and continuous or linear epitopes shared between PSA and hK2 located close to amino acids 3-11. In addition, several minor and partly overlapping domains were also identified. Clearly, the characterization of antibodies from this workshop and the location of their epitopes on the 3-D model of PSA illustrate the importance of selecting appropriate antibody pairs for use in immunoassays. It is hoped that these findings and the epitope nomenclature described in this TD-3 Workshop are used as a standard for future evaluation of anti-PSA antibodies.
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| 6. |
- Lerm, Maria, et al.
(författare)
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Deamidation of Cdc42 and Rac by Escherichia coli cytotoxic necrotizing factor 1 : activation of c-Jun N-terminal kinase in HeLa cells
- 1999
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Ingår i: Infection and Immunity. - : American Society for Microbiology. - 0019-9567 .- 1098-5522. ; 67:2, s. 496-503
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Tidskriftsartikel (refereegranskat)abstract
- Recently, Escherichia coli cytotoxic necrotizing factor 1 (CNF1) was shown to activate the low-molecular-mass GTPase RhoA by deamidation of Gln63, thereby inhibiting intrinsic and GTPase-activating protein (GAP)-stimulated GTPase activities (G. Schmidt, P. Sehr, M. Wilm, J. Selzer, M. Mann, and K. Aktories, Nature 387:725-729, 1997; G. Flatau, E. Lemichez, M. Gauthier, P. Chardin, S. Paris, C. Fiorentini, and P. Boquet, Nature 387:729-733, 1997). Here we report that in addition to RhoA, Cdc42 and Rac also are targets for CNF1 in vitro and in intact cells. Treatment of HeLa cells with CNF1 induced a transient formation of microspikes and formation of membrane ruffles. CNF1 caused a transient 10- to 50-fold increase in the activity of the c-Jun N-terminal kinase. Tryptic peptides of Cdc42 obtained from CNF1-treated cells by immunoprecipitation exhibited an increase in mass of 1 Da compared to control peptides, indicating the deamidation of glutamine 61 by the toxin. The same increase in mass was observed with the respective peptides obtained from CNF1-modified recombinant Cdc42 and Rac1. Modification of recombinant Cdc42 and Rac1 by CNF1 inhibited intrinsic and GAP-stimulated GTPase activities and retarded binding of 2'(3')-O-(N-methylanthraniloyl)GDP. The data suggest that recombinant as well as cellular Cdc42 and Rac are substrates for CNF1.
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