Fast DGT Based Receivers for GFDM in Broadband Channels

Generalized frequency division multiplexing (GFDM) is a recent multicarrier 5G waveform candidate with flexibility of pulse shaping filters. However, the flexibility of choosing a pulse shaping filter may result in inter carrier interference (ICI) and inter symbol interference (ISI), which becomes more severe in a broadband channel. In order to eliminate the ISI and ICI, based on discrete Gabor transform (DGT), in this paper, a transmit GFDM signal is first treated as an inverse DGT (IDGT), and then a frequency-domain DGT is formulated to recover (as a receiver) the GFDM signal. Furthermore, to reduce the complexity, a suboptimal frequency-domain DGT called local DGT (LDGT) is developed. Some analyses are also given for the proposed DGT based receivers.Comment: 28 pages, 8 figure

Dexmedetomidine post-treatment attenuates cardiac ischaemia/reperfusion injury by inhibiting apoptosis through HIF-1α signalling.

Hypoxia-inducible factor 1α (HIF-1α) plays a critical role in the apoptotic process during cardiac ischaemia/reperfusion (I/R) injury. This study aimed to investigate whether post-treatment with dexmedetomidine (DEX) could protect against I/R-induced cardiac apoptosis in vivo and in vitro via regulating HIF-1α signalling pathway. Rat myocardial I/R was induced by occluding the left anterior descending artery for 30 minutes followed by 6-hours reperfusion, and cardiomyocyte hypoxia/reoxygenation (H/R) was induced by oxygen-glucose deprivation for 6 hours followed by 3-hours reoxygenation. Dexmedetomidine administration at the beginning of reperfusion or reoxygenation attenuated I/R-induced myocardial injury or H/R-induced cell death, alleviated mitochondrial dysfunction, reduced the number of apoptotic cardiomyocytes, inhibited the activation of HIF-1α and modulated the expressions of apoptosis-related proteins including BCL-2, BAX, BNIP3, cleaved caspase-3 and cleaved PARP. Conversely, the HIF-1α prolyl hydroxylase-2 inhibitor IOX2 partly blocked DEX-mediated cardioprotection both in vivo and in vitro. Mechanistically, DEX down-regulated HIF-1α expression at the post-transcriptional level and inhibited the transcriptional activation of the target gene BNIP3. Post-treatment with DEX protects against cardiac I/R injury in vivo and H/R injury in vitro. These effects are, at least in part, mediated via the inhibition of cell apoptosis by targeting HIF-1α signalling