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A key question in the thermodynamics of open quantum systems is how to partition thermodynamic quantities such as entropy, work, and internal energy between the system and its environment. We show that the only partition under which entropy is nonsingular is based on a partition of Hilbert space, which assigns half the system-environment coupling to the system and half to the environment. However, quantum work partitions nontrivially under Hilbert-space partition, and we derive a work sum rule that accounts for quantum work at a distance. All state functions of the system are shown to be path independent once this nonlocal quantum work is properly accounted for. Our results are illustrated with application to a driven resonant level strongly coupled to a reservoir.

We present a partition of quantum observables in an open quantum system that is inherited from the division of the underlying Hilbert space or configuration space. It is shown that this partition leads to the definition of an inhomogeneous continuity equation for generic, non-local observables. This formalism is employed to describe the local evolution of the von Neumann entropy of a system of independent quantum particles out of equilibrium. Crucially, we find that all local fluctuations in the entropy are governed by an entropy current operator, implying that the production of entanglement entropy is not measured by this partitioned entropy. For systems linearly perturbed from equilibrium, it is shown that this entropy current is equivalent to a heat current, provided that the system-reservoir coupling is partitioned symmetrically. Finally, we show that any other partition of the coupling leads directly to a divergence of the von Neumann entropy. Thus, we conclude that Hilbert-space partitioning is the only partition of the von Neumann entropy that is consistent with the laws of thermodynamics.

The COVID-19 pandemic has affected all domains of human life, including the economic and social fabric of societies. One of the central strategies for managing public health throughout the pandemic has been through persuasive messaging and collective behaviour change. To help scholars better understand the social and moral psychology behind public health behaviour, we present a dataset comprising of 51,404 individuals from 69 countries. This dataset was collected for the International Collaboration on Social & Moral Psychology of COVID-19 project (ICSMP COVID-19). This social science survey invited participants around the world to complete a series of moral and psychological measures and public health attitudes about COVID-19 during an early phase of the COVID-19 pandemic (between April and June 2020). The survey included seven broad categories of questions: COVID-19 beliefs and compliance behaviours; identity and social attitudes; ideology; health and well-being; moral beliefs and motivation; personality traits; and demographic variables. We report both raw and cleaned data, along with all survey materials, data visualisations, and psychometric evaluations of key variables., (© 2023. The Author(s).)

The NLRP3 inflammasome plays a central role in antimicrobial defense as well as in the context of sterile inflammatory conditions. NLRP3 activity is governed by two independent signals: the first signal primes NLRP3, rendering it responsive to the second signal, which then triggers inflammasome formation. Our understanding of how NLRP3 priming contributes to inflammasome activation remains limited. Here, we show that IKKβ, a kinase activated during priming, induces recruitment of NLRP3 to phosphatidylinositol-4-phosphate (PI4P), a phospholipid enriched on the trans-Golgi network. NEK7, a mitotic spindle kinase that had previously been thought to be indispensable for NLRP3 activation, was redundant for inflammasome formation when IKKβ recruited NLRP3 to PI4P. Studying iPSC-derived human macrophages revealed that the IKKβ-mediated NEK7-independent pathway constitutes the predominant NLRP3 priming mechanism in human myeloid cells. Our results suggest that PI4P binding represents a primed state into which NLRP3 is brought by IKKβ activity., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Bacterial cell wall components provide various unique molecular structures that are detected by pattern recognition receptors (PRRs) of the innate immune system as non-self. Most bacterial species form a cell wall that consists of peptidoglycan (PGN), a polymeric structure comprising alternating amino sugars that form strands cross-linked by short peptides. Muramyl dipeptide (MDP) has been well documented as a minimal immunogenic component of peptidoglycan 1-3 . MDP is sensed by the cytosolic nucleotide-binding oligomerization domain-containing protein 2 4 (NOD2). Upon engagement, it triggers pro-inflammatory gene expression, and this functionality is of critical importance in maintaining a healthy intestinal barrier function 5 . Here, using a forward genetic screen to identify factors required for MDP detection, we identified N-acetylglucosamine kinase (NAGK) as being essential for the immunostimulatory activity of MDP. NAGK is broadly expressed in immune cells and has previously been described to contribute to the hexosamine biosynthetic salvage pathway 6 . Mechanistically, NAGK functions upstream of NOD2 by directly phosphorylating the N-acetylmuramic acid moiety of MDP at the hydroxyl group of its C6 position, yielding 6-O-phospho-MDP. NAGK-phosphorylated MDP-but not unmodified MDP-constitutes an agonist for NOD2. Macrophages from mice deficient in NAGK are completely deficient in MDP sensing. These results reveal a link between amino sugar metabolism and innate immunity to bacterial cell walls., (© 2022. The Author(s).)

The opioid crisis is a major public health challenge in the United States, killing about 70,000 people in 2020 alone. Long delays and feedbacks between policy actions and their effects on drug-use behavior create dynamic complexity, complicating policy decision-making. In 2017, the National Academies of Sciences, Engineering, and Medicine called for a quantitative systems model to help understand and address this complexity and guide policy decisions. Here, we present SOURCE (Simulation of Opioid Use, Response, Consequences, and Effects), a dynamic simulation model developed in response to that charge. SOURCE tracks the US population aged ≥12 y through the stages of prescription and illicit opioid (e.g., heroin, illicit fentanyl) misuse and use disorder, addiction treatment, remission, and overdose death. Using data spanning from 1999 to 2020, we highlight how risks of drug use initiation and overdose have evolved in response to essential endogenous feedback mechanisms, including: 1) social influence on drug use initiation and escalation among people who use opioids; 2) risk perception and response based on overdose mortality, influencing potential new initiates; and 3) capacity limits on treatment engagement; as well as other drivers, such as 4) supply-side changes in prescription opioid and heroin availability; and 5) the competing influences of illicit fentanyl and overdose death prevention efforts. Our estimates yield a more nuanced understanding of the historical trajectory of the crisis, providing a basis for projecting future scenarios and informing policy planning.

Changing collective behaviour and supporting non-pharmaceutical interventions is an important component in mitigating virus transmission during a pandemic. In a large international collaboration (Study 1, N = 49,968 across 67 countries), we investigated self-reported factors associated with public health behaviours (e.g., spatial distancing and stricter hygiene) and endorsed public policy interventions (e.g., closing bars and restaurants) during the early stage of the COVID-19 pandemic (April-May 2020). Respondents who reported identifying more strongly with their nation consistently reported greater engagement in public health behaviours and support for public health policies. Results were similar for representative and non-representative national samples. Study 2 (N = 42 countries) conceptually replicated the central finding using aggregate indices of national identity (obtained using the World Values Survey) and a measure of actual behaviour change during the pandemic (obtained from Google mobility reports). Higher levels of national identification prior to the pandemic predicted lower mobility during the early stage of the pandemic (r = -0.40). We discuss the potential implications of links between national identity, leadership, and public health for managing COVID-19 and future pandemics., (© 2022. The Author(s).)

Mixed lineage kinase domain-like (MLKL) is the executioner in the caspase-independent form of programmed cell death called necroptosis. Receptor-interacting serine/threonine protein kinase 3 (RIPK3) phosphorylates MLKL, triggering MLKL oligomerization, membrane translocation and membrane disruption. MLKL also undergoes ubiquitylation during necroptosis, yet neither the mechanism nor the significance of this event has been demonstrated. Here, we show that necroptosis-specific multi-mono-ubiquitylation of MLKL occurs following its activation and oligomerization. Ubiquitylated MLKL accumulates in a digitonin-insoluble cell fraction comprising organellar and plasma membranes and protein aggregates. Appearance of this ubiquitylated MLKL form can be reduced by expression of a plasma membrane-located deubiquitylating enzyme. Oligomerization-induced MLKL ubiquitylation occurs on at least four separate lysine residues and correlates with its proteasome- and lysosome-dependent turnover. Using a MLKL-DUB fusion strategy, we show that constitutive removal of ubiquitin from MLKL licences MLKL auto-activation independent of necroptosis signalling in mouse and human cells. Therefore, in addition to the role of ubiquitylation in the kinetic regulation of MLKL-induced death following an exogenous necroptotic stimulus, it also contributes to restraining basal levels of activated MLKL to avoid unwanted cell death., (© 2021 The Authors.)

Tumor necrosis factor (TNF) is one of the few cytokines successfully targeted by therapies against inflammatory diseases. However, blocking this well studied and pleiotropic ligand can cause dramatic side-effects. Here, we reason that a systems-level proteomic analysis of TNF signaling could dissect its diverse functions and offer a base for developing more targeted therapies. Therefore, we combine phosphoproteomics time course experiments with subcellular localization and kinase inhibitor analysis to identify functional modules of protein phosphorylation. The majority of regulated phosphorylation events can be assigned to an upstream kinase by inhibiting master kinases. Spatial proteomics reveals phosphorylation-dependent translocations of hundreds of proteins upon TNF stimulation. Phosphoproteome analysis of TNF-induced apoptosis and necroptosis uncovers a key role for transcriptional cyclin-dependent kinase activity to promote cytokine production and prevent excessive cell death downstream of the TNF signaling receptor. This resource of TNF-induced pathways and sites can be explored at http://tnfviewer.biochem.mpg.de/ ., (© 2021. The Author(s).)

Introduction: The opioid crisis is a pervasive public health threat in the U.S. Simulation modeling approaches that integrate a systems perspective are used to understand the complexity of this crisis and analyze what policy interventions can best address it. However, limitations in currently available data sources can hamper the quantification of these models., Methods: To understand and discuss data needs and challenges for opioid systems modeling, a meeting of federal partners, modeling teams, and data experts was held at the U.S. Food and Drug Administration in April 2019. This paper synthesizes the meeting discussions and interprets them in the context of ongoing simulation modeling work., Results: The current landscape of national-level quantitative data sources of potential use in opioid systems modeling is identified, and significant issues within data sources are discussed. Major recommendations on how to improve data sources are to: maintain close collaboration among modeling teams, enhance data collection to better fit modeling needs, focus on bridging the most crucial information gaps, engage in direct and regular interaction between modelers and data experts, and gain a clearer definition of policymakers' research questions and policy goals., Conclusions: This article provides an important step in identifying and discussing data challenges in opioid research generally and opioid systems modeling specifically. It also identifies opportunities for systems modelers and government agencies to improve opioid systems models., (Copyright © 2020 American Journal of Preventive Medicine. All rights reserved.)

Signaling via the intracellular pathogen receptors nucleotide-binding oligomerization domain-containing proteins NOD1 and NOD2 requires receptor interacting kinase 2 (RIPK2), an adaptor kinase that can be targeted for the treatment of various inflammatory diseases. However, the molecular mechanisms of how RIPK2 contributes to NOD signaling are not completely understood. We generated FLAG-tagged RIPK2 knock-in mice using CRISPR/Cas9 technology to study NOD signaling mechanisms at the endogenous level. Using cells from these mice, we were able to generate a detailed map of post-translational modifications on RIPK2. Similar to other reports, we did not detect ubiquitination of RIPK2 lysine 209 during NOD2 signaling. However, using site-directed mutagenesis we identified a new regulatory region on RIPK2, which dictates the crucial interaction with the E3 ligase XIAP and downstream signaling outcomes., (© 2020 The Authors.)

Cyclic GMP-AMP synthase (cGAS) is an innate immune sensor for cytosolic microbial DNA 1 . After binding DNA, cGAS synthesizes the messenger 2'3'-cyclic GMP-AMP (cGAMP) 2-4 , which triggers cell-autonomous defence and the production of type I interferons and pro-inflammatory cytokines via the activation of STING 5 . In addition to responding to cytosolic microbial DNA, cGAS also recognizes mislocalized cytosolic self-DNA and has been implicated in autoimmunity and sterile inflammation 6,7 . Specificity towards pathogen- or damage-associated DNA was thought to be caused by cytosolic confinement. However, recent findings place cGAS robustly in the nucleus 8-10 , where tight tethering of chromatin is important to prevent autoreactivity to self-DNA 8 . Here we show how cGAS is sequestered and inhibited by chromatin. We provide a cryo-electron microscopy structure of the cGAS catalytic domain bound to a nucleosome, which shows that cGAS does not interact with the nucleosomal DNA, but instead interacts with histone 2A-histone 2B, and is tightly anchored to the 'acidic patch'. The interaction buries the cGAS DNA-binding site B, and blocks the formation of active cGAS dimers. The acidic patch robustly outcompetes agonistic DNA for binding to cGAS, which suggests that nucleosome sequestration can efficiently inhibit cGAS, even when accessible DNA is nearby, such as in actively transcribed genomic regions. Our results show how nuclear cGAS is sequestered by chromatin and provides a mechanism for preventing autoreactivity to nuclear self-DNA.

Objective: We investigated the long-term cognitive effects of concussion in 19,261 members of the general population and a cohort of varsity American football players with a history of frequent head impacts, using tests that are known to be sensitive to small changes in performance., Methods: We asked 19,261 participants to complete a demographic questionnaire and 12 cognitive tests measuring aspects of executive function, including inhibitory control. We compared the performance of those reporting a history of concussion (post-concussion) to those reporting no history of concussion (non-concussed) on the cognitive battery and four non-cognitive variables. We used the results of this population-level study to predict the profile of cognitive performance in varsity American football players, who completed the same cognitive tasks., Results: Post-concussion and non-concussed participants did not differ on 11 of the 12 cognitive tasks employed. However, on a test of inhibitory control based on the classic Stroop paradigm, post-concussion participants showed accuracy-related impairments specific to the incongruent conditions of the task. Post-concussion participants reported higher levels of anxiety, depression, and trouble concentrating. An entirely independent sample of 74 varsity American football players demonstrated the same pattern of impairment: compared to healthy controls, they scored significantly lower on the test of inhibitory control but were indistinguishable from controls on the 11 other tasks., Interpretation: Self-reported concussion is not associated with long-term general effects on cognitive function. Nevertheless, those who report at least one concussion and those who expose themselves to long-term frequent sport-related head impacts do have a modest, but statistically robust, deficit of inhibitory control.

The inflammatory functions of the cytokine tumor necrosis factor (TNF) rely on its ability to induce cytokine production and to induce cell death. Caspase-dependent and caspase-independent pathways-apoptosis and necroptosis, respectively-regulate immunogenicity by the release of distinct sets of cellular proteins. To obtain an unbiased, systems-level understanding of this important process, we here applied mass spectrometry-based proteomics to dissect protein release during apoptosis and necroptosis. We report hundreds of proteins released from human myeloid cells in time course experiments. Both cell death types induce receptor shedding, but only apoptotic cells released nucleosome components. Conversely, necroptotic cells release lysosomal components by activating lysosomal exocytosis at early stages of necroptosis-induced membrane permeabilization and show reduced release of conventionally secreted cytokines., Competing Interests: Declaration of Interests The authors declare no competing interests., (Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.)

Innate immune signaling and programmed cell death are intimately linked, and many signaling pathways can regulate and induce both, transcription of inflammatory mediators or autonomous cell death. The best-characterized examples for these dual outcomes are members of the TNF superfamily, the inflammasome receptors, and the toll-like receptors. Signaling via the intracellular peptidoglycan receptors NOD1 and NOD2, however, does not appear to follow this trend, despite involving signaling proteins, or proteins with domains that are linked to programmed cell death, such as RIP kinases, inhibitors of apoptosis (IAP) proteins or the CARD domains on NOD1/2. To better understand the connections between NOD signaling and cell death induction, we here review the latest findings on the molecular regulation of signaling downstream of the NOD receptors and explore the links between this immune signaling pathway and the regulation of cell death., (Copyright © 2019 Heim, Stafford and Nachbur.)

The E3 ubiquitin ligase Parkin is a key effector of the removal of damaged mitochondria by mitophagy. Parkin determines cell fate in response to mitochondrial damage, with its loss promoting early onset Parkinson's disease and potentially also cancer progression. Controlling a cell's apoptotic response is essential to co-ordinate the removal of damaged mitochondria. We report that following mitochondrial damage-induced mitophagy, Parkin directly ubiquitinates the apoptotic effector protein BAK at a conserved lysine in its hydrophobic groove, a region that is crucial for BAK activation by BH3-only proteins and its homo-dimerisation during apoptosis. Ubiquitination inhibited BAK activity by impairing its activation and the formation of lethal BAK oligomers. Parkin also suppresses BAX-mediated apoptosis, but in the absence of BAX ubiquitination suggesting an indirect mechanism. In addition, we find that BAK-dependent mitochondrial outer membrane permeabilisation during apoptosis promotes PINK1-dependent Parkin activation. Hence, we propose that Parkin directly inhibits BAK to suppress errant apoptosis, thereby allowing the effective clearance of damaged mitochondria, but also promotes clearance of apoptotic mitochondria to limit their potential pro-inflammatory effect., (© 2018 The Authors.)

Objective: To investigate the structural integrity of fibre tracts underlying overt motor behaviour in PDOC., Methods: This cross-sectional study examined 15 PDOC patients and 22 healthy participants. Eight PDOC patients met the criteria for the vegetative state, 5 met the criteria for the minimally conscious state and 2 met the criteria for emerging from the minimally conscious state. We used fibre tractography to reconstruct the white matter fibres known to be involved in voluntary motor execution (i.e., those connecting thalamus with M1, M1 with cerebellum, and cerebellum with thalamus) and used fractional anisotropy (FA) as a measure of their integrity., Results: PDOC patients showed significantly reduced FA relative to controls on the fibres connecting thalamus and M1. This went above and beyond a widespread injury to the white matter and correlated with clinical severity. In a subset of patients, we also identified a similar pattern of injury in the fibres connecting M1 and cerebellum but a relative preservation of those connecting cerebellum and thalamus., Conclusions: Our results suggest that structural damage to motor fibres may lead to reduced responsiveness in PDOC patients across all diagnostic sub-categories, and therefore behavioural assessments may underestimate the level of retained cognitive function and awareness across the PDOC spectrum., (Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.)

The microscopic origins of Fourier's venerable law of thermal transport in quantum electron systems has remained somewhat of a mystery, given that previous derivations were forced to invoke intrinsic scattering rates far exceeding those occurring in real systems. We propose an alternative hypothesis, namely, that Fourier's law emerges naturally if many quantum states participate in the transport of heat across the system. We test this hypothesis systematically in a graphene flake junction and show that the temperature distribution becomes nearly classical when the broadening of the individual quantum states of the flake exceeds their energetic separation. We develop a thermal resistor network model to investigate the scaling of the sample and contact thermal resistances and show that the latter is consistent with classical thermal transport theory in the limit of large level broadening.

Inhibitors of apoptosis (IAPs) proteins are critical regulators of innate immune signaling pathways and therefore have potential as drug targets. X-linked IAP (XIAP) and cellular IAP1 and IAP2 (cIAP1 and cIAP2) are E3 ligases that have been shown to be required for signaling downstream of NOD2, an intracellular receptor for bacterial peptidoglycan. We used genetic and biochemical approaches to compare the responses of IAP-deficient mice and cells to NOD2 stimulation. In all cell types tested, XIAP is the only IAP required for signaling immediately downstream of NOD2, while cIAP1 and cIAP2 are dispensable for NOD2-induced nuclear factor κB (NF-κB) and mitogen-activated protein kinase (MAPK) activation. However, mice lacking cIAP1 or TNFR1 have a blunted cytokine response to NOD2 stimulation. We conclude that cIAPs regulate NOD2-dependent autocrine TNF signaling in vivo and highlight the importance of physiological context in the interplay of innate immune signaling pathways., (Copyright © 2018 The Author(s). Published by Elsevier Inc. All rights reserved.)

Hunting in the neotropics is a widespread form of resource extraction. However, there is increasing concern that current activities are leading to the decline and extirpation of vulnerable species; particulary ateline primates, large ungulates (such as tapirs and white-lipped peccaries) and large birds such as curassows. Hunting patterns are expected to be a product of two principal influences: the value of return for a given amount of effort invested into hunting, and cultural factors that determine the prestige and usefulness of prey. Previous work has suggested that hunting profiles change in a predictable way over time, becoming more diverse and more dependent on smaller bodied species as preferred, large-bodied prey become scarcer. In this paper, we evaluate the hunting profiles of 78 neotropical communities in Central and South America. We investigate the uniformity of species preferences, whether communities that are geographically closer have similar hunting profiles, and whether the age and size of settlements can be used to predict the type and diversity of species targeted. We found that there was only a weak correlation between the structure of communities' hunting profiles and their geographical proximity. Neither a community's size nor age was a good predictor of the shape and structure of its hunting profile. Our data suggest that either the availability of prey or the cultural influences dictating the value of different species can change rapidly over small distances, and that older and larger settlements do not impact prey species distributions in a predictable way., (© The Author(s) 2017.)

Increasing pressure on tropical forests is continually highlighting the need to find new solutions that mitigate the impact of human populations on biodiversity. However, developing solutions that can tackle the drivers of anthropogenic pressure, or at least take them into account, hinges upon building a good understanding of the culture and perceptions of local people. This study aims to provide an overview of the ethnoprimatology of an indigenous Kichwa community in the Ecuadorian Amazon that maintains a traditional lifestyle but also has good access to markets. We examine whether primates are seen as a distinctive group and their relative importance as sources of bushmeat and as household pets. Pile-sorting exercises revealed that although locals generally group members of the order Primates together, tree-dwelling non-primates including sloths, coatis, kinkajous and tamanduas are also frequently classified as 'monkeys'. The perceived importance of primates to the forest and the community lay more in their potential as bushmeat, and only 1 respondent identified an ecological role for the group in terms of seed dispersal. Gaining a better understanding of local perceptions will allow for better-informed conservation decisions that are more aware of potential impacts and are more likely to gain community support., (© 2016 The Author(s) Published by S. Karger AG, Basel.)

Intracellular nucleotide binding and oligomerization domain (NOD) receptors recognize antigens including bacterial peptidoglycans and initiate immune responses by triggering the production of pro-inflammatory cytokines through activating NF-κB and MAP kinases. Receptor interacting protein kinase 2 (RIPK2) is critical for NOD-mediated NF-κB activation and cytokine production. Here we develop and characterize a selective RIPK2 kinase inhibitor, WEHI-345, which delays RIPK2 ubiquitylation and NF-κB activation downstream of NOD engagement. Despite only delaying NF-κB activation on NOD stimulation, WEHI-345 prevents cytokine production in vitro and in vivo and ameliorates experimental autoimmune encephalomyelitis in mice. Our study highlights the importance of the kinase activity of RIPK2 for proper immune responses and demonstrates the therapeutic potential of inhibiting RIPK2 in NOD-driven inflammatory diseases.

A precise definition for a quantum electron thermometer is given, as an electron reservoir coupled locally (e.g., by tunneling) to a sample, and brought into electrical and thermal equilibrium with it. A realistic model of a scanning thermal microscope with atomic resolution is then developed, including the effect of thermal coupling of the probe to the ambient environment. We show that the temperatures of individual atomic orbitals or bonds in a conjugated molecule with a temperature gradient across it exhibit quantum oscillations, whose origin can be traced to a realization of Maxwell's demon at the single-molecule level. These oscillations may be understood in terms of the rules of covalence describing bonding in π-electron systems. Fourier's law of heat conduction is recovered as the resolution of the temperature probe is reduced, indicating that the macroscopic law emerges as a consequence of coarse graining.

Transport through an Anderson junction (two macroscopic electrodes coupled to an Anderson impurity) is dominated by a Kondo peak in the spectral function at zero temperature. We show that the single-particle Kohn-Sham potential of density-functional theory reproduces the linear transport, despite the lack of a Kondo peak in its spectral function. Using Bethe ansatz techniques, we calculate this potential for all coupling strengths, including the crossover from mean-field behavior to charge quantization caused by the derivative discontinuity. A simple and accurate interpolation formula is also given.

The majority of plant viruses rely on insect vectors for transmission. Insects with piercing-sucking mouthparts are the most common and efficient vectors because, they are able to inject viruses into specific plant tissues. Acquisition and inoculation of viruses occurs during specific vector feeding behaviors, and feeding behavior varies greatly among insects with piercing-sucking mouthparts. In this review we provide an overview of the feeding behavior of the major insect vectors with piercing sucking mouthparts: aphids, whiteflies, mealybugs, hoppers, and thrips. We briefly review the different mechanisms of plant virus transmission by these insects, and discuss how each mechanism requires a vector that engages in specific feeding behaviors, and how differences in feeding behavior among these insects can determine which viruses they are capable of transmitting. We also discuss recent findings indicating that plant viruses can directly modify their vector's behavior in a way that enhances transmission to a host plant.

Background: The transport through a quantum-scale device may be uniquely characterized by its transmission eigenvalues τ(n). Recently, highly conductive single-molecule junctions (SMJ) with multiple transport channels (i.e., several τ(n) > 0) have been formed from benzene molecules between Pt electrodes. Transport through these multichannel SMJs is a probe of both the bonding properties at the lead-molecule interface and of the molecular symmetry., Results: We use a many-body theory that properly describes the complementary wave-particle nature of the electron to investigate transport in an ensemble of Pt-benzene-Pt junctions. We utilize an effective-field theory of interacting π-electrons to accurately model the electrostatic influence of the leads, and we develop an ab initio tunneling model to describe the details of the lead-molecule bonding over an ensemble of junction geometries. We also develop a simple decomposition of transmission eigenchannels into molecular resonances based on the isolated resonance approximation, which helps to illustrate the workings of our many-body theory, and facilitates unambiguous interpretation of transmission spectra., Conclusion: We confirm that Pt-benzene-Pt junctions have two dominant transmission channels, with only a small contribution from a third channel with τ(n) << 1. In addition, we demonstrate that the isolated resonance approximation is extremely accurate and determine that transport occurs predominantly via the HOMO orbital in Pt-benzene-Pt junctions. Finally, we show that the transport occurs in a lead-molecule coupling regime where the charge carriers are both particle-like and wave-like simultaneously, requiring a many-body description.

We investigate electronic transport through molecular radicals and predict a correlation-induced transmission node arising from destructive interference between transport contributions from different charge states of the molecule. This quantum interference effect has no single-particle analog and cannot be described by effective single-particle theories. Large errors in the thermoelectric properties and nonlinear current-voltage response of molecular radical junctions are introduced when the complementary wave and particle aspects of the electron are not properly treated. A method to accurately calculate the low-energy transport through a radical-based junction using an Anderson model is given.

Vector infection by some animal-infecting parasites results in altered feeding that enhances transmission. Modification of vector behavior is of broad adaptive significance, as parasite fitness relies on passage to a new host, and vector feeding is nearly always essential for transmission. Although several plant viruses infect their insect vectors, we have shown that vector infection by a plant virus alters feeding behavior. Here we show that infection with Tomato spotted wilt virus (TSWV), type member of the only plant-infecting genus in the Bunyaviridae, alters the feeding behavior of its thrips vector, Frankliniella occidentalis (Pergande). Male thrips infected with TSWV fed more than uninfected males, with the frequency of all feeding behaviors increasing by up to threefold, thus increasing the probability of virus inoculation. Importantly, infected males made almost three times more noningestion probes (probes in which they salivate, but leave cells largely undamaged) compared with uninfected males. A functional cell is requisite for TSWV infection and cell-to-cell movement; thus, this behavior is most likely to establish virus infection. Some animal-infecting members of the Bunyaviridae (La Crosse virus and Rift Valley fever virus) also cause increased biting rates in infected vectors. Concomitantly, these data support the hypothesis that capacity to modify vector feeding behavior is a conserved trait among plant- and animal-infecting members of the Bunyaviridae that evolved as a mechanism to enhance virus transmission. Our results underscore the evolutionary importance of vector behavioral modification to diverse parasites with host ranges spanning both plant and animal kingdoms.

We calculate transmission eigenvalue distributions for Pt-benzene-Pt and Pt-butadiene-Pt junctions using realistic state-of-the-art many-body techniques. An effective field theory of interacting π-electrons is used to include screening and van der Waals interactions with the metal electrodes. We find that the number of dominant transmission channels in a molecular junction is equal to the degeneracy of the molecular orbital closest to the metal Fermi level.

Quantum interference effects offer opportunities to tune the electronic and thermoelectric response of a quantum-scale device over orders of magnitude. Here we focus on single-molecule devices, in which interference features may be strongly affected by both chemical and electronic modifications to the system. Although not always desirable, such a susceptibility offers insight into the importance of "small" terms, such as through-space coupling and many-body charge-charge correlations. Here we investigate the effect of these small terms using different Hamiltonian models with Hückel, gDFTB and many-body theory to calculate the transport through several single-molecule junctions, finding that terms that are generally thought to only slightly perturb the transport instead produce significant qualitative changes in the transport properties. In particular, we show that coupling of multiple interference features in cross-conjugated molecules by through-space coupling will lead to splitting of the features, as can correlation effects. The degeneracy of multiple interference features in cross-conjugated molecules appears to be significantly more sensitive to perturbations than those observed in equivalent cyclic systems and this needs to be considered if such supernodes are required for molecular thermoelectric devices.

We predict an enormous order-dependent quantum enhancement of thermoelectric effects in the vicinity of higher-order interferences in the transmission spectrum of a nanoscale junction. Single-molecule junctions based on 3,3'-biphenyl and polyphenyl ether (PPE) are investigated in detail. The nonequilibrium thermodynamic efficiency and power output of a thermoelectric heat engine based on a 1,3-benzene junction are calculated using many-body theory and compared to the predictions of the figure-of-merit ZT.

An exact expression for the heat current in an interacting nanostructure is derived and used to calculate the thermoelectric response of three representative single-molecule junctions formed from isoprene, 1,3-benzenedithiol, and [18]-annulene. Dramatic enhancements of the thermopower S and Lorenz number L are predicted when the junction is tuned across a node in the transmission function, with universal maximum values S(max) = (pi/3(1/2))(k(B)/e) and L(max) = (7pi(2)/5)(k(B)(2)/e(2)). The effect of a finite minimum transmission probability due, e.g., to incoherent processes or additional nonresonant channels, is also considered.

A spatially extended classical system with metastable states subject to weak spatiotemporal noise can exhibit a transition in its activation behavior when one or more external parameters are varied. Depending on the potential, the transition can be first or second order, but there exists no systematic theory of the relation between the order of the transition and the shape of the potential barrier. In this paper, we address that question in detail for a general class of systems whose order parameter is describable by a classical field that can vary in both space and time, and whose zero-noise dynamics are governed by a smooth polynomial potential. We show that a quartic potential barrier can have only second-order transitions, confirming an earlier conjecture [D. L. Stein, J. Stat. Phys. 114, 1537 (2004)]. We then derive, through a combination of analytical and numerical arguments, both necessary and sufficient conditions to have a first-order vs a second-order transition in noise-induced activation behavior, for a large class of systems with smooth polynomial potentials of arbitrary order. We find in particular that the order of the transition is especially sensitive to the potential behavior near the top of the barrier.

We give a detailed discussion of the quantum interference effect transistor (QuIET), a proposed device which exploits the interference between electron paths through aromatic molecules to modulate the current flow. In the off state, perfect destructive interference stemming from the molecular symmetry blocks the current, while in the on state, the current is allowed to flow by locally introducing either decoherence or elastic scattering. Details of a model calculation demonstrating the efficacy of the QuIET are presented, and various fabrication scenarios are proposed, including the possibility of using conducting polymers to connect the QuIET with multiple leads.

We report experiments on aluminium nanowires in ultra-high vacuum at room temperature that reveal a periodic spectrum of exceptionally stable structures. Two 'magic' series of stable structures are observed: at low conductance, the formation of stable nanowires is governed by electronic shell effects whereas for larger contacts atomic packing dominates. The crossover between the two regimes is found to be smooth. A detailed comparison of the experimental results to a theoretical stability analysis indicates that, while the main features of the observed electron-shell structure are similar to those of alkali and noble metals, a sequence of extremely stable wires plays a unique role in aluminium. This series appears isolated in conductance histograms and can be attributed to 'superdeformed' non-axisymmetric nanowires.

We experimentally investigated the decay behavior with time t of resonances near and at exceptional points, where two complex eigenvalues and also the associated eigenfunctions coalesce. The measurements were performed with a dissipative microwave billiard, whose shape depends on two parameters. The t2 dependence predicted at the exceptional point on the basis of a two-state matrix model could be verified. Outside the exceptional point the predicted Rabi oscillations, also called quantum echoes in this context, were detected.

We investigate multiterminal quantum transport through single monocyclic aromatic annulene molecules, and their derivatives, using the nonequilibrium Green function approach within the self-consistent Hartree-Fock approximation. We propose a new device concept, the quantum interference effect transistor, that exploits perfect destructive interference stemming from molecular symmetry and controls current flow by introducing decoherence and/or elastic scattering that break the symmetry. This approach overcomes the fundamental problems of power dissipation and environmental sensitivity that beset nanoscale device proposals.

Thermally induced conductance jumps of metal nanowires are modeled using stochastic Ginzburg-Landau field theories. Changes in radius are predicted to occur via the nucleation of surface kinks at the wire ends, consistent with recent electron microscopy studies. The activation rate displays nontrivial dependence on nanowire length, and undergoes first- or second-order-like transitions as a function of length. The activation barriers of the most stable structures are predicted to be universal, i.e., independent of the radius of the wire, and proportional to the square root of the surface tension. The reduction of the activation barrier under strain is also determined.