Joint Satellite-Transmitter and Ground-Receiver Digital Pre-Distortion for Active Phased Arrays in LEO Satellite Communications

A novel joint satellite-transmitter and ground-receiver (JSG) digital pre-distortion (DPD) (JSG-DPD) technique is proposed to improve the linearity and power efficiency of the space-borne active phased arrays (APAs) in low Earth orbit (LEO) satellite communications. Different from the conventional DPD technique that requires a complex RF feedback loop, the DPD coefficients based on a generalized memory polynomial (GMP) model are extracted at the ground-receiver and then transmitted to the digital baseband front-end of the LEO satellite-transmitter via a satellite–ground bi-directional transmission link. The issue of the additive white Gaussian noise (AWGN) of the satellite–ground channel affecting the extraction of DPD coefficients is tackled using a superimposing training sequences (STS) method. The proposed technique has been experimentally verified using a 28 GHz phased array. The performance improvements in terms of error vector amplitude (EVM) and adjacent channel power ratio (ACPR) are 7.5% and 3.6 dB, respectively. Requiring limited space-borne resources, this technique offers a promising solution to achieve APA DPD for LEO satellite communications

A Digital Signal Recovery Technique Using DNNs for LEO Satellite Communication Systems

This article proposes a new digital signal recovery (DSR) technique for next-generation power efficient low Earth orbit (LEO) satellite-To-ground communication systems, which feature additive white Gaussian noise (AWGN) channel and significant power variation. This technique utilizes the prior knowledge [i.e., nonlinearities of radio frequency power amplifiers (RF-PAs)] of space-borne transmitters to improve the quality of the signal received at ground stations by modeling and mitigating the imperfection using deep neural networks (DNNs). Benefiting from its robustness against noise and power variation, the proposed DNN based DSR technique (DNN-DSR), can correct high signal distortions caused by the nonlinearities and hence allows RF-PAs to work close to their saturation region, leading to a high power efficiency of the LEO satellites. This work has been validated by both simulations and experiments, in comparison with the power back-off technique as well as memory polynomial-based DSR solutions. Experimental results show that the DNN-DSR technique can increase the drain efficiency of the space-borne RF-PA from 32.6% to 45% while maintaining the same error vector magnitude as the power back-off technique. It has also been demonstrated that the proposed DNN-DSR technique can handle a signal power variation of 12 dB, which is challenging for conventional solutions.</p

Robust Digital Signal Recovery for LEO Satellite Communications Subject to High SNR Variation and Transmitter Memory Effects

This paper proposes a robust digital signal recovery (DSR) technique to tackle the high signal-to-noise ratio (SNR) variation and transmitter memory effects for broadband power efficient down-link in next-generation low Earth orbit (LEO) satellite constellations. The robustness against low SNR is achieved by concurrently integrating magnitude normalization and noise feature filtering using a filtering block built with one batch normalization (BN) layer and two bidirectional long short-term memory (BiLSTM) layers. Moreover, unlike existing deep neural network-based DSR techniques (DNN-DSR), which failed to effectively take into account the memory effects of radio-frequency power amplifiers (RF-PAs) in the model design, the proposed BiLSTM-DSR technique can extracts the sequential characteristics of the adjacent in-phase (I) and quadrature (Q) samples, and hence can obtain superior memory effects compensation compared with the DNN-DSR technique. Experimental validation results of the proposed BiLSTM-DSR with a 100 MHz bandwidth OFDM signal demonstrate an excellent performance of 11.83 dB and 9.4% improvement for adjacent channel power ratio (ACPR) and error vector magnitude (EVM), respectively. BiLSTM-DSR also outperforms the existing DNN-DSR technique in terms of the ACPR and EVM by 2.4 dB and 0.9%, which provides a promising solution for developing deep learning-assisted receivers for high-throughput LEO satellite networks

Functional imaging of interleukin 1 beta expression in inflammatory process using bioluminescence imaging in transgenic mice

<p>Abstract</p> <p>Background</p> <p>Interleukin 1 beta (IL-1β) plays an important role in a number of chronic and acute inflammatory diseases. To understand the role of IL-1β in disease processes and develop an <it>in vivo </it>screening system for anti-inflammatory drugs, a transgenic mouse line was generated which incorporated the transgene firefly luciferase gene driven by a 4.5-kb fragment of the human IL-1β gene promoter. Luciferase gene expression was monitored in live mice under anesthesia using bioluminescence imaging in a number of inflammatory disease models.</p> <p>Results</p> <p>In a LPS-induced sepsis model, dramatic increase in luciferase activity was observed in the mice. This transgene induction was time dependent and correlated with an increase of endogenous IL-1β mRNA and pro-IL-1β protein levels in the mice. In a zymosan-induced arthritis model and an oxazolone-induced skin hypersensitivity reaction model, luciferase expression was locally induced in the zymosan injected knee joint and in the ear with oxazolone application, respectively. Dexamethasone suppressed the expression of luciferase gene both in the acute sepsis model and in the acute arthritis model.</p> <p>Conclusion</p> <p>Our data suggest that the transgenic mice model could be used to study transcriptional regulation of the IL-1β gene expression in the inflammatory process and evaluation the effect of anti-inflammatory drug <it>in vivo</it>.</p

Removal of Hsf4 leads to cataract development in mice through down-regulation of γS-crystallin and Bfsp expression

<p>Abstract</p> <p>Background</p> <p>Heat-shock transcription factor 4 (HSF4) mutations are associated with autosomal dominant lamellar cataract and Marner cataract. Disruptions of the <it>Hsf4 </it>gene cause lens defects in mice, indicating a requirement for HSF4 in fiber cell differentiation during lens development. However, neither the relationship between HSF4 and crystallins nor the detailed mechanism of maintenance of lens transparency by HSF4 is fully understood.</p> <p>Results</p> <p>In an attempt to determine how the underlying biomedical and physiological mechanisms resulting from loss of HSF4 contribute to cataract formation, we generated an <it>Hsf4 </it>knockout mouse model. We showed that the <it>Hsf4 </it>knockout mouse (<it>Hsf4</it>^-/-) partially mimics the human cataract caused by HSF4 mutations. Q-PCR analysis revealed down-regulation of several cataract-relevant genes, including <it>γS-crystallin (Crygs) </it>and lens-specific beaded filament proteins 1 and 2 (<it>Bfsp1 </it>and <it>Bfsp2</it>), in the lens of the <it>Hsf4</it>^-/-mouse. Transcription activity analysis using the dual-luciferase system suggested that these cataract-relevant genes are the direct downstream targets of HSF4. The effect of HSF4 on <it>γS-crystallin </it>is exemplified by the cataractogenesis seen in the <it>Hsf4</it>^-/-,<it>rncat </it>intercross. The 2D electrophoretic analysis of whole-lens lysates revealed a different expression pattern in 8-week-old <it>Hsf4</it>^-/-mice compared with their wild-type counterparts, including the loss of some αA-crystallin modifications and reduced expression of γ-crystallin proteins.</p> <p>Conclusion</p> <p>Our results indicate that HSF4 is sufficiently important to lens development and disruption of the <it>Hsf4 </it>gene leads to cataracts via at least three pathways: 1) down-regulation of <it>γ-crystallin</it>, particularly <it>γS-crystallin</it>; 2) decreased lens beaded filament expression; and 3) loss of post-translational modification of αA-crystallin.</p

Comparison of the Distinct, Host-Specific Response of Three Solanaceae Hosts Induced by <i>Phytophthora infestans</i>

Three Solanaceae hosts (TSHs), S. tuberosum, N. benthamiana and S. lycopersicum, represent the three major phylogenetic clades of Solanaceae plants infected by Phytophthora infestans, which causes late blight, one of the most devastating diseases seriously affecting crop production. However, details regarding how different Solanaceae hosts respond to P. infestans are lacking. Here, we conducted RNA-seq to analyze the transcriptomic data from the TSHs at 12 and 24 h post P. infestans inoculation to capture early expression effects. Macroscopic and microscopic observations showed faster infection processes in S. tuberosum than in N. benthamiana and S. lycopersicum under the same conditions. Analysis of the number of genes and their level of expression indicated that distinct response models were adopted by the TSHs in response to P. infestans. The host-specific infection process led to overlapping but distinct in GO terms and KEGG pathways enriched for differentially expressed genes; many were tightly linked to the immune response in the TSHs. S. tuberosum showed the fastest response and strongest accumulation of reactive oxygen species compared with N. benthamiana and S. lycopersicum, which also had similarities and differences in hormone regulation. Collectively, our study provides an important reference for a better understanding of late blight response mechanisms of different Solanaceae host interactions

QTL Mapping of Fiber-Related Traits Based on a High-Density Genetic Map in Flax (Linum usitatissimum L.)

A genetic map is an important and valuable tool for quantitative trait locus (QTL) mapping, marker-assisted selection (MAS)-based breeding, and reference-assisted chromosome assembly. In this study, 112 F2 plants from a cross between Linum usitatissimum L. “DIANE” and “NY17” and parent plants were subjected to high-throughput sequencing and specific-locus amplified fragment (SLAF) library construction. After preprocessing, 61.64 Gb of raw data containing 253.71 Mb paired-end reads, each 101 bp in length, were obtained. A total of 192,797 SLAFs were identified, of which 23,115 were polymorphic, with a polymorphism rate of 11.99%. Finally, 2,339 SLAFs were organized into a linkage map consisting of 15 linkage groups (LGs). The total length of the genetic map was 1483.25 centimorgans (cM) and the average distance between adjacent markers was 0.63 cM. Combined with flax chromosome-scale pseudomolecules, 12 QTLs associating with 6 flax fiber-related traits were mapped on the chromosomal scaffolds. This high-density genetic map of flax should serve as a foundation for flax fine QTL mapping, draft genome assembly, and MAS-guided breeding. Ultimately, the genomic regions identified in this research could potentially be valuable for improving flax fiber cultivars, as well as for identification of candidate genes involved in flax fiber formation processes.Significance statementA high-density genetic map of flax was constructed, and QTLs were identified on the sequence scaffolds to be interrelated with fiber-related traits. The results of this study will not only provide a platform for gene/QTL fine mapping, map-based gene isolation, and molecular breeding for flax, but also provide a reference to help position sequence scaffolds on the physical map and assist in the process of assembling the flax genome sequence

Tumor-Initiating Cells Are Enriched in CD44hi Population in Murine Salivary Gland Tumor

Tumor-initiating cells (T-ICs) discovered in various tumors have been widely reported. However, T-IC populations in salivary gland tumors have yet to be elucidated. Using the established Pleomorphic Adenoma Gene-1 (Plag1) transgenic mouse model of a salivary gland tumor, we identified CD44high (CD44hi) tumor cells, characterized by high levels of CD44 cell surface expression, as the T-ICs for pleomorphic adenomas. These CD44hi tumor cells incorporated 5-bromo-2-deoxyuridine (BrdU), at a lower rate than their CD44negative (CD44neg) counterparts, and also retained BrdU for a long period of time. Cell surface maker analysis revealed that 25% of the CD44hi tumor cells co-express other cancer stem cell markers such as CD133 and CD117. As few as 500 CD44hi tumor cells were sufficient to initiate pleomorphic adenomas in one third of the wildtype mice, whereas more than 1×104 CD44neg cells were needed for the same purpose. In NIH 3T3 cells, Plag1 was capable of activating the gene transcription of Egr1, a known upregulator for CD44. Furthermore, deletion of sequence 81–96 in the Egr1 promoter region abolished the effect of Plag1 on Egr1 upregulation. Our results establish the existence of T-ICs in murine salivary gland tumors, and suggest a potential molecular mechanism for CD44 upregulation