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MIT科学家开发出可用于山体滑坡和地震预测的新技术 快报文章
地球科学快报,2024年第7期
作者:  王立伟
Microsoft Word(14Kb)  |  收藏  |  浏览/下载:609/0  |  提交时间:2024/04/10
mechanisms  landslides and earthquakes  
The timing and effect of the earliest human arrivals in North America 期刊论文
NATURE, 2020
作者:  Lorena Becerra-Valdivia;  Thomas Higham
收藏  |  浏览/下载:26/0  |  提交时间:2020/08/09

The peopling of the Americas marks a major expansion of humans across the planet. However, questions regarding the timing and mechanisms of this dispersal remain, and the previously accepted model (termed '  Clovis-first'  )-suggesting that the first inhabitants of the Americas were linked with the Clovis tradition, a complex marked by distinctive fluted lithic points(1)-has been effectively refuted. Here we analyse chronometric data from 42 North American and Beringian archaeological sites using a Bayesian age modelling approach, and use the resulting chronological framework to elucidate spatiotemporal patterns of human dispersal. We then integrate these patterns with the available genetic and climatic evidence. The data obtained show that humans were probably present before, during and immediately after the Last Glacial Maximum (about 26.5-19 thousand years ago)(2,3)but that more widespread occupation began during a period of abrupt warming, Greenland Interstadial 1 (about 14.7-12.9 thousand years beforead 2000)(4). We also identify the near-synchronous commencement of Beringian, Clovis and Western Stemmed cultural traditions, and an overlap of each with the last dates for the appearance of 18 now-extinct faunal genera. Our analysis suggests that the widespread expansion of humans through North America was a key factor in the extinction of large terrestrial mammals.


A Bayesian age model suggests that human dispersal to the Americas probably began before the Last Glacial Maximum, overlapping with the last dates of appearance for several faunal genera.


  
Current European flood-rich period exceptional compared with past 500 years 期刊论文
NATURE, 2020, 583 (7817) : 560-+
作者:  ;  nter Blö;  schl;  Andrea Kiss;  Alberto Viglione;  Mariano Barriendos;  Oliver Bö;  hm;  Rudolf Brá;  zdil;  Denis Coeur;  Gaston Demaré;  e;  Maria Carmen Llasat;  Neil Macdonald;  Dag Retsö;  Lars Roald;  Petra Schmocker-Fackel;  Inê;  s Amorim;  Monika Bě;  ;  nová;  Gerardo Benito;  Chiara Bertolin;  Dario Camuffo;  Daniel Cornel;  Radosł;  aw Doktor;  ;  bor Elleder;  Silvia Enzi;  Joã;  o Carlos Garcia;  ;  diger Glaser;  Julia Hall;  Klaus Haslinger;  Michael Hofstä;  tter;  ;  rgen Komma;  Danuta Limanó;  wka;  David Lun;  Andrei Panin;  Juraj Parajka;  Hrvoje Petrić;  Fernando S. Rodrigo;  Christian Rohr;  Johannes Schö;  nbein;  Lothar Schulte;  Luí;  s Pedro Silva;  Willem H. J. Toonen;  Peter Valent;  ;  rgen Waser;  Oliver Wetter
收藏  |  浏览/下载:40/0  |  提交时间:2020/08/09

There are concerns that recent climate change is altering the frequency and magnitude of river floods in an unprecedented way(1). Historical studies have identified flood-rich periods in the past half millennium in various regions of Europe(2). However, because of the low temporal resolution of existing datasets and the relatively low number of series, it has remained unclear whether Europe is currently in a flood-rich period from a long-term perspective. Here we analyse how recent decades compare with the flood history of Europe, using a new database composed of more than 100 high-resolution (sub-annual) historical flood series based on documentary evidence covering all major regions of Europe. We show that the past three decades were among the most flood-rich periods in Europe in the past 500 years, and that this period differs from other flood-rich periods in terms of its extent, air temperatures and flood seasonality. We identified nine flood-rich periods and associated regions. Among the periods richest in floods are 1560-1580 (western and central Europe), 1760-1800 (most of Europe), 1840-1870 (western and southern Europe) and 1990-2016 (western and central Europe). In most parts of Europe, previous flood-rich periods occurred during cooler-than-usual phases, but the current flood-rich period has been much warmer. Flood seasonality is also more pronounced in the recent period. For example, during previous flood and interflood periods, 41 per cent and 42 per cent of central European floods occurred in summer, respectively, compared with 55 per cent of floods in the recent period. The exceptional nature of the present-day flood-rich period calls for process-based tools for flood-risk assessment that capture the physical mechanisms involved, and management strategies that can incorporate the recent changes in risk.


Analysis of thousands of historical documents recording floods in Europe shows that flooding characteristics in recent decades are unlike those of previous centuries.


  
The Orinoco Low-Level Jet: An Investigation of Its Mechanisms of Formation Using the WRF Model 期刊论文
JOURNAL OF GEOPHYSICAL RESEARCH-ATMOSPHERES, 2020, 125 (13)
作者:  Jimenez-Sanchez, Giovanni;  Markowski, Paul M.;  Young, George S.;  Stensrud, David J.
收藏  |  浏览/下载:9/0  |  提交时间:2020/08/18
Orinoco low-level jet  forcing mechanisms  dynamical downscaling  momentum balance analysis  LLJs near the equator may originate from processes other than the inertial oscillation  LLJs near the equator may originate from processes other than topographic thermal forcing  
Coupling delay controls synchronized oscillation in the segmentation clock 期刊论文
NATURE, 2020
作者:  Yoshioka-Kobayashi, Kumiko;  Matsumiya, Marina;  Niino, Yusuke;  Isomura, Akihiro;  Kori, Hiroshi;  Miyawaki, Atsushi;  Kageyama, Ryoichiro
收藏  |  浏览/下载:7/0  |  提交时间:2020/07/03

Individual cellular activities fluctuate but are constantly coordinated at the population level via cell-cell coupling. A notable example is the somite segmentation clock, in which the expression of clock genes (such as Hes7) oscillates in synchrony between the cells that comprise the presomitic mesoderm (PSM)(1,2). This synchronization depends on the Notch signalling pathway  inhibiting this pathway desynchronizes oscillations, leading to somite fusion(3-7). However, how Notch signalling regulates the synchronicity of HES7 oscillations is unknown. Here we establish a live-imaging system using a new fluorescent reporter (Achilles), which we fuse with HES7 to monitor synchronous oscillations in HES7 expression in the mouse PSM at a single-cell resolution. Wild-type cells can rapidly correct for phase fluctuations in HES7 oscillations, whereas the absence of the Notch modulator gene lunatic fringe (Lfng) leads to a loss of synchrony between PSM cells. Furthermore, HES7 oscillations are severely dampened in individual cells of Lfng-null PSM. However, when Lfng-null PSM cells were completely dissociated, the amplitude and periodicity of HES7 oscillations were almost normal, which suggests that LFNG is involved mostly in cell-cell coupling. Mixed cultures of control and Lfng-null PSM cells, and an optogenetic Notch signalling reporter assay, revealed that LFNG delays the signal-sending process of intercellular Notch signalling transmission. These results-together with mathematical modelling-raised the possibility that Lfng-null PSM cells shorten the coupling delay, thereby approaching a condition known as the oscillation or amplitude death of coupled oscillators(8). Indeed, a small compound that lengthens the coupling delay partially rescues the amplitude and synchrony of HES7 oscillations in Lfng-null PSM cells. Our study reveals a delay control mechanism of the oscillatory networks involved in somite segmentation, and indicates that intercellular coupling with the correct delay is essential for synchronized oscillation.


Monitoring cells of the mouse presomitic mesoderm using the Achilles reporter fused to HES7 sheds light on the mechanisms that underpin synchronous oscillations in the expression of clock genes between neighbouring cells.


  
Frequent mutations that converge on the NFKBIZ pathway in ulcerative colitis 期刊论文
NATURE, 2020, 577 (7789) : 260-+
作者:  Kakiuchi, Nobuyuki;  Yoshida, Kenichi;  Uchino, Motoi;  Kihara, Takako;  Akaki, Kotaro;  Inoue, Yoshikage;  Kawada, Kenji;  Nagayama, Satoshi;  Yokoyama, Akira;  Yamamoto, Shuji;  Matsuura, Minoru;  Horimatsu, Takahiro;  Hirano, Tomonori;  Goto, Norihiro;  Takeuchi, Yasuhide;  Ochi, Yotaro;  Shiozawa, Yusuke;  Kogure, Yasunori;  Watatani, Yosaku;  Fujii, Yoichi;  Kim, Soo Ki;  Kon, Ayana;  Kataoka, Keisuke;  Yoshizato, Tetsuichi;  Nakagawa, Masahiro M.;  Yoda, Akinori;  Nanya, Yasuhito;  Makishima, Hideki;  Shiraishi, Yuichi;  Chiba, Kenichi;  Tanaka, Hiroko;  Sanada, Masashi;  Sugihara, Eiji;  Sato, Taka-aki;  Maruyama, Takashi;  Miyoshi, Hiroyuki;  Taketo, Makoto Mark;  Oishi, Jun;  Inagaki, Ryosaku;  Ueda, Yutaka;  Okamoto, Shinya;  Okajima, Hideaki;  Sakai, Yoshiharu;  Sakurai, Takaki;  Haga, Hironori;  Hirota, Seiichi;  Ikeuchi, Hiroki;  Nakase, Hiroshi;  Marusawa, Hiroyuki;  Chiba, Tsutomu;  Takeuchi, Osamu;  Miyano, Satoru;  Seno, Hiroshi;  Ogawa, Seishi
收藏  |  浏览/下载:77/0  |  提交时间:2020/07/03

Chronic inflammation is accompanied by recurring cycles of tissue destruction and repair and is associated with an increased risk of cancer(1-3). However, how such cycles affect the clonal composition of tissues, particularly in terms of cancer development, remains unknown. Here we show that in patients with ulcerative colitis, the inflamed intestine undergoes widespread remodelling by pervasive clones, many of which are positively selected by acquiring mutations that commonly involve the NFKBIZ, TRAF3IP2, ZC3H12A, PIGR and HNRNPF genes and are implicated in the downregulation of IL-17 and other pro-inflammatory signals. Mutational profiles vary substantially between colitis-associated cancer and non-dysplastic tissues in ulcerative colitis, which indicates that there are distinct mechanisms of positive selection in both tissues. In particular, mutations in NFKBIZ are highly prevalent in the epithelium of patients with ulcerative colitis but rarely found in both sporadic and colitis-associated cancer, indicating that NFKBIZ-mutant cells are selected against during colorectal carcinogenesis. In further support of this negative selection, we found that tumour formation was significantly attenuated in Nfkbiz-mutant mice and cell competition was compromised by disruption of NFKBIZ in human colorectal cancer cells. Our results highlight common and discrete mechanisms of clonal selection in inflammatory tissues, which reveal unexpected cancer vulnerabilities that could potentially be exploited for therapeutics in colorectal cancer.


  
The arms race between bacteria and their phage foes 期刊论文
NATURE, 2020, 577 (7790) : 327-336
作者:  Hirschey, Matthew
收藏  |  浏览/下载:20/0  |  提交时间:2020/07/03

Bacteria are under immense evolutionary pressure from their viral invaders-bacteriophages. Bacteria have evolved numerous immune mechanisms, both innate and adaptive, to cope with this pressure. The discovery and exploitation of CRISPR-Cas systems have stimulated a resurgence in the identification and characterization of anti-phage mechanisms. Bacteriophages use an extensive battery of counter-defence strategies to co-exist in the presence of these diverse phage defence mechanisms. Understanding the dynamics of the interactions between these microorganisms has implications for phage-based therapies, microbial ecology and evolution, and the development of new biotechnological tools. Here we review the spectrum of anti-phage systems and highlight their evasion by bacteriophages.


  
A GPR174-CCL21 module imparts sexual dimorphism to humoral immunity 期刊论文
NATURE, 2020, 577 (7790) : 416-+
作者:  Morley, Jessica;  Cowls, Josh;  Taddeo, Mariarosaria;  Floridi, Luciano
收藏  |  浏览/下载:16/0  |  提交时间:2020/07/03

Humoral immune responses to immunization and infection and susceptibilities to antibody-mediated autoimmunity are generally lower in males(1-3). However, the mechanisms underlying such sexual dimorphism are not well understood. Here we show that there are intrinsic differences between the B cells that produce germinal centres in male and female mice. We find that antigen-activated male B cells do not position themselves as efficiently as female B cells in the centre of follicles in secondary lymphoid organs, in which germinal centres normally develop. Moreover, GPR174-an X-chromosome-encoded G-protein-coupled receptor-suppresses the formation of germinal centres in male, but not female, mice. This effect is intrinsic to B cells, and correlates with the GPR174-enhanced positioning of B cells towards the T-cell-B-cell border of follicles, and the distraction of male, but not female, B cells from S1PR2-driven follicle-centre localization. Biochemical fractionation of conditioned media that induce B-cell migration in a GPR174-dependent manner identifies CCL21 as a GPR174 ligand. In response to CCL21, GPR174 triggers a calcium flux and preferentially induces the migration of male B cells  GPR174 also becomes associated with more G alpha i protein in male than in female B cells. Male B cells from orchidectomized mice exhibit impaired GPR174-mediated migration to CCL21, and testosterone treatment rescues this defect. Female B cells from testosterone-treated mice exhibit male-like GPR174-G alpha i association and GPR174-mediated migration. Deleting GPR174 from male B cells causes more efficient positioning towards the follicular centre, the formation of more germinal centres and an increased susceptibility to B-cell-dependent experimental autoimmune encephalomyelitis. By identifying GPR174 as a receptor for CCL21 and demonstrating its sex-dependent control of B-cell positioning and participation in germinal centres, we have revealed a mechanism by which B-cell physiology is fine-tuned to impart sexual dimorphism to humoral immunity.


  
RGF1 controls root meristem size through ROS signalling 期刊论文
NATURE, 2020, 577 (7788) : 85-+
作者:  Yamada, Masashi;  Han, Xinwei;  Benfey, Philip N.
收藏  |  浏览/下载:11/0  |  提交时间:2020/07/03

The stem cell niche and the size of the root meristem in plants are maintained by intercellular interactions and signalling networks involving a peptide hormone, root meristem growth factor 1 (RGF1)(1). Understanding how RGF1 regulates the development of the root meristem is essential for understanding stem cell function. Although five receptors for RGF1 have been identified(2-4), the downstream signalling mechanism remains unknown. Here we report a series of signalling events that follow RGF1 activity. We find that the RGF1-receptor pathway controls the distribution of reactive oxygen species (ROS) along the developmental zones of the Arabidopsis root. We identify a previously uncharacterized transcription factor, RGF1-INDUCIBLE TRANSCRIPTION FACTOR 1 (RITF1), that has a central role in mediating RGF1 signalling. Manipulating RITF1 expression leads to the redistribution of ROS along the root developmental zones. Changes in ROS distribution in turn enhance the stability of the PLETHORA2 protein, a master regulator of root stem cells. Our results thus clearly depict a signalling cascade that is initiated by RGF1, linking this peptide to mechanisms that regulate ROS.


  
IL-17a promotes sociability in mouse models of neurodevelopmental disorders 期刊论文
NATURE, 2020, 577 (7789) : 249-+
作者:  Reed, Michael Douglas;  Yim, Yeong Shin;  Wimmer, Ralf D.;  Kim, Hyunju;  Ryu, Changhyeon;  Welch, Gwyneth Margaret;  Andina, Matias;  King, Hunter Oren;  Waisman, Ari;  Halassa, Michael M.;  Huh, Jun R.;  Choi, Gloria B.
收藏  |  浏览/下载:11/0  |  提交时间:2020/07/03

A subset of children with autism spectrum disorder appear to show an improvement in their behavioural symptoms during the course of a fever, a sign of systemic inflammation(1,2). Here we elucidate the molecular and neural mechanisms that underlie the beneficial effects of inflammation on social behaviour deficits in mice. We compared an environmental model of neurodevelopmental disorders in which mice were exposed to maternal immune activation (MIA) during embryogenesis(3,4) with mouse models that are genetically deficient for contactin-associated protein-like 2 (Cntnap2)(5), fragile X mental retardation-1 (Fmr1)(6) or Sh3 and multiple ankyrin repeat domains 3 (Shank3)(7). We establish that the social behaviour deficits in offspring exposed to MIA can be temporarily rescued by the inflammatory response elicited by the administration of lipopolysaccharide (LPS). This behavioural rescue was accompanied by a reduction in neuronal activity in the primary somatosensory cortex dysgranular zone (S1DZ), the hyperactivity of which was previously implicated in the manifestation of behavioural phenotypes associated with offspring exposed to MIA(8). By contrast, we did not observe an LPS-induced rescue of social deficits in the monogenic models. We demonstrate that the differences in responsiveness to the LPS treatment between the MIA and the monogenic models emerge from differences in the levels of cytokine production. LPS treatment in monogenic mutant mice did not induce amounts of interleukin-17a (IL-17a) comparable to those induced in MIA offspring  bypassing this difference by directly delivering IL-17a into S1DZ was sufficient to promote sociability in monogenic mutant mice as well as in MIA offspring. Conversely, abrogating the expression of IL-17 receptor subunit a (IL-17Ra) in the neurons of the S1DZ eliminated the ability of LPS to reverse the sociability phenotypes in MIA offspring. Our data support a neuroimmune mechanism that underlies neurodevelopmental disorders in which the production of IL-17a during inflammation can ameliorate the expression of social behaviour deficits by directly affecting neuronal activity in the central nervous system.