bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hotspots of pest-induced US urban tree death, 2020-2050
Authors: Hudgins Emma J. , Koch Frank H. , Ambrose Mark J. , Leung Brian 
Published: April 2021

AbstractUrban trees are important nature-based solutions for future wellbeing and livability but are at high risk of mortality from insect pests. In the United States (US), 82% of the population live in urban settings and this number is growing, making urban tree mortality a matter of concern for most of its population. Until now, the magnitudes and spatial distributions of risks were unknown.Here, we combine new models of street tree populations in ∼30,000 US communities, species-specific spread predictions for 57 invasive insect species, and estimates of tree death due to insect exposure for 48 host tree genera.We estimate that 1.4 million street trees will be killed by invasive insects from 2020 through 2050, costing an annualized average of US$ 30M. However, these estimates hide substantial variation: 23% of urban centers will experience 95% of all insect-induced mortality. Further, 90% of all mortality will be due to emerald ash borer (Agrilus planipennis, EAB), which is expected to kill virtually all ash trees (Fraxinusspp.) in >6000 communities.We define an EAB high-impact zone spanning 902,500km2, largely within the southern and central US, within which we predict the death of 98.8% of all ash trees. “Mortality hotspot cities” include Milwaukee, WI; Chicago, IL; and New York, NY.We identify Asian wood borers of maple and oak trees as the highest risk future invaders, where a new establishment could cost US$ 4.9B over 30 years.Policy implications:To plan effective mitigation, managers must know which tree species in which communities will be at the greatest risk, as well as the highest-risk insects. We provide the first country-wide, spatial forecast of urban tree mortality due to invasive insect pests. This framework identifies dominant pest insects and spatial impact hotspots, which can provide the basis for spatial prioritization of spread control efforts such as quarantines and biological control release sites. Our results highlight the need for EAB early-detection efforts as far from current infestations as Seattle, WA. Further, these findings produce a list of biotic and spatiotemporal risk factors for future high-impact US urban forest insect pests.
Encoding model for continuous motion-sensitive neurons in the intermediate and deep layers of pigeon Optic Tectum
Authors: Wang Songwei , Zhao Mengyu , Qian Longlong , Wang Zhizhong , Shi Li 
Published: April 2021

AbstractThere are typical neurons in the intermediate and deep layers of the optic tectum of avian, which are sensitive to small continuous moving targets. Based on this sensitivity of these neurons to continuous moving targets, the hypothesis of directed energy accumulation in dendrite field of these neurons is proposed. Based on the phenomenon that single dendrite activation can induce somatic spikes in vitro, the hypothesis of sequential probability activation mechanism of soma is proposed. Combined with the above hypotheses, the information encoding model of these typical neurons is constructed. Moreover, electrophysiological experiments and model simulations are carried out to obtain the response of neurons to visual stimuli of sequential motion, random motion and random sequential motion. Results show that the encoding model fits the response properties of continuous motion-sensitive neurons well. This study is of great significance for understanding the neurophysiological process of small-target perception for avian tectofugal pathway and the construction of the brain-inspired small-target detection algorithm.
Honey bee queen health is unaffected by contact exposure to pesticides commonly found in beeswax
Authors: McAfee Alison , Milone Joseph P , Metz Bradley , McDermott Erin , Foster Leonard J , Tarpy David R 
Published: April 2021

AbstractHoney bee queen health is crucial for colony health and productivity, and pesticides have been previously associated with queen loss and premature supersedure. Prior research has investigated the effects of indirect pesticide exposure on queens via workers, as well as direct effects on queens during development. However, as adults, queens are in constant contact with wax as they walk on comb and lay eggs; therefore, direct pesticide contact with adult queens is a relevant but seldom investigated exposure route. Here, we conducted laboratory and field experiments to investigate the impacts of topical pesticide exposure on adult queens. We tested dose-response relationships of six pesticides commonly found in wax: coumaphos, tau-fluvalinate, atrazine, 2,4-DMPF, chlorpyriphos, chlorothalonil, and a cocktail of all six, each dosed up to 32 times the concentrations typically found in wax. We found no effect of any treatment on queen mass or sperm viability. Furthermore, none of the 1,568 proteins quantified in the queens’ fat bodies (a major site of detoxification enzyme production) were differentially expressed. In a field trial with N = 30 queens exposed to either a handling control, a solvent control, or a pesticide cocktail, we again found no impact on queen egg-laying pattern, mass, or emergence mass of daughter workers. Further, of the 3,127 proteins identified in fluid from the spermatheca (sperm storage organ), none were differentially expressed. These experiments consistently show that at realistic exposure levels, pesticides commonly found in wax have no direct impact on queen performance, reproduction, or quality metrics. We suggest that previously reported associations between high levels of pesticide residues in wax and queen failure are most likely driven by indirect effects of worker exposure (either through wax or other hive products) on queen care or queen perception.
Pan-cancer survey of tumour mass dormancy and underlying mutational processes
Authors: Wiecek Anna Julia , Jacobson Daniel Hadar , Lason Wojciech , Secrier Maria 
Published: April 2021

AbstractTumour mass dormancy is the key intermediate step between immune surveillance and cancer progression, yet due to its transitory nature it has been difficult to capture and characterise. Little is understood of its prevalence across cancer types and of the mutational background that may favour such a state. While this balance is finely tuned internally by the equilibrium between cell proliferation and cell death, the main external factors contributing to tumour mass dormancy are immunological and angiogenic. To understand the genomic and cellular context in which tumour mass dormancy may develop, we comprehensively profiled signals of immune and angiogenic dormancy in 9,631 cancers from the Cancer Genome Atlas and linked them to tumour mutagenesis. We find evidence for immunological and angiogenic dormancy-like signals in 16.5% of bulk sequenced tumours, with a frequency of up to 33% in certain tissues. Mutations in theCASP8andHRASoncogenes were positively selected in dormant tumours, suggesting an evolutionary pressure for controlling cell growth/apoptosis signals. By surveying the mutational damage patterns left in the genome by known cancer risk factors, we found that ageing-induced mutations were relatively depleted in these tumours, while patterns of smoking and defective base excision repair were linked with increased tumour mass dormancy. Furthermore, we identified a link between APOBEC mutagenesis and dormancy, which comes in conjunction with immune exhaustion and may partly depend on the expression of the angiogenesis regulatorPLGas well as interferon and chemokine signals. Tumour mass dormancy also appeared to be impaired in hypoxic conditions in the majority of cancers. The microenvironment of dormant cancers was enriched in cytotoxic and regulatory T cells, as expected, but also in macrophages and showed a reduction in inflammatory Th17 signals. Finally, tumour mass dormancy was linked with improved patient survival outcomes. Our analysis sheds light onto the complex interplay between dormancy, exhaustion, APOBEC activity and hypoxia, and sets directions for future mechanistic explorations.
Independent Promoter Recognition by TcpP Precedes Cooperative Promoter Activation by TcpP and ToxR
Authors: Calkins A.L. , Demey L.M. , Karslake J.D. , Donarski E.D. , Biteen J.S. , DiRita V.J. 
Published: April 2021

AbstractCholera is a diarrheal disease caused by the Gram-negative bacteriumVibrio cholerae. To reach the surface of intestinal epithelial cells, proliferate, and cause disease,V. choleraetightly regulates the production of virulence factors such as cholera toxin (ctxAB) and the toxin co-regulated pilus (tcpA-F). ToxT is directly responsible for regulating these major virulence factors while TcpP and ToxR indirectly regulate virulence factor production by stimulatingtoxTexpression. TcpP and ToxR are membrane-localized transcription activators (MLTAs) required to activatetoxTexpression. To gain a deeper understanding of how MLTAs identify promoter DNA while in the membrane, we tracked the dynamics of single TcpP-PAmCherry molecules in live cells using photoactivated localization microscopy and identified heterogeneous diffusion patterns. Our results provide evidence that: 1) TcpP exists in three biophysical states (fast diffusion, intermediate diffusion, and slow diffusion); 2) TcpP transitions between these different diffusion states; 3) TcpP molecules in the slow diffusion state are interacting with thetoxTpromoter; and 4) ToxR is not essential for TcpP to localize thetoxTpromoter. These data refine the current model of cooperativity between TcpP and ToxR in stimulatingtoxTexpression and demonstrate that TcpP locates thetoxTpromoter independent of ToxR.
Genome-wide mapping of G-quadruplex structures with CUT&Tag
Authors: Lyu Jing , Shao Rui , Elsässer Simon J 
Published: April 2021

ABSTRACTSingle-stranded genomic DNA can fold into G-quadruplex (G4) structures or form DNA:RNA hybrids (R loops). Recent evidence suggests that such non-canonical DNA structures affect gene expression, DNA methylation, replication fork progression and genome stability. When and how G4 structures form and are resolved remains unclear. Here we report the use of Cleavage Under Targets and Tagmentation (CUT&Tag) for mapping native G4 in mammalian cell lines at high resolution and low background. Mild native conditions used for the procedure retain more G4 structures and provide a higher signal-to-noise ratio than ChIP-based methods. We determine the G4 landscape of mouse embryonic stem cells (mESC), observing widespread G4 formation at active promoters, active and poised enhancers. We discover that the presence of G4 motifs and G4 structures distinguishes active and primed enhancers in mESCs. Further, performing R-loop CUT&Tag, we demonstrate the genome-wide co-occurence of single-stranded DNA, G4s and R loops, suggesting an intricate relationship between transcription and non-canonical DNA structures.
Coronary blood vessels from distinct origins converge to equivalent states during mouse and human development
Authors: Phansalkar Ragini , Krieger Josephine , Zhao Mingming , Kolluru Sai Saroja , Jones Robert C. , Quake Stephen R , Weissman Irving , Bernstein Daniel , Winn Virginia D. , D’Amato Gaetano , Red-Horse Kristy 
Published: April 2021

AbstractMost cell fate trajectories during development follow a diverging, tree-like branching pattern, but the opposite can occur when distinct progenitors contribute to the same cell type. During this convergent differentiation, it is unknown if cells “remember” their origins transcriptionally or whether this influences cell behavior. Most coronary blood vessels of the heart develop from two different progenitor sources—the endocardium (Endo) and sinus venosus (SV)—but whether transcriptional or functional differences related to origin are retained is unknown. We addressed this by combining lineage tracing with single-cell RNA sequencing (scRNAseq) in embryonic and adult mouse hearts. Shortly after coronary development begins, capillary ECs transcriptionally segregated into two states that retained progenitor-specific gene expression. Later in development, when the coronary vasculature is well-established but still remodeling, capillary Ecs again segregated into two populations, but transcriptional differences were primarily related to tissue localization rather than lineage. Specifically, ECs in the heart septum expressed genes indicative of increased local hypoxia and decreased blood flow. Adult capillary ECs were more homogeneous with respect to both lineage and location. In agreement, SV- and Endo-derived ECs in adult hearts displayed similar responses to injury. Finally, scRNAseq of developing human coronary vessels indicated that the human heart followed similar principles. Thus, over the course of development, transcriptional heterogeneity in coronary ECs is first influenced by lineage, then by location, until heterogeneity declines in the homeostatic adult heart. These results highlight the plasticity of ECs during development, and the validity of the mouse as a model for human coronary development.
The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis
Authors: Alejo-Valle Oriol , Weigert Karoline , Bhayadia Raj , Ng Michelle , Emmrich Stephan , Beyer Christoph , Schuschel Konstantin , Ihling Christian , Sinz Andrea , Flasinski Marius , Issa Hasan , Regenyi Eniko , Labuhn Maurice , Reinhardt Dirk , Yaspo Marie-Laure , Heckl Dirk , Klusmann Jan-Henning 
Published: April 2021

AbstractGiven the plasticity of hematopoietic stem/progenitor cells, multiple routes of differentiation must be blocked during acute myeloid leukemia pathogenesis – the molecular basis of which is incompletely understood. Here we report that post-transcriptional repression of transcription factor ARID3A by miR-125b is a key event in megakaryoblastic leukemia (AMKL) pathogenesis. AMKL is frequently associated with trisomy 21 andGATA1mutations (GATA1s), and children with Down syndrome are at a high risk of developing this disease. We show that chromosome 21-encoded miR-125b synergizes withGata1sto drive leukemogenesis in this context. Leveraging forward and reverse genetics, we uncoverArid3aas the main miR-125b target underlying this synergy. We demonstrate that during normal hematopoiesis this transcription factor promotes megakaryocytic differentiation in concert with GATA1 and mediates TGFβ-induced apoptosis and cell cycle arrest in complex with SMAD2/3. WhileGata1smutations perturb erythroid differentiation and induce hyperproliferation of megakaryocytic progenitors, intact ARID3A expression assures their megakaryocytic differentiation and growth restriction. Upon knockdown, these tumor suppressive functions are revoked, causing a dual megakaryocytic/erythroid differentiation blockade and subsequently AMKL. Inversely, restoringARID3Aexpression relieves the megakaryocytic differentiation arrest in AMKL patient-derived xenografts. This work illustrates how mutations in lineage-determining transcription factors and perturbation of post-transcriptional gene regulation interplay to block multiple routes of hematopoietic differentiation and cause leukemia. Surmounting this differentiation blockade in megakaryoblastic leukemia by restoring the tumor suppressor ARID3A represents a promising strategy for treating this lethal pediatric disease.Key pointsRepression of megakaryocytic transcription factorARID3Aby miR-125b synergizes withGATA1sto induce leukemiaRestoring ARID3A expression relieves megakaryocytic differentiation arrest in megakaryoblastic leukemiaGraphical abstract
Remodeling tumor microenvironment by liposomal co-delivery of DMXAA and simvastatin inhibits malignant melanoma progression
Authors: Rauca Valentin-Florian , Patras Laura , Luput Lavinia , Licarete Emilia , Toma Vlad-Alexandru , Porfire Alina , Mot Augustin-Catalin , Rakosy-Tican Elena , Sesarman Alina , Banciu Manuela 
Published: April 2021

AbstractAnti-angiogenic therapies for melanoma have not yet been translated into meaningful clinical benefit for patients, due to development of drug-induced resistance in cancer cells, mainly caused by hypoxia-inducible factor 1α (HIF-1α) overexpression and enhanced oxidative stress mediated by tumor-associated macrophages (TAMs). Our previous study demonstrated synergistic antitumor actions of simvastatin (SIM) and 5,6-dimethylxanthenone-4-acetic acid (DMXAA) on anin vitromelanoma modelviasuppression of the aggressive phenotype of melanoma cells and inhibition of TAMs-mediated angiogenesis. Therefore, we took the advantage of long circulating liposomes (LCL) superior tumor targeting capacity to efficiently deliver SIM and DMXAA to B16.F10 melanomain vivo, with the final aim of improving the outcome of the anti-angiogenic therapy. Thus, we assessed the effects of this novel combined tumor-targeted treatment ons.c. B16.F10 murine melanoma growth and on the production of critical markers involved in tumor development and progression. Our results showed that the combined liposomal therapy inhibited almost totally the growth of melanoma tumors, due to the enhancement of anti-angiogenic effects of LCL-DMXAA by LCL-SIM and induction of a pro-apoptotic state in the tumor microenvironment (TME). These effects were favoured by the partial re-education of TAMs towards a M1 phenotype and maintained via suppression of major invasion and metastasis promoters (HIF-1α, pAP-1 c-Jun, and MMPs). Thus, this novel therapy holds the potential to remodel the tumor microenvironment, by suppressing its most important malignant biological capabilities.HighlightsNovel combined liposomal delivery of SIM and DMXAA inhibits melanoma tumor growthLCL-SIM augments the anti-angiogenic effects of LCL-DMXAACombined liposomal therapy inhibits HIF-1α/VEGF axis, induces apoptosis and TAM re-education in tumorsThis novel therapy suppresses the most important malignant capabilities of melanoma
Evaluating population affinity estimates in forensic anthropology: Insights from the forensic anthropology database for assessing methods accuracy (FADAMA)
Authors: Winburn Allysha P. , Algee‐Hewitt Bridget 
Published: April 2021

AbstractUsing a sample of anonymized U.S. forensic anthropology cases (n = 251) from the FADAMA database, we assess the degree of concordance between decedents’ social identifiers and anthropologists’ continental‐based classifications. We report high success rates (>90%) that generally support previous findings, yet we acknowledge the limitations of assessing “ancestry” accuracy based on resolved cases and draw attention to situations in which our methods fail. For example, forensic anthropologists achieve just 20% accuracy when classifying individuals as “other” or “mixed”—problematic categories that we argue should be rejected. Leveraging our findings, we ask: what are we really estimating when we perform a skeletal assessment of “ancestry” in the US context? We argue that the “ancestry estimates” historically and routinely produced in forensic anthropology instead give information on population affinity: a measure of how similar a given case is to one among several socially relevant groups of interest. Distancing forensic anthropology from genetics and other disciplines that estimate ancestry, the approach of population affinity assesses similarities to both social and biological groupings, potentially at a fine‐grained level, attempting to account for the complex histories, shared biologies, and wide ranges of diversity that characterize our communities and our casework. Population affinity is a flexible and inclusive approach that more accurately describes current forensic anthropological analyses of human variation. Going forward, we must acknowledge and build on the contributions of previous scholars as we work together toward our shared goal of theoretically grounded analyses of human variation that accurately and equitably serve all casework decedents.
Large‐Scale Carbon Dioxide Removal to Meet the 1.5°C Limit: Key Governance Gaps, Challenges and Priority Responses
Authors: Mace M.J. , Fyson Claire L. , Schaeffer Michiel , Hare William L. 
Published: April 2021

AbstractParties to the UNFCCC and Paris Agreement have agreed to pursue efforts to limit the global average temperature increase to 1.5°C. To meet this goal, the international community will have to aggressively reduce emissions and also remove CO2 from the atmosphere on an unprecedented scale, through an array of biological and technical Carbon Dioxide Removal (CDR) options. This paper considers governance challenges that arise from the need to rely on CDR to meet the Paris Agreement’s long‐term temperature goal. It looks at how heavy this reliance may have to be, over what timeframe, involving what options and, crucially, how best to ensure that CDR does not, while trying to address one problem, create many other challenges for sustainable development. After identifying the potential scale and pace of CO2 removal needed to meet the 1.5°C goal, we identify key governance gaps and challenges that arise from large‐scale CDR implementation and propose a series of policy responses to be addressed by policy makers as a matter of priority, to enable CDR to contribute to 1.5°C‐consistent pathways at the scale and pace required.
Collaborative economy, a society service? Involvement with ethics and the common good
Authors: Chivite Cebolla María Peana , Jorge Vázquez Javier , Chivite Cebolla Carmen Mª 
Published: April 2021

AbstractThe company at the service of today's society is reinventing itself to satisfy people's needs in a more efficient and adapted way. Globalization and digitization promote increasing interaction and new forms of economic organization such as collaborative economy. However, can it be understood that this new business model, more than others, has as its raison d'être in the search for the “common good”? A first approach suggests the presence of values related to collaboration between equals aiming at a common good. However, the possible existence of a profit motive and the labor relations framework in which certain activities are carried out have created a debate on their ethical qualification. In this context, considering 278 companies in the collaborative economy sector, the relationship between the concept of “common good” and the collaborative economy is analyzed, while examining whether these new realities have an explicit ethical intention (of search for goods for people). According to the results, it is not possible to assert that these platforms have an ethical concern, but it is observed that they are in line with the common good and implicitly contribute to the service of society.