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Sökning: WFRF:(Kuchta A.)

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  • Kuchta, D.M., et al. (författare)
  • 70+ Gb/s VCSEL-based multimode fiber links
  • 2016
  • Ingår i: Proceedings IEEE Compound Semiconductor Integrated Circuit Symposium (CSICS). - 1550-8781. - 9781509016082 ; 2016-November, s. art. no. 7751010-
  • Konferensbidrag (refereegranskat)abstract
    • We report on an 850nm VCSEL based link operating error free to 71 Gb/s using an NRZ modulation format. This optical link uses custom transmitter and receiver ICs with 2-tap Feed Forward Equalization implemented in 130nm BiCMOS and GaAs based VCSELs and photodiodes. This paper covers new aspects of the circuits and packaging.
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  • Kuchta, D.M., et al. (författare)
  • A 50 Gb/s NRZ Modulated 850nm VCSEL Transmitter Operating Error Free to 90°C
  • 2015
  • Ingår i: Journal of Lightwave Technology. - 0733-8724 .- 1558-2213. ; 33:4, s. 802-810
  • Tidskriftsartikel (refereegranskat)abstract
    • We report on the properties of an 850nm VCSEL transmitter running at 50Gb/s with NRZ modulation from 30°C to 90°C. This is the highest transmitter operating temperature at 50Gb/s for a VCSEL link of any wavelength. This achievement is made possible by a combination of a high speed VCSEL design and driver and receiver circuits that incorporate equalization. Without equalization, the highest temperature attained with BER
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  • Lyons, Oliver, et al. (författare)
  • Mutations in EPHB4 cause human venous valve aplasia
  • 2021
  • Ingår i: JCI Insight. - : American Society For Clinical Investigation. - 2379-3708. ; 6:18
  • Tidskriftsartikel (refereegranskat)abstract
    • Venous valve (VV) failure causes chronic venous insufficiency, but the molecular regulation of valve development is poorly understood. A primary lymphatic anomaly, caused by mutations in the receptor tyrosine kinase EPHB4, was recently described, with these patients also presenting with venous insufficiency. Whether the venous anomalies are the result of an effect on VVs is not known. VV formation requires complex "organization" of valve-forming endothelial cells, including their reorientation perpendicular to the direction of blood flow. Using quantitative ultrasound, we identified substantial VV aplasia and deep venous reflux in patients with mutations in EPHB4. We used a GFP reporter in mice to study expression of its ligand, ephrinB2, and analyzed developmental phenotypes after conditional deletion of floxed Ephb4 and Efnb2 alleles. EphB4 and ephrinB2 expression patterns were dynamically regulated around organizing valve-forming cells. Efnb2 deletion disrupted the normal endothelial expression patterns of the gap junction proteins connexin37 and connexin43 (both required for normal valve development) around reorientating valve-forming cells and produced deficient valve-forming cell elongation, reorientation, polarity, and proliferation. Ephb4 was also required for valve-forming cell organization and subsequent growth of the valve leaflets. These results uncover a potentially novel cause of primary human VV aplasia.
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  • Resultat 1-6 av 6

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