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CHLOROQUINE HYPE DERAILS CORONAVIRUS DRUG TRIALS 期刊论文
NATURE, 2020, 580 (7805) : 573-573
作者:  Hu, Minjie;  Zheng, Xiaobin;  Fan, Chen-Ming;  Zheng, Yixian
收藏  |  浏览/下载:16/0  |  提交时间:2020/07/03

With politicians touting the potential benefits of malaria drugs to fight COVID-19, some people are turning away from clinical trials of other therapies.


With politicians touting the potential benefits of malaria drugs to fight COVID-19, some people are turning away from clinical trials of other therapies.


  
Submicrosecond entangling gate between trapped ions via Rydberg interaction 期刊论文
NATURE, 2020, 580 (7803) : 345-+
作者:  Chatterjee, Sourav;  Guidi, Mara;  Seeberger, Peter H.;  Gilmore, Kerry
收藏  |  浏览/下载:16/0  |  提交时间:2020/07/03

Generating quantum entanglement in large systems on timescales much shorter than the coherence time is key to powerful quantum simulation and computation. Trapped ions are among the most accurately controlled and best isolated quantum systems(1) with low-error entanglement gates operated within tens of microseconds using the vibrational motion of few-ion crystals(2,3). To exceed the level of complexity tractable by classical computers the main challenge is to realize fast entanglement operations in crystals made up of many ions (large ion crystals)(4). The strong dipole-dipole interactions in polar molecule(5) and Rydberg atom(6,7) systems allow much faster entangling gates, yet stable state-independent confinement comparable with trapped ions needs to be demonstrated in these systems(8). Here we combine the benefits of these approaches: we report a two-ion entangling gate with 700-nanosecond gate time that uses the strong dipolar interaction between trapped Rydberg ions, which we use to produce a Bell state with 78 per cent fidelity. The sources of gate error are identified and a total error of less than 0.2 per cent is predicted for experimentally achievable parameters. Furthermore, we predict that residual coupling to motional modes contributes an approximate gate error of 10(-4) in a large ion crystal of 100 ions. This provides a way to speed up and scale up trapped-ion quantum computers and simulators substantially.


  
AGEING RATS SEE THE BENEFITS OF CUTTING CALORIES 期刊论文
NATURE, 2020, 579 (7797) : 10-10
作者:  Callaway, Ewen;  Cyranoski, David
收藏  |  浏览/下载:6/0  |  提交时间:2020/07/03
Targeting of temperate phages drives loss of type I CRISPR-Cas systems 期刊论文
NATURE, 2020, 578 (7793) : 149-+
作者:  Xiang, Lifeng;  Yin, Yu;  Zheng, Yun;  Ma, Yanping;  Li, Yonggang;  Zhao, Zhigang;  Guo, Junqiang;  Ai, Zongyong;  Niu, Yuyu;  Duan, Kui;  He, Jingjing;  Ren, Shuchao;  Wu, Dan;  Bai, Yun;  Shang, Zhouchun;  Dai, Xi;  Ji, Weizhi;  Li, Tianqing
收藏  |  浏览/下载:30/0  |  提交时间:2020/07/03

On infection of their host, temperate viruses that infect bacteria (bacteriophages  hereafter referred to as phages) enter either a lytic or a lysogenic cycle. The former results in lysis of bacterial cells and phage release (resulting in horizontal transmission), whereas lysogeny is characterized by the integration of the phage into the host genome, and dormancy (resulting in vertical transmission)(1). Previous co-culture experiments using bacteria and mutants of temperate phages that are locked in the lytic cycle have shown that CRISPR-Cas systems can efficiently eliminate the invading phages(2,3). Here we show that, when challenged with wild-type temperate phages (which can become lysogenic), type I CRISPR-Cas immune systems cannot eliminate the phages from the bacterial population. Furthermore, our data suggest that, in this context, CRISPR-Cas immune systems are maladaptive to the host, owing to the severe immunopathological effects that are brought about by imperfect matching of spacers to the integrated phage sequences (prophages). These fitness costs drive the loss of CRISPR-Cas from bacterial populations, unless the phage carries anti-CRISPR (acr) genes that suppress the immune system of the host. Using bioinformatics, we show that this imperfect targeting is likely to occur frequently in nature. These findings help to explain the patchy distribution of CRISPR-Cas immune systems within and between bacterial species, and highlight the strong selective benefits of phage-encoded acr genes for both the phage and the host under these circumstances.


CRISPR-Cas systems cannot eliminate temperate bacteriophages from bacterial populations and-in this context-the systems impose immunopathological costs on the host, creating selective pressures that may explain their patchy distribution in bacteria.