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Transparent ferroelectric crystals with ultrahigh piezoelectricity 期刊论文
NATURE, 2020, 577 (7790) : 350-+
作者:  Qiu, Chaorui;  Wang, Bo;  Zhang, Nan;  Zhang, Shujun;  Liu, Jinfeng;  Walker, David;  Wang, Yu;  Tian, Hao;  Shrout, Thomas R.;  Xu, Zhuo;  Chen, Long-Qing;  Li, Fei
收藏  |  浏览/下载:16/0  |  提交时间:2020/07/03

Transparent piezoelectrics are highly desirable for numerous hybrid ultrasound-optical devices ranging from photoacoustic imaging transducers to transparent actuators for haptic applications(1-7). However, it is challenging to achieve high piezoelectricity and perfect transparency simultaneously because most high-performance piezoelectrics are ferroelectrics that contain high-density light-scattering domain walls. Here, through a combination of phase-field simulations and experiments, we demonstrate a relatively simple method of using an alternating-current electric field to engineer the domain structures of originally opaque rhombohedral Pb(Mg1/3Nb2/3)O-3-PbTiO3 (PMN-PT) crystals to simultaneously generate near-perfect transparency, an ultrahigh piezoelectric coefficient d(33) (greater than 2,100 picocoulombs per newton), an excellent electromechanical coupling factor k(33) (about 94 per cent) and a large electro-optical coefficient gamma(33) (approximately 220 picometres per volt), which is far beyond the performance of the commonly used transparent ferroelectric crystal LiNbO3. We find that increasing the domain size leads to a higher d(33) value for the [001]-oriented rhombohedral PMN-PT crystals, challenging the conventional wisdom that decreasing the domain size always results in higher piezoelectricity(8-10). This work presents a paradigm for achieving high transparency and piezoelectricity by ferroelectric domain engineering, and we expect the transparent ferroelectric crystals reported here to provide a route to a wide range of hybrid device applications, such as medical imaging, self-energy-harvesting touch screens and invisible robotic devices.


  
Controls on surface water carbonate chemistry along North American ocean margins 期刊论文
NATURE COMMUNICATIONS, 2020, 11 (1)
作者:  Cai, Wei-Jun;  Xu, Yuan-Yuan;  Feely, Richard A.;  Wanninkhof, Rik;  Jonsson, Bror;  Alin, Simone R.;  Barbero, Leticia;  Cross, Jessica N.;  Azetsu-Scott, Kumiko;  Fassbender, Andrea J.;  Carter, Brendan R.;  Jiang, Li-Qing;  Pepin, Pierre;  Chen, Baoshan;  Hussain, Najid;  Reimer, Janet J.;  Xue, Liang;  Salisbury, Joseph E.;  Martin Hernandez-Ayon, Jose;  Langdon, Chris;  Li, Qian;  Sutton, Adrienne J.;  Chen, Chen-Tung A.;  Gledhill, Dwight K.
收藏  |  浏览/下载:14/0  |  提交时间:2020/06/09
Mutations that prevent caspase cleavage of RIPK1 cause autoinflammatory disease 期刊论文
NATURE, 2020, 577 (7788) : 103-+
作者:  Lalaoui, Najoua;  Boyden, Steven E.;  Oda, Hirotsugu;  Wood, Geryl M.;  Stone, Deborah L.;  Chau, Diep;  Liu, Lin;  Stoffels, Monique;  Kratina, Tobias;  Lawlor, Kate E.;  Zaal, Kristien J. M.;  Hoffmann, Patrycja M.;  Etemadi, Nima;  Shield-Artin, Kristy;  Biben, Christine;  Tsai, Wanxia Li;  Blake, Mary D.;  Kuehn, Hye Sun;  Yang, Dan;  Anderton, Holly;  Silke, Natasha;  Wachsmuth, Laurens;  Zheng, Lixin;  Moura, Natalia Sampaio;  Beck, David B.;  Gutierrez-Cruz, Gustavo;  Ombrello, Amanda K.;  Pinto-Patarroyo, Gineth P.;  Kueh, Andrew J.;  Herold, Marco J.;  Hall, Cathrine;  Wang, Hongying;  Chae, Jae Jin;  Dmitrieva, Natalia I.;  McKenzie, Mark;  Light, Amanda;  Barham, Beverly K.;  Jones, Anne;  Romeo, Tina M.;  Zhou, Qing;  Aksentijevich, Ivona;  Mullikin, James C.;  Gross, Andrew J.;  Shum, Anthony K.;  Hawkins, Edwin D.;  Masters, Seth L.;  Lenardo, Michael J.;  Boehm, Manfred;  Rosenzweig, Sergio D.;  Pasparakis, Manolis;  Voss, Anne K.;  Gadina, Massimo;  Kastner, Daniel L.;  Silke, John
收藏  |  浏览/下载:23/0  |  提交时间:2020/07/03

RIPK1 is a key regulator of innate immune signalling pathways. To ensure an optimal inflammatory response, RIPK1 is regulated post-translationally by well-characterized ubiquitylation and phosphorylation events, as well as by caspase-8-mediated cleavage1-7. The physiological relevance of this cleavage event remains unclear, although it is thought to inhibit activation of RIPK3 and necroptosis8. Here we show that the heterozygous missense mutations D324N, D324H and D324Y prevent caspase cleavage of RIPK1 in humans and result in an early-onset periodic fever syndrome and severe intermittent lymphadenopathy-a condition we term '  cleavage-resistant RIPK1-induced autoinflammatory syndrome'  . To define the mechanism for this disease, we generated a cleavage-resistant Ripk1(D325A) mutant mouse strain. Whereas Ripk1(-/-) mice died postnatally from systemic inflammation, Ripk1(D325A/D325A) mice died during embryogenesis. Embryonic lethality was completely prevented by the combined loss of Casp8 and Ripk3, but not by loss of Ripk3 or Mlkl alone. Loss of RIPK1 kinase activity also prevented Ripk1(D325A/D325A) embryonic lethality, although the mice died before weaning from multi-organ inflammation in a RIPK3-dependent manner. Consistently, Ripk1(D325A/D325A) and Ripk1(D325A/+) cells were hypersensitive to RIPK3-dependent TNF-induced apoptosis and necroptosis. Heterozygous Ripk1(D325A/+) mice were viable and grossly normal, but were hyper-responsive to inflammatory stimuli in vivo. Our results demonstrate the importance of caspase-mediated RIPK1 cleavage during embryonic development and show that caspase cleavage of RIPK1 not only inhibits necroptosis but also maintains inflammatory homeostasis throughout life.


  
A dominant autoinflammatory disease caused by non-cleavable variants of RIPK1 期刊论文
NATURE, 2020, 577 (7788) : 109-+
作者:  Tao, Panfeng;  Sun, Jinqiao;  Wu, Zheming;  Wang, Shihao;  Wang, Jun;  Li, Wanjin;  Pan, Heling;  Bai, Renkui;  Zhang, Jiahui;  Wang, Ying;  Lee, Pui Y.;  Ying, Wenjing;  Zhou, Qinhua;  Hou, Jia;  Wang, Wenjie;  Sun, Bijun;  Yang, Mi;  Liu, Danru;  Fang, Ran;  Han, Huan;  Yang, Zhaohui;  Huang, Xin;  Li, Haibo;  Deuitch, Natalie;  Zhang, Yuan;  Dissanayake, Dilan;  Haude, Katrina;  McWalter, Kirsty;  Roadhouse, Chelsea;  MacKenzie, Jennifer J.;  Laxer, Ronald M.;  Aksentijevich, Ivona;  Yu, Xiaomin;  Wang, Xiaochuan;  Yuan, Junying;  Zhou, Qing
收藏  |  浏览/下载:23/0  |  提交时间:2020/07/03

Activation of RIPK1 controls TNF-mediated apoptosis, necroptosis and inflammatory pathways(1). Cleavage of human and mouse RIPK1 after residues D324 and D325, respectively, by caspase-8 separates the RIPK1 kinase domain from the intermediate and death domains. The D325A mutation in mouse RIPK1 leads to embryonic lethality during mouse development(2,3). However, the functional importance of blocking caspase-8-mediated cleavage of RIPK1 on RIPK1 activation in humans is unknown. Here we identify two families with variants in RIPK1 (D324V and D324H) that lead to distinct symptoms of recurrent fevers and lymphadenopathy in an autosomaldominant manner. Impaired cleavage of RIPK1 D324 variants by caspase-8 sensitized patients'  peripheral blood mononuclear cells to RIPK1 activation, apoptosis and necroptosis induced by TNF. The patients showed strong RIPK1-dependent activation of inflammatory signalling pathways and overproduction of inflammatory cytokines and chemokines compared with unaffected controls. Furthermore, we show that expression of the RIPK1 mutants D325V or D325H in mouse embryonic fibroblasts confers not only increased sensitivity to RIPK1 activation-mediated apoptosis and necroptosis, but also induction of pro-inflammatory cytokines such as IL-6 and TNF. By contrast, patient-derived fibroblasts showed reduced expression of RIPK1 and downregulated production of reactive oxygen species, resulting in resistance to necroptosis and ferroptosis. Together, these data suggest that human non-cleavable RIPK1 variants promote activation of RIPK1, and lead to an autoinflammatory disease characterized by hypersensitivity to apoptosis and necroptosis and increased inflammatory response in peripheral blood mononuclear cells, as well as a compensatory mechanism to protect against several pro-death stimuli in fibroblasts.


  
Nanoplasma-enabled picosecond switches for ultrafast electronics (vol 579, pg 534, 2020) 期刊论文
NATURE, 2020, 580 (7803) : E8-E8
作者:  Li, Jing;  Xu, Chuanliang;  Lee, Hyung Joo;  Ren, Shancheng;  Zi, Xiaoyuan;  Zhang, Zhiming;  Wang, Haifeng;  Yu, Yongwei;  Yang, Chenghua;  Gao, Xiaofeng;  Hou, Jianguo;  Wang, Linhui;  Yang, Bo;  Yang, Qing;  Ye, Huamao;  Zhou, Tie;  Lu, Xin;  Wang, Yan;  Qu, Min;  Yang, Qingsong;  Zhang, Wenhui;  Shah, Nakul M.;  Pehrsson, Erica C.;  Wang, Shuo;  Wang, Zengjun;  Jiang, Jun;  Zhu, Yan;  Chen, Rui;  Chen, Huan;  Zhu, Feng;  Lian, Bijun;  Li, Xiaoyun;  Zhang, Yun;  Wang, Chao;  Wang, Yue;  Xiao, Guangan;  Jiang, Junfeng;  Yang, Yue;  Liang, Chaozhao;  Hou, Jianquan;  Han, Conghui;  Chen, Ming;  Jiang, Ning;  Zhang, Dahong;  Wu, Song;  Yang, Jinjian;  Wang, Tao;  Chen, Yongliang;  Cai, Jiantong;  Yang, Wenzeng;  Xu, Jun;  Wang, Shaogang;  Gao, Xu;  Wang, Ting;  Sun, Yinghao
收藏  |  浏览/下载:18/0  |  提交时间:2020/07/03
Z-nucleic-acid sensing triggers ZBP1-dependent necroptosis and inflammation 期刊论文
NATURE, 2020, 580 (7803) : 391-+
作者:  Zhang, Zhibin;  Zhang, Ying;  Xia, Shiyu;  Kong, Qing;  Li, Shunying;  Liu, Xing;  Junqueira, Caroline;  Meza-Sosa, Karla F.;  Mok, Temy Mo Yin;  Ansara, James;  Sengupta, Satyaki;  Yao, Yandan;  Wu, Hao;  Lieberman, Judy
收藏  |  浏览/下载:11/0  |  提交时间:2020/07/03

The biological function of Z-DNA and Z-RNA, nucleic acid structures with a left-handed double helix, is poorly understood(1-3). Z-DNA-binding protein 1 (ZBP1  also known as DAI or DLM-1) is a nucleic acid sensor that contains two Z alpha domains that bind Z-DNA(4,5) and Z-RNA(6-8). ZBP1 mediates host defence against some viruses(6,7,9-14) by sensing viral nucleic acids(6,7,10). RIPK1 deficiency, or mutation of its RIP homotypic interaction motif (RHIM), triggers ZBP1-dependent necroptosis and inflammation in mice(15,16). However, the mechanisms that induce ZBP1 activation in the absence of viral infection remain unknown. Here we show that Z alpha-dependent sensing of endogenous ligands induces ZBP1-mediated perinatal lethality in mice expressing RIPK1 with mutated RHIM (Ripk1(mR/mR)), skin inflammation in mice with epidermis-specific RIPK1 deficiency (RIPK1(E-KO)) and colitis in mice with intestinal epithelial-specific FADD deficiency (FADD(IEC-KO)). Consistently, functional Z alpha domains were required for ZBP1-induced necroptosis in fibroblasts that were treated with caspase inhibitors or express RIPK1 with mutated RHIM. Inhibition of nuclear export triggered the Z alpha-dependent activation of RIPK3 in the nucleus resulting in cell death, which suggests that ZBP1 may recognize nuclear Z-form nucleic acids. We found that ZBP1 constitutively bound cellular double-stranded RNA in a Z alpha-dependent manner. Complementary reads derived from endogenous retroelements were detected in epidermal RNA, which suggests that double-stranded RNA derived from these retroelements may act as a Z alpha-domain ligand that triggers the activation of ZBP1. Collectively, our results provide evidence that the sensing of endogenous Z-form nucleic acids by ZBP1 triggers RIPK3-dependent necroptosis and inflammation, which could underlie the development of chronic inflammatory conditions-particularly in individuals with mutations in RIPK1 and CASP8(17-20).


  
PIK3CA variants selectively initiate brain hyperactivity during gliomagenesis 期刊论文
NATURE, 2020, 578 (7793) : 166-+
作者:  Qiu, Chaorui;  Wang, Bo;  Zhang, Nan;  Zhang, Shujun;  Liu, Jinfeng;  Walker, David;  Wang, Yu;  Tian, Hao;  Shrout, Thomas R.;  Xu, Zhuo;  Chen, Long-Qing;  Li, Fei
收藏  |  浏览/下载:7/0  |  提交时间:2020/07/03

Glioblastoma is a universally lethal form of brain cancer that exhibits an array of pathophysiological phenotypes, many of which are mediated by interactions with the neuronal microenvironment(1,2). Recent studies have shown that increases in neuronal activity have an important role in the proliferation and progression of glioblastoma(3,4). Whether there is reciprocal crosstalk between glioblastoma and neurons remains poorly defined, as the mechanisms that underlie how these tumours remodel the neuronal milieu towards increased activity are unknown. Here, using a native mouse model of glioblastoma, we develop a high-throughput in vivo screening platform and discover several driver variants of PIK3CA. We show that tumours driven by these variants have divergent molecular properties that manifest in selective initiation of brain hyperexcitability and remodelling of the synaptic constituency. Furthermore, secreted members of the glypican (GPC) family are selectively expressed in these tumours, and GPC3 drives gliomagenesis and hyperexcitability. Together, our studies illustrate the importance of functionally interrogating diverse tumour phenotypes driven by individual, yet related, variants and reveal how glioblastoma alters the neuronal microenvironment.


Glioblastoma tumours expressing oncogenic PIK3CA variants secrete the glycan GPC3, which promotes the formation of neural synapses, brain synaptic hyperexcitability and gliomagenesis.


  
The evolutionary history of 2,658 cancers 期刊论文
NATURE, 2020, 578 (7793) : 122-+
作者:  Tao, Panfeng;  Sun, Jinqiao;  Wu, Zheming;  Wang, Shihao;  Wang, Jun;  Li, Wanjin;  Pan, Heling;  Bai, Renkui;  Zhang, Jiahui;  Wang, Ying;  Lee, Pui Y.;  Ying, Wenjing;  Zhou, Qinhua;  Hou, Jia;  Wang, Wenjie;  Sun, Bijun;  Yang, Mi;  Liu, Danru;  Fang, Ran;  Han, Huan;  Yang, Zhaohui;  Huang, Xin;  Li, Haibo;  Deuitch, Natalie;  Zhang, Yuan;  Dissanayake, Dilan;  Haude, Katrina;  McWalter, Kirsty;  Roadhouse, Chelsea;  MacKenzie, Jennifer J.;  Laxer, Ronald M.;  Aksentijevich, Ivona;  Yu, Xiaomin;  Wang, Xiaochuan;  Yuan, Junying;  Zhou, Qing
收藏  |  浏览/下载:33/0  |  提交时间:2020/07/03

Cancer develops through a process of somatic evolution(1,2). Sequencing data from a single biopsy represent a snapshot of this process that can reveal the timing of specific genomic aberrations and the changing influence of mutational processes(3). Here, by whole-genome sequencing analysis of 2,658 cancers as part of the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA)(4), we reconstruct the life history and evolution of mutational processes and driver mutation sequences of 38 types of cancer. Early oncogenesis is characterized by mutations in a constrained set of driver genes, and specific copy number gains, such as trisomy 7 in glioblastoma and isochromosome 17q in medulloblastoma. The mutational spectrum changes significantly throughout tumour evolution in 40% of samples. A nearly fourfold diversification of driver genes and increased genomic instability are features of later stages. Copy number alterations often occur in mitotic crises, and lead to simultaneous gains of chromosomal segments. Timing analyses suggest that driver mutations often precede diagnosis by many years, if not decades. Together, these results determine the evolutionary trajectories of cancer, and highlight opportunities for early cancer detection.


  
Super-elastic ferroelectric single-crystal membrane with continuous electric dipole rotation 期刊论文
SCIENCE, 2019, 366 (6464) : 475-+
作者:  Dong, Guohua;  Li, Suzhi;  Yao, Mouteng;  Zhou, Ziyao;  Zhang, Yong-Qiang;  Han, Xu;  Luo, Zhenlin;  Yao, Junxiang;  Peng, Bin;  Hu, Zhongqiang;  Huang, Houbing;  Jia, Tingting;  Li, Jiangyu;  Ren, Wei;  Ye, Zuo-Guang;  Ding, Xiangdong;  Sun, Jun;  Nan, Ce-Wen;  Chen, Long-Qing;  Li, Ju;  Liu, Ming
收藏  |  浏览/下载:9/0  |  提交时间:2019/11/27
Ultrahigh-energy density lead-free dielectric films via polymorphic nanodomain design 期刊论文
SCIENCE, 2019, 365 (6453) : 578-582
作者:  Pan, Hao;  Li, Fei;  Liu, Yao;  Zhang, Qinghua;  Wang, Meng;  Lan, Shun;  Zheng, Yunpeng;  Ma, Jing;  Gu, Lin;  Shen, Yang;  Yu, Pu;  Zhang, Shujun;  Chen, Long-Qing;  Lin, Yuan-Hua;  Nan, Ce-Wen
收藏  |  浏览/下载:13/0  |  提交时间:2019/11/27