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An ultra-high bandwidth (BW) and a low Vπ InP Mach-Zehnder modulator with an n-i-p-n heterostructure is proposed. The combination of the n-i-p-n heterostructure and the capacitive-loaded travelling-wave electrode provides a modulator with extremely low electrical loss. The device exhibits a 3 dB electro-optic BW of over 67 GHz and a Vπ of 2.0 V. A 100 Gb/s non-return-to-zero on-off keying modulation with an extinction ratio of over 10 dB is also realised. [ABSTRACT FROM AUTHOR]

We report an athermal InP (110) optical modulator with a simple planar n-SI-n heterostructure. A symmetrical push-pull operation provides a high-extinction ratio of >25 dB over the entire C-band and zero-chirp modulation. A Mach-Zehnder optical modulator (MZM) exhibits a 3 dB-EO bandwidth of 30 GHz and 40-Gb/s NRZ high-speed modulation with wavelength and temperature insensitive operation. We also successfully demonstrate an MZM integrated twin-IQ modulator that exhibits 56-Gb/s × 2 athermal QPSK modulation at constant drive and bias voltages.

We report the design and fabrication of a hybrid-integration-type coherent receiver. We optimize the receiver building blocks, and achieve a -25-dB common-mode rejection ratio and a 20-dB signal input power dynamic range., (© 2011 Optical Society of America)

Cellular senescence is a tumor-suppressing mechanism that is accompanied by characteristic chromatin condensation called senescence-associated heterochromatic foci (SAHFs). We found that individual SAHFs originate from individual chromosomes. SAHFs do not show alterations of posttranslational modifications of core histones that mark condensed chromatin in mitotic chromosomes, apoptotic chromatin, or transcriptionally inactive heterochromatin. Remarkably, SAHF-positive senescent cells lose linker histone H1 and exhibit increased levels of chromatin-bound high mobility group A2 (HMGA2). The expression of N-terminally enhanced green fluorescent protein (EGFP)-tagged histone H1 induces premature senescence phenotypes, including increased levels of phosphorylated p53, p21, and hypophosphorylated Rb, and a decrease in the chromatin-bound endogenous histone H1 level but not in p16 level accumulation or SAHF formation. However, the simultaneous ectopic expression of hemagglutinin-tagged HMGA2 and N-terminally EGFP-tagged histone H1 leads to significant SAHF formation (P < 0.001). It is known that histone H1 and HMG proteins compete for a common binding site, the linker DNA. These results suggest that SAHFs are a novel type of chromatin condensation involving alterations in linker DNA-binding proteins.