Color-Shift-Keying Embedded Direct-Current Optical-Orthogonal-Frequency-Division-Multiplexing (CSK-DCO-OFDM) for Visible Light Communications (VLC)
IEEE PHOTONICS JOURNAL
Authors: Gunawan, Wahyu Hendra; Liu, Yang; Yeh, Chien-Hung; Chow, Chi-Wai
Abstract
We propose and experimentally demonstrate a color-shift-keying embedded direct-current-optical-orthogonal-frequency-division-multiplexing (CSK-DCO-OFDM) scheme for the VLC systems. The proposed scheme can provide not only non-flickering aggregated optical power to reduce human health concerns, but also offers additional modulation dimension or flexibility to the CSK by including high data rate OFDM signal. The data rate is increased from 10 Mbit/s in the original CSK signal to 70.43 Mbit/s in the CSK-DCO-OFDM signal, and both the CSK and OFDM signals satisfy the forward-error-correction (FEC) threshold.
c-Src-Dependent and -Independent Functions of Matk in Osteoclasts and Osteoblasts
JOURNAL OF IMMUNOLOGY
Authors: Kim, Jung Ha; Kim, Kabsun; Kim, Inyoung; Seong, Semun; Kim, Nacksung
Abstract
The non-receptor tyrosine kinase c-Src participates in bone metabolism by regulating the activities of both the bone-resorbing osteoclasts and bone-forming osteoblasts. In this study, we investigated whether megakaryocyte-associated tyrosine kinase ( Matk), a potent inhibitor of c-Src, affects the functions of murine osteoclasts and osteoblasts. Results revealed that the formation of osteoclasts with actin rings was attenuated by Matk overexpression in osteoclast precursor cells but was enhanced by Matk knockdown. The inhibitory effect of Matk on osteoclasts was closely related with the inhibition of c-Src activity. Intriguingly, Matk overexpression in osteoblasts reduced bone nodule formation. Conversely, Matk knockdown increased osteoblast function. Most importantly, binding of Matk to Runx2 resulted in the inhibition of Runx2 translocation into the nucleus and downregulation of Runx2 target genes. Taken together, our findings demonstrated that Matk plays a critical role in bone metabolism by impairing the functions of osteoclasts and osteoblasts via distinct mechanisms involving inhibition of c-Src-dependent and -independent signaling pathways.