MIMO Channel Information Feedback Using Deep Recurrent Network

In a multiple-input multiple-output (MIMO) system, the availability of channel state information (CSI) at the transmitter is essential for performance improvement. Recent convolutional neural network (NN) based techniques show competitive ability in realizing CSI compression and feedback. By introducing a new NN architecture, we enhance the accuracy of quantized CSI feedback in MIMO communications. The proposed NN architecture invokes a module named long short-term memory (LSTM) which admits the NN to benefit from exploiting temporal and frequency correlations of wireless channels. Compromising performance with complexity, we further modify the NN architecture with a significantly reduced number of parameters to be trained. Finally, experiments show that the proposed NN architectures achieve better performance in terms of both CSI compression and recovery accuracy

(E)-3-Dimethyl­amino-1-(4-pyrid­yl)prop-2-en-1-one

The title compound, C10H12N2O, is approximately planar, the r.m.s. deviation of the non-H atoms from the mean plane being 0.099 Å

Inhibition of EGFR nuclear shuttling decreases irradiation resistance in HeLa cells

Introduction. Cervical cancer is a leading cause of mortality in women worldwide. The resistance to irradiation at the advanced stage is the main reason for the poor prognosis and high mortality. This work aims to elucidate the molecular mechanism underlying the radio-resistance. Material and methods. In this study, we determined the pEGFR-T654 and pDNA-PK-T2609 expression level changes in irradiated HeLa cells treated with T654 peptide, a nuclear localization signal (NLS) inhibitor, to inhibit EGFR nuclear transport. Cell viability, cell cycle and migratory capacity were analyzed. Xenograft animal model was used to evaluate the effect of EGFR nuclear transport inhibition on the tumor growth in vivo. Results. The enhanced translocation of nuclear EGFR in the irradiated HeLa cells correlated with the increasing level of pEGFR-T654 and pDNA-PK-T2609. Inhibition of EGFR nuclear translocation by NLS peptide inhibitor attenuated DNA damage repair in the irradiated HeLa cells, decreased cell viability and promoted cell death through arrest at G0 phase. NLS peptide inhibitor impaired the migratory capacity of irradiated HeLa cells, and negatively affected tumorigenesis in xenograft mice. Conclusions. This work puts forward a potential molecular mechanism of the irradiation resistance in cervical cancer cells, providing a promising direction towards an efficient therapy of cervical cancer

Inhibition of EGFR nuclear shuttling decreases irradiation resistance in HeLa cells

Introduction. Cervical cancer is a leading cause of mortality in women worldwide. The resistance to irradiation at the advanced stage is the main reason for the poor prognosis and high mortality. This work aims to elucidate the molecular mechanism underlying the radio-resistance. Material and methods. In this study, we determined the pEGFR-T654 and pDNA-PK-T2609 expression level changes in irradiated HeLa cells treated with T654 peptide, a nuclear localization signal (NLS) inhibitor, to inhibit EGFR nuclear transport. Cell viability, cell cycle and migratory capacity were analyzed. Xenograft animal model was used to evaluate the effect of EGFR nuclear transport inhibition on the tumor growth in vivo. Results. The enhanced translocation of nuclear EGFR in the irradiated HeLa cells correlated with the increasing level of pEGFR-T654 and pDNA-PK-T2609. Inhibition of EGFR nuclear translocation by NLS peptide inhibitor attenuated DNA damage repair in the irradiated HeLa cells, decreased cell viability and promoted cell death through arrest at G0 phase. NLS peptide inhibitor impaired the migratory capacity of irradiated HeLa cells, and negatively affected tumorigenesis in xenograft mice. Conclusions. This work puts forward a potential molecular mechanism of the irradiation resistance in cervical cancer cells, providing a promising direction towards an efficient therapy of cervical cancer. (Folia Histochemica et Cytobiologica 2017, Vol. 55, No. 2, 43–51