The trapped-ion quantum charge-coupled device (QCCD) proposal
lays out a blueprint for a universal quantum computer that uses mobile ions as qubits. Analogous to a charge-coupled device (CCD) camera, ...which stores and processes imaging information as movable electrical charges in coupled pixels, a QCCD computer stores quantum information in the internal state of electrically charged ions that are transported between different processing zones using dynamic electric fields. The promise of the QCCD architecture is to maintain the low error rates demonstrated in small trapped-ion experiments
by limiting the quantum interactions to multiple small ion crystals, then physically splitting and rearranging the constituent ions of these crystals into new crystals, where further interactions occur. This approach leverages transport timescales that are fast relative to the coherence times of the qubits, the insensitivity of the qubit states of the ion to the electric fields used for transport, and the low crosstalk afforded by spatially separated crystals. However, engineering a machine capable of executing these operations across multiple interaction zones with low error introduces many difficulties, which have slowed progress in scaling this architecture to larger qubit numbers. Here we use a cryogenic surface trap to integrate all necessary elements of the QCCD architecture-a scalable trap design, parallel interaction zones and fast ion transport-into a programmable trapped-ion quantum computer that has a system performance consistent with the low error rates achieved in the individual ion crystals. We apply this approach to realize a teleported CNOT gate using mid-circuit measurement
, negligible crosstalk error and a quantum volume
of 2
= 64. These results demonstrate that the QCCD architecture provides a viable path towards high-performance quantum computers.
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GEOZS, IJS, IMTLJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBMB, UL, UM, UPUK, ZAGLJ
This article employs a long‐term historical and anthropological perspective to examine questions of resilience through a case study of Cabo Pulmo, BCS, Mexico. Using the recent COVID‐19 crisis as a ...starting point, this article discusses the crises, shocks, booms, and busts that have affected and shaped the people, landscapes, and ecologies of the coastline that now includes Cabo Pulmo. While the community of Cabo Pulmo has been able to withstand several crises and disruptions, and could be considered “resilient” in many senses, I argue that this resilience is ongoing and conditional. Furthermore, the production of this resilience in Cabo Pulmo is highly contingent upon a strategic politics, enacted by the local community, that establishes, protects, and maintains claims to both land and place. Resilience, I argue, can be seen as an ongoing politics and strategic positionality, rooted in historical relations and connections to place, that people seek to create, maintain, and deploy at various scales to mediate and resist periodic shocks, threats, and disruptions.
Resumen
Este artículo utiliza una perspectiva histórica y antropológica de largo plazo para examinar cuestiones de resiliencia a través de un estudio de caso de Cabo Pulmo, BCS, México. Usando la crisis reciente de COVID como punto de partida, este artículo discute las crisis, los choques, los auges y las caídas que han afectado y modelado las personas, los paisajes, y las ecologías de la línea costera que ahora incluye Cabo Pulmo. Mientras la comunidad de Cabo Pulmo ha sido capaz de resistir varias crisis y disrupciones, y puede ser considerada “resiliente” en muchos sentidos, argumento que esta resiliencia está en desarrollo y es condicional. Adicionalmente, la producción de esta resiliencia en Cabo Pulmo es altamente dependiente de una política estratégica puesta en efecto por la comunidad local, que establece, protege y mantiene reclamaciones tanto de tierra como de lugar. La resiliencia, argumento, puede ser vista como una política en marcha y una posicionalidad estratégica enraizada en relaciones históricas y conexiones a lugar que las personas buscan crear, mantener y utilizar a varias escalas para mediar y resistir choques, amenazas, y disrupciones periódicas. tierra, ecología política, resiliencia, vulnerabilidad, México
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
3.
A survival guide to Landsat preprocessing Young, Nicholas E.; Anderson, Ryan S.; Chignell, Stephen M. ...
Ecology (Durham),
April 2017, Volume:
98, Issue:
4
Journal Article
Peer reviewed
Open access
Landsat data are increasingly used for ecological monitoring and research. These data often require preprocessing prior to analysis to account for sensor, solar, atmospheric, and topographic effects. ...However, ecologists using these data are faced with a literature containing inconsistent terminology, outdated methods, and a vast number of approaches with contradictory recommendations. These issues can, at best, make determining the correct preprocessing workflow a difficult and time-consuming task and, at worst, lead to erroneous results. We address these problems by providing a concise overview of the Landsat missions and sensors and by clarifying frequently conflated terms and methods. Preprocessing steps commonly applied to Landsat data are differentiated and explained, including georeferencing and co-registration, conversion to radiance, solar correction, atmospheric correction, topographic correction, and relative correction. We then synthesize this information by presenting workflows and a decision tree for determining the appropriate level of imagery preprocessing given an ecological research question, while emphasizing the need to tailor each workflow to the study site and question at hand. We recommend a parsimonious approach to Landsat preprocessing that avoids unnecessary steps and recommend approaches and data products that are well tested, easily available, and sufficiently documented. Our focus is specific to ecological applications of Landsat data, yet many of the concepts and recommendations discussed are also appropriate for other disciplines and remote sensing platforms.
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BFBNIB, FZAB, GIS, IJS, INZLJ, KILJ, NLZOH, NMLJ, NUK, OILJ, PNG, SAZU, SBCE, SBMB, UL, UM, UPUK, ZRSKP
Heat stress management in underground mines Ryan, Anderson; Euler, De Souza
International journal of mining science and technology,
07/2017, Volume:
27, Issue:
4
Journal Article
Peer reviewed
Open access
Heat management must be maintained within the mine working environment to minimize stress on equipment and personnel. The issue is a growing concern as mines continue to expand in size, depth and ...infrastructure. Heat management is a concern as it relates to both heat sensitive equipment and more importantly the health and safety of the workers found within the mine. Proper application of engineering protocols and work practice controls will have a direct impact on the health and safety of workers and increased productivity. Using continuous monitoring stations placed in strategic locations throughout the mine to capture the environmental conditions, various strategies can be used in the planning and prevention of potential hazard exposure. Economic analysis is used to select the most feasible strategy for heat stress control. This paper presents a step by step methodology that may be considered by ventilation specialists to effectively implement a heat management control system. A case study based on a detailed heat management assessment conducted for a potash mine in Saskatchewan, Canada is presented.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Histone H3K36 trimethylation (H3K36me3) is frequently lost in multiple cancer types, identifying it as an important therapeutic target. Here we identify a synthetic lethal interaction in which ...H3K36me3-deficient cancers are acutely sensitive to WEE1 inhibition. We show that RRM2, a ribonucleotide reductase subunit, is the target of this synthetic lethal interaction. RRM2 is regulated by two pathways here: first, H3K36me3 facilitates RRM2 expression through transcription initiation factor recruitment; second, WEE1 inhibition degrades RRM2 through untimely CDK activation. Therefore, WEE1 inhibition in H3K36me3-deficient cells results in RRM2 reduction, critical dNTP depletion, S-phase arrest, and apoptosis. Accordingly, this synthetic lethality is suppressed by increasing RRM2 expression or inhibiting RRM2 degradation. Finally, we demonstrate that WEE1 inhibitor AZD1775 regresses H3K36me3-deficient tumor xenografts.
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•WEE1 inhibition selectively kills H3K36me3-deficient cancer cells•These cells are killed through dNTP starvation because of RRM2 depletion•RRM2 is regulated by H3K36me3 through transcription and WEE1 via degradation•WEE1 inhibitor AZD1775 regresses H3K36me3-deficient tumors in vivo
Pfister et al. show that WEE1 inhibition selectively kills H3K36me3-deficient cancer cells through dNTP starvation resulting from RRM2 depletion. Pfister et al. further show that H3K36me3 facilitates RRM2 transcription whereas WEE1 inhibition promotes RRM2 degradation via CDK activation.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Lung cancer remains the leading cause of cancer‐related death due to poor treatment responses and resistance arising from tumour heterogeneity. Here, we show that adverse prognosis associated with ...epigenetic silencing of the tumour suppressor RASSF1A is due to increased deposition of extracellular matrix (ECM), tumour stiffness and metastatic dissemination in vitro and in vivo. We find that lung cancer cells with RASSF1A promoter methylation display constitutive nuclear YAP1 accumulation and expression of prolyl 4‐hydroxylase alpha‐2 (P4HA2) which increases collagen deposition. Furthermore, we identify that elevated collagen creates a stiff ECM which in turn triggers cancer stem‐like programming and metastatic dissemination in vivo. Re‐expression of RASSF1A or inhibition of P4HA2 activity reverses these effects and increases markers of lung differentiation (TTF‐1 and Mucin 5B). Our study identifies RASSF1A as a clinical biomarker associated with mechanical properties of ECM which increases the levels of cancer stemness and risk of metastatic progression in lung adenocarcinoma. Moreover, we highlight P4HA2 as a potential target for uncoupling ECM signals that support cancer stemness.
Synopsis
The hippo signaling regulator RASSF1A is established as tumor suppressor in solid cancers, but the in vivo consequences of its loss have been difficult to discern. This study finds epigenetic suppression of RASSF1A in lung cancer to promote YAP‐dependent collagen deposition, leading to increased tumor stiffness, cancer stem‐cell reprograming, and risk of metastasis.
RASSF1A suppresses metastatic dissemination in lung adenocarcinoma.
Loss of RASSF1A leads to YAP‐dependent expression of collagen prolyl hydroxylase P4HA2 and elevated extracellular matrix (ECM) stiffness.
ECM stiffness overrides RASSF1A‐mediated restriction of oncogenic YAP transcription.
High stiffness triggers emergence of cancer stem‐like cells.
Epigenetic silencing of tumor suppressor RASSF1A promotes nuclear YAP1 accumulation and collagen deposition in the ECM.
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FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
The circadian clock integrates temporal information with environmental cues in regulating plant development and physiology. Recently, the circadian clock has been shown to affect plant responses to ...biotic cues. To further examine this role of the circadian clock, we tested disease resistance in mutants disrupted in CCA1 and LHY, which act synergistically to regulate clock activity. We found that cca1 and lhy mutants also synergistically affect basal and resistance gene-mediated defense against Pseudomonas syringae and Hyaloperonospora arabidopsidis. Disrupting the circadian clock caused by overexpression of CCA1 or LHY also resulted in severe susceptibility to P. syringae. We identified a downstream target of CCA1 and LHY, GRP7, a key constituent of a slave oscillator regulated by the circadian clock and previously shown to influence plant defense and stomatal activity. We show that the defense role of CCA1 and LHY against P. syringae is at least partially through circadian control of stomatal aperture but is independent of defense mediated by salicylic acid. Furthermore, we found defense activation by P. syringae infection and treatment with the elicitor flg22 can feedback-regulate clock activity. Together this data strongly supports a direct role of the circadian clock in defense control and reveal for the first time crosstalk between the circadian clock and plant innate immunity.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Recent Progress in RXLR Effector Research Anderson, Ryan G; Deb, Devdutta; Fedkenheuer, Kevin ...
Molecular plant-microbe interactions
28, Issue:
10
Journal Article
Peer reviewed
Open access
Some of the most devastating oomycete pathogens deploy effector proteins, with the signature amino acid motif RXLR, that enter plant cells to promote virulence. Research on the function and evolution ...of RXLR effectors has been very active over the decade that has transpired since their discovery. Comparative genomics indicate that RXLR genes play a major role in virulence for Phytophthora and downy mildew species. Importantly, gene-for-gene resistance against these oomycete lineages is based on recognition of RXLR proteins. Comparative genomics have revealed several mechanisms through which this resistance can be broken, most notably involving epigenetic control of RXLR gene expression. Structural studies have revealed a core fold that is present in the majority of RXLR proteins, providing a foundation for detailed mechanistic understanding of virulence and avirulence functions. Finally, functional studies have demonstrated that suppression of host immunity is a major function for RXLR proteins. Host protein targets are being identified in a variety of plant cell compartments. Some targets comprise hubs that are also manipulated by bacteria and fungi, thereby revealing key points of vulnerability in the plant immune network.
Coupling aromatic heteronucleophiles to arenes is a common way to assemble drug‐like molecules. Many methods operate via nucleophiles intercepting organometallic intermediates, via Pd‐, Cu‐, and ...Ni‐catalysis, that facilitate carbon‐heteroatom bond formation and a variety of protocols. We present an alternative, unified strategy where phosphonium salts can replicate the behavior of organometallic intermediates. Under a narrow set of reaction conditions, a variety of aromatic heteronucleophile classes can be coupled to pyridines and diazines that are often problematic in metal‐catalyzed couplings, such as where (pseudo)halide precursors are unavailable in complex structures with multiple polar functional groups.
Aromatic heteronucleophiles are frequently coupled to pyridine and diazine heterocycles to make drug‐like molecules. An alternative approach where seven distinct classes of nucleophiles are coupled to azine phosphonium salts via a nucleophile addition‐P‐ligand coupling mechanism is presented. A narrow range of reaction conditions and applicability to drug‐like fragments and complex bioactive molecules are advantages of this approach.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
Plant nucleotide-binding leucine-rich repeat (NLR) immune receptors activate cell death and confer disease resistance by unknown mechanisms. We demonstrate that plant Toll/interleukin-1 receptor ...(TIR) domains of NLRs are enzymes capable of degrading nicotinamide adenine dinucleotide in its oxidized form (NAD
). Both cell death induction and NAD
cleavage activity of plant TIR domains require known self-association interfaces and a putative catalytic glutamic acid that is conserved in both bacterial TIR NAD
-cleaving enzymes (NADases) and the mammalian SARM1 (sterile alpha and TIR motif containing 1) NADase. We identify a variant of cyclic adenosine diphosphate ribose as a biomarker of TIR enzymatic activity. TIR enzymatic activity is induced by pathogen recognition and functions upstream of the genes
(
) and
(
), which encode regulators required for TIR immune function. Thus, plant TIR-NLR receptors require NADase function to transduce recognition of pathogens into a cell death response.
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