《自然》（20190103出版）一周論文導讀

Nature, 3 January 2019, Volume 565 Issue 7737

《自然》2019年1月3日第7737期565卷

物理學Physics

An ultrafast symmetry switch in a Weyl semimetal

Weyl半金屬的超快對稱性開關

作者：Edbert J. Sie、Clara M. Nyby、C. D. Pemmaraju、Su Ji Park、Xijie Wang、Aaron M. Lindenberg， et al

鏈接：

https://www.nature.com/articles/s41586-018-0809-4

摘要：

晶體材料按照其電子結構的不同可以劃分為金屬和絕緣體兩大類。拓撲金屬具有特殊的能帶結構，它包含一些能帶結構的奇點。

在絕大多數金屬材料中，這樣的Weyl點都會遠離費米面，但是如果這樣的點恰好坐落在費米面上，就會給出一類非常特殊的電子結構：拓撲半金屬——其費米面縮小為費米點，能隙為0，且具有線性色散。

但集成到功能設備中需要超越材料的拓撲保護特性並在高速下操縱拓撲的能力。

本文利用相對論電子衍射的晶體測量結果證明，太赫茲光脈衝可以在Weyl半金屬WTe₂中誘發太赫茲頻層間剪切應變，且應變幅較大，從而形成拓撲上不同的亞穩態相。

這項工作證明了超快操縱固體拓撲特性的可能性，以及開發以太赫茲頻率工作的拓撲開關的可能性。

Abstract

Topological quantum materials exhibit fascinating properties, with important applications for dissipationless electronics and fault-tolerant quantum computers. Manipulating the topological invariants in these materials would allow the development of topological switching applications analogous to switching of transistors. Lattice strain provides the most natural means of tuning these topological invariants because it directly modifies the electron–ion interactions and potentially alters the underlying crystalline symmetry on which the topological properties depend. However, conventional means of applying strain through heteroepitaxial lattice mismatch and dislocations are not extendable to controllable time-varying protocols, which are required in transistors. Integration into a functional device requires the ability to go beyond the robust, topologically protected properties of materials and to manipulate the topology at high speeds. Here we use crystallographic measurements by relativistic electron diffraction to demonstrate that terahertz light pulses can be used to induce terahertz-frequency interlayer shear strain with large strain amplitude in the Weyl semimetal WTe₂, leading to a topologically distinct metastable phase. Separate nonlinear optical measurements indicate that this transition isassociated with a symmetry change to a centrosymmetric, topologically trivialphase. We further show that such shear strain provides an ultrafast, energy-efficient way of inducing robust, well separated Weyl points or of annihilating all Weyl points of opposite chirality. This work demonstrates possibilities for ultrafast manipulation of the topological properties of solids and for the development of a topological switch operating at terahertz frequencies.

Scalable energy-efficient magnetoelectric spin–orbit logic

高擴展、高效能磁電自旋邏輯電路

作者：SasikanthManipatruni、Dmitri E.Nikonov、Chia-ChingLin、Tanay A.Gosavi，et al

鏈接：

https://www.nature.com/articles/s41586-018-0770-2

摘要：

自上世紀80年代初以來，大多數電子產品都依賴於使用互補的金屬氧化物半導體（CMOS）晶體管。

然而，CMOS工作原理，包括由絕緣柵控制的可開關半導體電導，在很大程度上保持不變，即使晶體管被縮小到10納米。而在當今數據時代，數據爆炸帶來了對更高效計算機的需求。

文章中，研究者展示了一種製作新型邏輯器件和存儲器件的方法。相比於傳統 CMOS 集成的微處理器，新微處理器能效可以得到顯著增強。

結果顯示，與CMOS技術相比，新設備具有更高的轉換能量、較低的開關電壓和增強的邏輯密度。

Abstract

Since the early 1980s, most electronics have relied on the use of complementary metal–oxide–semiconductor (CMOS) transistors. However, the principles of CMOS operation, involving a switchable semiconductor conductance controlled by aninsulating gate, have remained largely unchanged, even as transistors are miniaturized to sizes of 10 nanometres. We investigated what dimensionally scalable logic technology beyond CMOS could provide improvements in efficiency and performance for von Neumann architectures and enable growth in emerging computing such as artifical intelligence. Such a computing technology needs to allow progressive miniaturization, reduce switching energy, improve device interconnection and provide a complete logic and memory family. Here we propose a scalable spintronic logic device that operates via spin–orbit transduction (the coupling of an electron』s angular momentum with its linear momentum) combined with magnetoelectric switching. The device uses advanced quantum materials, especially correlated oxides and topological states of matter, for collective switching and detection. We describe progress in magnetoelectric switching and spin–orbit detection of state, and show that in comparison with CMOS technology our devicehas superior switching energy (by a factor of 10 to 30), lower switching voltage (by a factor of 5) and enhanced logic density (by a factor of 5). Inaddition, its non-volatility enables ultralow standby power, which is critical to modern computing. The properties of our device indicate that the proposed technology could enable the development of multi-generational computing.

環境Enviroment

Greenland melt drives continuous export of methane from the ice-sheet bed

格陵蘭島融化推動了冰蓋甲烷的持續輸出

作者：Guillaume Lamarche-Gagnon、Barbara Sherwood Lollar、Sandra Arndt, Peer Fietzek、Alexander D. Beaton,et al

鏈接：

https://www.nature.com/articles/s41586-018-0800-0

摘要：

在全球甲烷預算中，冰蓋目前被忽略了。儘管有人提出，冰蓋中蘊藏著大量甲烷，如果這些氣體在冰層快速消退期間釋放，可能會導致大氣甲烷濃度上升，但目前還沒有關於冰蓋甲烷足跡的數據。

在這裡，研究人員發現，格陵蘭冰蓋的冰川下集水區的有效排水系統迅速地將冰川下產生的甲烷驅動到冰川邊緣。

他們報告了在融化季節，甲烷—過飽和水（CH_4(aq)）持續從冰蓋中的連續輸出。

結果表明，冰蓋覆蓋著廣泛的、生物活性強的產甲烷濕地，冰川下水文學對於控制來自冰蓋的甲烷通量至關重要，此類環境因素以前被低估了，應該在地球的甲烷預算中加以考慮。

Abstract

Ice sheets are currently ignored in global methane budgets. Although ice sheets have been proposed to contain large reserves of methane that may contribute to a rise in atmospheric methane concentration if released during periods of rapid iceretreat, no data exist on the current methane footprint of ice sheets. Here we find that subglacially produced methane is rapidly driven to the ice margin by the efficient drainage system of a subglacial catchment of the Greenland ice sheet. We report the continuous export of methane-supersaturated waters (CH_4(aq)) from the ice-sheet bed during the melt season. Pulses of high CH_4(aq)concentration coincide with supraglacially forced subglacial flushing events, confirming a subglacial source and highlighting the influence of melt on methane export. Sustained methane fluxes over the melt season are indicative of subglacial methane reserves that exceed methane export, with an estimated 6.3 tonnes (discharge-weighted mean; range from 2.4 to 11 tonnes) of CH_4(aq)transported laterally from the ice-sheet bed. Stable-isotope analyses reveal a microbial origin for methane, probably from a mixture of inorganic and ancient organic carbon buried beneath the ice. We show that subglacial hydrology is crucial for controlling methane fluxes from the ice sheet, with efficient drainage limiting the extent of methane oxidation to about 17 per cent of methane exported. Atmospheric evasion is the main methane sink once run off reaches the ice margin, with estimated diffusive fluxes (4.4 to 28 millimoles of CH₄per square metre per day) rivalling that of major world rivers. Overall, our results indicate that ice sheets overlie extensive, biologically active methanogenic wetlands and that high rates of methane export to the atmospherecan occur via efficient subglacial drainage pathways. Our findings suggest that such environments have been previously underappreciated and should be consideredin Earth』s methane budget.

Capture of nebular gases during Earth』s accretion is preserved in deep-mantle neon

地球吸積過程中捕捉到的星雲氣體保存在深地幔氖中

作者：Curtis D. Williams、Sujoy Mukhopadhyay

鏈接：

https://www.nature.com/articles/s41586-018-0771-1

摘要：

行星內部捕獲星雲氣體的證據將對行星形成模型造成重要的限制。這些約束包括吸積時間尺度、熱演化、揮發性成分和行星氧化還原態。

目前，在地球內部存在這種氣體的證據仍然存在爭議。與其他生命必須的化學元素不同，氖（Ne）是惰性的，意味著它不會隨化學和生物過程發生變化。

在本文中，同位素測量深地幔揭示²⁰Ne/²²Ne比率高達13.03±0.04。這些比值明顯高於太陽—風輻照物質和CI球粒隕石的比值，這需要在地幔深處存在星雲氖。

Abstract

Evidence for the capture of nebular gases by planetary interiors would place important constraints on models of planet formation. These constraints include accretion timescales, thermal evolution, volatile compositions and planetary redox states. Retention of nebular gases by planetary interiors also constrains the dynamics of outgassing and volatile loss associated with the assembly and ensuing evolution of terrestrial planets. But evidence for such gases in Earth』s interior remains controversia. The ratio of the two primordial neon isotopes, ²⁰Ne/²²Ne, is significantly different for the three potential sources of Earth』s volatiles: nebular gas, solar-wind-irradiated material and CI chondrites. Therefore, the²⁰Ne/²²Ne ratio is a powerful tool for assessingthe source of volatiles in Earth』s interior. Here we present neon is otope measurements from deep mantle plumes that reveal²⁰Ne/²²Ne ratios of up to 13.03 ± 0.04 (2 standard deviations). These ratiosare demonstrably higher than those for solar-wind-irradiated material and CI chondrites, requiring the presence of nebular neon in the deep mantle. Furthermore, we determine a²⁰Ne/²²Ne ratio for the primordial plume mantle of 13.23 ± 0.22 (2 standard deviations), which is indistinguishable from the nebular ratio, providing robust evidence for a reservoir of nebular gas preserved in the deep mantle today. The acquisition of nebular gases requires planetary embryos to grow to sufficiently large mass before the dissipation of the protoplanetary disk. Our observations also indicate distinct²⁰Ne/²²Ne ratios between deep mantle plumes and mid-ocean-ridge basalts, which is best explained by addition of a chondritic component to the shallower mantle during the main phase of Earth』s accretion and by subsequent recycling of seawater-derived neon in platetectonic processes.

生物學Biology

Identifying the pathways required for coping behaviours associated with sustained pain

識別與持續疼痛相關的應對行為所需的途徑

作者：Tianwen Huang、Shing-Hong Lin、Nathalie M. Malewicz、Qiufu Ma , et al

鏈接：

https://www.nature.com/articles/s41586-018-0793-8

摘要：

動物和人類對傷害刺激有兩種反應。第一種包括防止或限制傷害的反射性防禦反應，例如一個人的手在接觸熱的物體時迅速縮回。

當第一行反應不能阻止損傷時，產生的疼痛會引發第二種應對反應——比如舔受傷部位以緩解疼痛。

這是兩種不同的進化反應，但科學家一直無法解釋這種現象的分子起源和信號傳導路徑。

本研究確定了深層次持續痛疼背後的神經信號通路，這種持續性疼痛在受傷後立刻發生。

同時還揭示了促使反射性戒斷以避免傷害，以及隨後的疼痛應對反應，存在不同的信號傳導路徑。這是首次闡明這些反應是如何在大腦以外的地方產生的。

Abstract

Animals and humans display two types of response to noxious stimuli. The first includes reflexive defensive responses that prevent or limit injury; a well-known example of these responses is the quick withdrawal of one』s hand upon touching a hot object. When the first-line response fails to prevent tissue damage (for example, a finger is burnt), the resulting pain invokes a second-line coping response—such as licking the injured area to soothe suffering. However, the underlying neural circuits that drive these two strings of behaviour remain poorly understood. Here we show in mice that spinal neurons marked by coexpression of TAC1^Creand LBX1^Flpodrive coping responses associated with pain. Ablation of these spinal neurons led to the loss of both persistent licking and conditioned aversion evoked by stimuli (including skin pinching and burn injury) that—in humans—produce sustained pain, without affecting any of the reflexive defensive reactions that we tested. This selective in difference to sustained pain resembles the phenotype seen in humans with lesions of medial thalamic nuclei. Consistently, spinal TAC1-lineage neuronsare connected to medial thalamic nuclei by direct projections and via indirect routes through the superior lateral parabrachial nuclei. Furthermore, the anatomical and functional segregation observed at the spinal level also applies to primary sensory neurons. For example, in response to noxious mechanical stimuli, MRGPRD- and TRPV1-positive nociceptors are required to elicit reflexive and coping responses, respectively. Our study therefore reveals a fundamental subdivision within the cutaneous somatosensory system, and challenges the validity of using reflexive defensive responses to measure sustained pain.

Structure of Plasmodium falciparum Rh5–CyRPA–Ripr invasion complex

惡性瘧原蟲體內由 Rh5–CyRPA–Ripr組成的蛋白複合物

作者：WilsonWong、RickHuang、SebastienMenant、ZhihengYu、AlanF. Cowman, et al

鏈接：

https://www.nature.com/articles/s41586-018-0779-6

摘要：

瘧疾每年導致全球約50萬人死亡，其中惡性瘧原蟲是常見的一種瘧原蟲，導致了許多瘧疾死亡病例。它在入侵人體細胞時，依靠一種蛋白複合物進入細胞內部。

本文中，研究人員利用低溫冷凍電子顯微鏡技術，首次描繪出惡性瘧原蟲體內由Rh5、CyPRA和Ripr三種蛋白質組成的蛋白複合物的三維結構圖。

瘧原蟲依靠這種蛋白複合物與人體血液中紅細胞內部的受體建立聯繫，從而進入紅細胞內部並導致疾病。

揭示這種蛋白複合物的三維結構，有助深入理解瘧原蟲入侵細胞機制，並找出阻斷其感染的方法，在此基礎上有可能開發出針對惡性瘧原蟲的疫苗。

Abstract

Plasmodium falciparum causes the severe form of malaria that has high levels of mortality in humans. Blood-stage merozoites of P. falciparum invade erythrocytes, and this requires interactions between multiple ligands from the parasite and receptors in hosts. These interactions include the binding of the Rh5–CyRPA–Ripr complex with the erythrocyte receptor basigin1, which is an essential step for entry into human erythrocytes. Here we show thatthe Rh5–CyRPA–Ripr complex binds the erythrocyte cell line JK-1 significantlybetter than does Rh5 alone, and that this binding occurs through the insertion of Rh5 and Ripr into host membranes as a complex with high molecular weight. We report a cryo-electron microscopy structure of the Rh5–CyRPA–Ripr complex at subnanometre resolution, which reveals the organization of this essential invasion complex and the mode of interactions between members of the complex, and shows that CyRPA is a critical mediator of complex assembly. Our structure identifies blades 4–6 of the β-propeller of CyRPA as contact sites for Rh5 and Ripr. The limited contacts between Rh5–CyRPA and CyRPA–Ripr are consistent with the dissociation of Rh5 and Ripr from CyRPA for membrane insertion. A comparision of the crystal structure of Rh5–basigin with the cryo-electron microscopy structure of Rh5–CyRPA–Ripr suggests that Rh5 and Ripr are positioned parallel to the erythrocyte membrane before membrane insertion. This provides information on the function of this complex, and thereby provides insights into invasion by P.falciparum.

Loss of ADAR1 in tumours overcomesresistance to immune checkpoint blockade

腫瘤中的ADAR1缺失能影響免疫療法效果

作者：Jeffrey J. Ishizuka、Robert T. Manguso、W. Nicholas Haining, etal

鏈接：

https://www.nature.com/articles/s41586-018-0768-9

摘要：

大多數癌症患者要麼對免疫檢查點阻滯沒有響應，要麼對其產生耐藥性，這往往是因為獲得性突變削弱了抗原呈現。

在這裡，研究人員展示了腫瘤細胞中RNA編輯酶ADAR1功能的喪失，使腫瘤對免疫治療具有敏感性，並克服了對檢查點阻滯的抵抗。

在ADAR1缺失的情況下，干擾素誘導的RNA的A-to-I編輯減少，導致PKR和MDA5檢測雙鏈RNA配體；這分別導致生長抑制和腫瘤炎症。該成果有助於開發針對免疫療法失效的一般策略。

Abstract

Most patients with cancer either do not respond to immune checkpoint blockade or develop resistance to it, often because of acquired mutations that impair antigen presentation. Here we show that loss of function of the RNA-editing enzyme ADAR1 in tumour cells profoundly sensitizes tumours to immunotherapy and overcomes resistance to checkpoint blockade. In the absence of ADAR1, A-to-I editing of interferon-inducible RNA species is reduced, leading to double-stranded RNA ligand sensing by PKR and MDA5; this results in growth inhibition and tumour inflammation, respectively. Loss of ADAR1 overcomes resistance to PD-1 checkpoint blockade caused by inactivation of antigen presentation by tumour cells. Thus, effective anti-tumour immunity is constrained by inhibitory checkpoints such as ADAR1 that limit the sensing of innate ligands. The induction of sufficient inflammation in tumours that are sensitized to interferon can bypass the therapeutic requirement for CD8+ T cell recognition of cancer cells and may provide a general strategy to overcome immunotherapy resistance.

（唐一塵）

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