Digital radio-over-fiber system based on differential pulse code modulation and space division multiplexing.

In this paper, we present and experimentally demonstrate a digital-radio-over-fiber (D-RoF) architecture based on differential pulse code modulation (DPCM) and space division multiplexing (SDM). At low quantization resolution, DPCM can effectively reduce quantization noise and obtain significant signal-to-quantization noise ratio (SQNR) gain. We experimentally study the 7-core and 8-core multicore fiber transmission of 64-ary quadrature amplitude modulation (64QAM) orthogonal frequency division multiplexing (OFDM) signals with a bandwidth of 100 MHz in a fiber-wireless hybrid transmission link. Compared to PCM-based D-RoF, the error vector magnitude (EVM) performance in the DPCM-based D-RoF is effectively improved when the quantization bits (QBs) are 3-5 bits. In particular, when the QB is 3 bits, the EVM of the DPCM-based D-RoF is 6.5% and 7% lower than that of the PCM-based system in 7-core- and 8-core-multicore fiber-wireless hybrid transmission links, respectively.

[Inhibition effect of gambogic acid on MUTZ-1 cell line and its possible mechanism].

This study was aimed to investigate the effects of gambogic acid on the cells of high-risk patients with myelodysplastic syndrome (MDS) in vitro and its mechanism. The inhibition effect of gambogic acid on growth of MUTZ-1 cell line of MDS-RAEB was detected by MTT method. Apoptosis and cell cycle were detected by morphological observation and flow cytometry respectively. The expressions of bax/bcl-2 gene at mRNA level were detected by RT-PCR. The results indicated that the Gambogic acid inhibited the growth of MUTZ-1 cells, the inhibitory rate of gambogic acid with the range of 0.2 - 0.8 microg/ml was enhanced along with increasing of drug concentration. Flow cytometric assay showed that the apoptotic rate of MUTZ-1 cells treated by gambogic acid also was enhanced along with increasing of drug concentration, the apoptotic rates resulting from gambogic acid (0, 0.4, 0.6, 0.8 microg/ml) were (5 +/- 0.5)%, (13 +/- 0.5)%, (37 +/- 0.7)% and (56 +/- 0.6)% respectively. The characteristic changes of apoptosis emerged in MUTZ-1 cells after being exposed to gambogic acid. Gambogic acid could significantly down-regulate the expressions of bcl-2 gene in a dose dependent manner, however, it had no effects on bax gene. It is concluded that within the range of concentration from 0.4 to 0. 8 microg/ml, gambogic acid can inhibit the growth of MUTZ-1 cells by inducing their apoptosis and down-regulating the expression of bcl-2 gene, which may be one of the main mechanisms underlying its antitumor effects.