Converting normal insulators into topological insulators via tuning orbital levels

Tuning the spin-orbit coupling strength via foreign element doping and/or modifying bonding strength via strain engineering are the major routes to convert normal insulators to topological insulators. We here propose an alternative strategy to realize topological phase transition by tuning the orbital level. Following this strategy, our first-principles calculations demonstrate that a topological phase transition in some cubic perovskite-type compounds CsGeBr$_3$ and CsSnBr$_3$ could be facilitated by carbon substitutional doping. Such unique topological phase transition predominantly results from the lower orbital energy of the carbon dopant, which can pull down the conduction bands and even induce band inversion. Beyond conventional approaches, our finding of tuning the orbital level may greatly expand the range of topologically nontrivial materials

Optimizing Data Intensive Flows for Networks on Chips

Data flow analysis and optimization is considered for homogeneous rectangular mesh networks. We propose a flow matrix equation which allows a closed-form characterization of the nature of the minimal time solution, speedup and a simple method to determine when and how much load to distribute to processors. We also propose a rigorous mathematical proof about the flow matrix optimal solution existence and that the solution is unique. The methodology introduced here is applicable to many interconnection networks and switching protocols (as an example we examine toroidal networks and hypercube networks in this paper). An important application is improving chip area and chip scalability for networks on chips processing divisible style loads

Deep Generative Fixed-filter Active Noise Control

Due to the slow convergence and poor tracking ability, conventional LMS-based adaptive algorithms are less capable of handling dynamic noises. Selective fixed-filter active noise control (SFANC) can significantly reduce response time by selecting appropriate pre-trained control filters for different noises. Nonetheless, the limited number of pre-trained control filters may affect noise reduction performance, especially when the incoming noise differs much from the initial noises during pre-training. Therefore, a generative fixed-filter active noise control (GFANC) method is proposed in this paper to overcome the limitation. Based on deep learning and a perfect-reconstruction filter bank, the GFANC method only requires a few prior data (one pre-trained broadband control filter) to automatically generate suitable control filters for various noises. The efficacy of the GFANC method is demonstrated by numerical simulations on real-recorded noises.Comment: Accepted by ICASSP 2023. Code will be available after publicatio

Roles of arabidopsis WRKY18, WRKY40 and WRKY60 transcription factors in plant responses to abscisic acid and abiotic stress

<p>Abstract</p> <p>Background</p> <p>WRKY transcription factors are involved in plant responses to both biotic and abiotic stresses. Arabidopsis WRKY18, WRKY40, and WRKY60 transcription factors interact both physically and functionally in plant defense responses. However, their role in plant abiotic stress response has not been directly analyzed.</p> <p>Results</p> <p>We report that the three WRKYs are involved in plant responses to abscisic acid (ABA) and abiotic stress. Through analysis of single, double, and triple mutants and overexpression lines for the WRKY genes, we have shown that <it>WRKY18 </it>and <it>WRKY60 </it>have a positive effect on plant ABA sensitivity for inhibition of seed germination and root growth. The same two WRKY genes also enhance plant sensitivity to salt and osmotic stress. <it>WRKY40</it>, on the other hand, antagonizes <it>WRKY18 </it>and <it>WRKY60 </it>in the effect on plant sensitivity to ABA and abiotic stress in germination and growth assays. Both <it>WRKY18 </it>and <it>WRKY40 </it>are rapidly induced by ABA, while induction of <it>WRKY60 </it>by ABA is delayed. ABA-inducible expression of <it>WRKY60 </it>is almost completely abolished in the <it>wrky18 </it>and <it>wrky40 </it>mutants. WRKY18 and WRKY40 recognize a cluster of W-box sequences in the <it>WRKY60 </it>promoter and activate WRKY60 expression in protoplasts. Thus, <it>WRKY60 </it>might be a direct target gene of WRKY18 and WRKY40 in ABA signaling. Using a stable transgenic reporter/effector system, we have shown that both WRKY18 and WRKY60 act as weak transcriptional activators while WRKY40 is a transcriptional repressor in plant cells.</p> <p>Conclusions</p> <p>We propose that the three related WRKY transcription factors form a highly interacting regulatory network that modulates gene expression in both plant defense and stress responses by acting as either transcription activator or repressor.</p

Nicotinic Receptor β2 Determines Nk Cell-Dependent Metastasis In A Murine Model Of Metastatic Lung Cancer

Cigarette smoke exposure markedly compromises the ability of the immune system to protect against invading pathogens and tumorigenesis. Nicotine is a psychoactive component of tobacco products that acts as does the natural neurotransmitter, acetylcholine, on nicotinic receptors (nAChRs). Here we demonstrate that natural killer (NK) cells strongly express nAChR β2. Nicotine exposure impairs the ability of NK cells to kill target cells and release cytokines, a process that is largely abrogated by nAChR β2 deficiency. Further, nicotinic suppression of NF-κB-induced transcriptional activity in NK cells is dependent on nAChR β2. This nAChR subtype also plays a large role in the NK cell-mediated control of melanoma lung metastasis, in a murine lung metastasis model exposed to nicotine. Our findings suggest nAChR β2 as a prominent pathway for nicotine induced impairment of NK cell functions which contributes to the occurrence of smoking-related pathologies. © 2013 Hao et al

Inflammation-Mediated Memory Dysfunction and Effects of a Ketogenic Diet in a Murine Model of Multiple Sclerosis

A prominent clinical symptom in multiple sclerosis (MS), a progressive disorder of the central nervous system (CNS) due to heightened neuro-inflammation, is learning and memory dysfunction. Here, we investigated the effects of a ketogenic diet (KD) on memory impairment and CNS-inflammation in a murine model of experimental autoimmune encephalomyelitis (EAE), using electrophysiological, behavioral, biochemical and in vivo imaging approaches. Behavioral spatial learning deficits were associated with motor disability in EAE mice, and were observed concurrently with brain inflammation. The KD improved motor disability in the EAE model, as well as CA1 hippocampal synaptic plasticity (long-term potentiation) and spatial learning and memory (assessed with the Morris Water Maze). Moreover, hippocampal atrophy and periventricular lesions in EAE mice were reversed in KD-treated EAE mice. Finally, we found that the increased expression of inflammatory cytokines and chemokines, as well as the production of reactive oxygen species (ROS), in our EAE model were both suppressed by the KD. Collectively, our findings indicate that brain inflammation in EAE mice is associated with impaired spatial learning and memory function, and that KD treatment can exert protective effects, likely via attenuation of the robust immune response and increased oxidative stress seen in these animals