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短期内温度过高和降水不足会降低女性生育意愿 快报文章
气候变化快报,2022年第07期
作者:  秦冰雪
Microsoft Word(15Kb)  |  收藏  |  浏览/下载:737/0  |  提交时间:2022/04/05
Climate Change  Population Growth  Sub-saharan Africa  
气候变化可能导致北美第四纪晚期巨型动物减少 快报文章
气候变化快报,2021年第5期
作者:  董利苹
Microsoft Word(14Kb)  |  收藏  |  浏览/下载:467/0  |  提交时间:2021/03/05
Climate Change  Human Population Growth  North America  Late Quaternary  Megafauna  
The social and environmental influences of population growth rate and demographic pressure deserve greater attention in ecological economics 期刊论文
ECOLOGICAL ECONOMICS, 2020, 172
作者:  O&;  39;Sullivan, Jane N.
收藏  |  浏览/下载:14/0  |  提交时间:2020/07/02
Capital widening  Demographic dynamics  Family planning  Inequality  Overpopulation  Population growth rate  Population pressure  
Rapid non-uniform adaptation to conformation-specific KRAS(G12C) inhibition 期刊论文
NATURE, 2020, 577 (7790) : 421-+
作者:  Xue, Jenny Y.;  Zhao, Yulei;  Aronowitz, Jordan;  Mai, Trang T.;  Vides, Alberto;  Qeriqi, Besnik;  Kim, Dongsung;  Li, Chuanchuan;  de Stanchina, Elisa;  Mazutis, Linas;  Risso, Davide;  Lito, Piro
收藏  |  浏览/下载:12/0  |  提交时间:2020/07/03

KRAS GTPases are activated in one-third of cancers, and KRAS(G12C) is one of the most common activating alterations in lung adenocarcinoma(1,2). KRAS(G12C) inhibitors(3,4) are in phase-I clinical trials and early data show partial responses in nearly half of patients with lung cancer. How cancer cells bypass inhibition to prevent maximal response to therapy is not understood. Because KRAS(G12C) cycles between an active and inactive conformation(4-6), and the inhibitors bind only to the latter, we tested whether isogenic cell populations respond in a non-uniform manner by studying the effect of treatment at a single-cell resolution. Here we report that, shortly after treatment, some cancer cells are sequestered in a quiescent state with low KRAS activity, whereas others bypass this effect to resume proliferation. This rapid divergent response occurs because some quiescent cells produce new KRAS(G12C) in response to suppressed mitogen-activated protein kinase output. New KRAS(G12C) is maintained in its active, drug-insensitive state by epidermal growth factor receptor and aurora kinase signalling. Cells without these adaptive changes-or cells in which these changes are pharmacologically inhibited-remain sensitive to drug treatment, because new KRAS(G12C) is either not available or exists in its inactive, drug-sensitive state. The direct targeting of KRAS oncoproteins has been a longstanding objective in precision oncology. Our study uncovers a flexible non-uniform fitness mechanism that enables groups of cells within a population to rapidly bypass the effect of treatment. This adaptive process must be overcome if we are to achieve complete and durable responses in the clinic.


  
Population flow drives spatio-temporal distribution of COVID-19 in China 期刊论文
NATURE, 2020
作者:  Fernandez, Diego Carlos;  Komal, Ruchi;  Langel, Jennifer;  Ma, Jun;  Duy, Phan Q.;  Penzo, Mario A.;  Zhao, Haiqing;  Hattar, Samer
收藏  |  浏览/下载:69/0  |  提交时间:2020/07/03

Sudden, large-scale and diffuse human migration can amplify localized outbreaks of disease into widespread epidemics(1-4). Rapid and accurate tracking of aggregate population flows may therefore be epidemiologically informative. Here we use 11,478,484 counts of mobile phone data from individuals leaving or transiting through the prefecture of Wuhan between 1 January and 24 January 2020 as they moved to 296 prefectures throughout mainland China. First, we document the efficacy of quarantine in ceasing movement. Second, we show that the distribution of population outflow from Wuhan accurately predicts the relative frequency and geographical distribution of infections with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) until 19 February 2020, across mainland China. Third, we develop a spatio-temporal '  risk source'  model that leverages population flow data (which operationalize the risk that emanates from epidemic epicentres) not only to forecast the distribution of confirmed cases, but also to identify regions that have a high risk of transmission at an early stage. Fourth, we use this risk source model to statistically derive the geographical spread of COVID-19 and the growth pattern based on the population outflow from Wuhan  the model yields a benchmark trend and an index for assessing the risk of community transmission of COVID-19 over time for different locations. This approach can be used by policy-makers in any nation with available data to make rapid and accurate risk assessments and to plan the allocation of limited resources ahead of ongoing outbreaks.


Modelling of population flows in China enables the forecasting of the distribution of confirmed cases of COVID-19 and the identification of areas at high risk of SARS-CoV-2 transmission at an early stage.


  
Population growth and land development: Investigating the bi-directional interactions 期刊论文
ECOLOGICAL ECONOMICS, 2020, 169
作者:  Tong, Qingmeng;  Qiu, Feng
收藏  |  浏览/下载:10/0  |  提交时间:2020/07/02
Population growth  Land development  Spatial spillovers  Spatial regression model  
Bacterial coexistence driven by motility and spatial competition 期刊论文
NATURE, 2020, 578 (7796) : 588-+
作者:  Micke, P.;  Leopold, T.;  King, S. A.;  Benkler, E.;  Spiess, L. J.;  Schmoeger, L.;  Schwarz, M.;  Crespo Lopez-Urrutia, J. R.;  Schmidt, P. O.
收藏  |  浏览/下载:8/0  |  提交时间:2020/07/03

Elucidating elementary mechanisms that underlie bacterial diversity is central to ecology(1,2) and microbiome research(3). Bacteria are known to coexist by metabolic specialization(4), cooperation(5) and cyclic warfare(6-8). Many species are also motile(9), which is studied in terms of mechanism(10,11), benefit(12,13), strategy(14,15), evolution(16,17) and ecology(18,19). Indeed, bacteria often compete for nutrient patches that become available periodically or by random disturbances(2,20,21). However, the role of bacterial motility in coexistence remains unexplored experimentally. Here we show that-for mixed bacterial populations that colonize nutrient patches-either population outcompetes the other when low in relative abundance. This inversion of the competitive hierarchy is caused by active segregation and spatial exclusion within the patch: a small fast-moving population can outcompete a large fast-growing population by impeding its migration into the patch, while a small fast-growing population can outcompete a large fast-moving population by expelling it from the initial contact area. The resulting spatial segregation is lost for weak growth-migration trade-offs and a lack of virgin space, but is robust to population ratio, density and chemotactic ability, and is observed in both laboratory and wild strains. These findings show that motility differences and their trade-offs with growth are sufficient to promote diversity, and suggest previously undescribed roles for motility in niche formation and collective expulsion-containment strategies beyond individual search and survival.


In mixed bacterial populations that colonize nutrient patches, a growth-migration trade-off can lead to spatial exclusion that provides an advantage to populations that become rare, thereby stabilizing the community.


  
Feeding-dependent VIP neuron-ILC3 circuit regulates the intestinal barrier 期刊论文
NATURE, 2020, 579 (7800) : 575-+
作者:  Bhaduri, Aparna;  Andrews, Madeline G.;  Mancia Leon, Walter;  Jung, Diane;  Shin, David;  Allen, Denise;  Jung, Dana;  Schmunk, Galina;  Haeussler, Maximilian;  Salma, Jahan;  Pollen, Alex A.;  Nowakowski, Tomasz J.;  Kriegstein, Arnold R.
收藏  |  浏览/下载:37/0  |  提交时间:2020/07/03

The intestinal mucosa serves both as a conduit for the uptake of food-derived nutrients and microbiome-derived metabolites, and as a barrier that prevents tissue invasion by microorganisms and tempers inflammatory responses to the myriad contents of the lumen. How the intestine coordinates physiological and immune responses to food consumption to optimize nutrient uptake while maintaining barrier functions remains unclear. Here we show in mice how a gut neuronal signal triggered by food intake is integrated with intestinal antimicrobial and metabolic responses that are controlled by type-3 innate lymphoid cells (ILC3)(1-3). Food consumption rapidly activates a population of enteric neurons that express vasoactive intestinal peptide (VIP)(4). Projections of VIP-producing neurons (VIPergic neurons) in the lamina propria are in close proximity to clusters of ILC3 that selectively express VIP receptor type 2 (VIPR2  also known as VPAC2). Production of interleukin (IL)-22 by ILC3, which is upregulated by the presence of commensal microorganisms such as segmented filamentous bacteria(5-7), is inhibited upon engagement of VIPR2. As a consequence, levels of antimicrobial peptide derived from epithelial cells are reduced but the expression of lipid-binding proteins and transporters is increased(8). During food consumption, the activation of VIPergic neurons thus enhances the growth of segmented filamentous bacteria associated with the epithelium, and increases lipid absorption. Our results reveal a feeding- and circadian-regulated dynamic neuroimmune circuit in the intestine that promotes a trade-off between innate immune protection mediated by IL-22 and the efficiency of nutrient absorption. Modulation of this pathway may therefore be effective for enhancing resistance to enteropathogens(2,3,9) and for the treatment of metabolic diseases.


Feeding controls a neuroimmune circuit comprising VIP-producing neurons and type-3 innate lymphoid cells that helps to regulate the efficiency of nutrient uptake and IL-22-mediated immune protection in the intestine.


  
Biotic and anthropogenic forces rival climatic/abiotic factors in determining global plant population growth and fitness 期刊论文
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2020, 117 (2) : 1107-1112
作者:  Morris, William F.;  Ehrlen, Johan;  Dahlgren, Johan P.;  Loomis, Alexander K.;  Louthan, Allison M.
收藏  |  浏览/下载:8/0  |  提交时间:2020/05/13
population growth rate  climate change  environmental driver  species interactions  anthropogenic impacts  
AQP5 enriches for stem cells and cancer origins in the distal stomach 期刊论文
NATURE, 2020, 578 (7795) : 437-+
作者:  Athukoralage, Januka S.;  McMahon, Stephen A.;  Zhang, Changyi;  Grueschow, Sabine;  Graham, Shirley;  Krupovic, Mart;  Whitaker, Rachel J.;  Gloster, Tracey M.;  White, Malcolm F.
收藏  |  浏览/下载:17/0  |  提交时间:2020/07/03

LGR5 marks resident adult epithelial stem cells at the gland base in the mouse pyloric stomach(1), but the identity of the equivalent human stem cell population remains unknown owing to a lack of surface markers that facilitate its prospective isolation and validation. In mouse models of intestinal cancer, LGR5(+) intestinal stem cells are major sources of cancer following hyperactivation of the WNT pathway(2). However, the contribution of pyloric LGR5(+) stem cells to gastric cancer following dysregulation of the WNT pathway-a frequent event in gastric cancer in humans(3)-is unknown. Here we use comparative profiling of LGR5(+) stem cell populations along the mouse gastrointestinal tract to identify, and then functionally validate, the membrane protein AQP5 as a marker that enriches for mouse and human adult pyloric stem cells. We show that stem cells within the AQP5(+) compartment are a source of WNT-driven, invasive gastric cancer in vivo, using newly generated Aqp5-creERT2 mouse models. Additionally, tumour-resident AQP5(+) cells can selectively initiate organoid growth in vitro, which indicates that this population contains potential cancer stem cells. In humans, AQP5 is frequently expressed in primary intestinal and diffuse subtypes of gastric cancer (and in metastases of these subtypes), and often displays altered cellular localization compared with healthy tissue. These newly identified markers and mouse models will be an invaluable resource for deciphering the early formation of gastric cancer, and for isolating and characterizing human-stomach stem cells as a prerequisite for harnessing the regenerative-medicine potential of these cells in the clinic.


AQP5 is identified as a marker for pyloric stem cells in humans and mice, and stem cells in the AQP5(+) compartment are shown to be a source of invasive gastric cancer in mouse models.