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56 result(s) for "Weitz, Stefan"
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Search : how the data explosion makes us smarter
\"Search is as old as language. We've always needed to find something in the jumble of human creation. The first web was nothing more than passing verbal histories down the generations so others could find and remember how not to get eaten; the first search used the power of written language to build simple indexes in printed books, leading to the Dewey Decimal system and reverse indices in more modern times. Then digital happened. Besides having profound societal impacts, it also made the act of searching almost impossibly complex for both engines and searchers. Information isn't just words; it is pictures, videos, thoughts tagged with geocode data, routes, physical world data, and, increasingly, the machines themselves reporting their condition and listening to others'. Search: How the Data Explosion Makes Us Smarter holds up a mirror to our time to see if search can keep up. Author Stefan Weitz explores the idea of access to help readers understand how we are inventing new ways to search and access data through devices in more places and with more capabilities. We are at the cusp of imbuing our generation with superpowers, but only if we fundamentally rethink what search is, how people can use it, and what we should demand of it. \"-- Provided by publisher.
Microcracking in On-Chip Interconnect Stacks: FEM Simulation and Concept for Fatigue Test
The semiconductor industry is continuing the scaling down of both device and on-chip interconnect features, for performance and economic reasons. This trend has implications for the design of guard ring structures, i.e. metallic non-functional structures in the back-end-of-line (BEoL) stack designed to be efficient to stop microcracks. In this work, we present a sample design for an in situ experiment to study mechanical degradation and failure mechanisms of crack stop structures in the BEoL stack, to ensure the mechanical robustness of microchips for future technology nodes. Additional finite element method (FEM) simulations provide supplementary understanding of the crack kinetics. To examine the effects of mechanical loading on crack stop elements of the BEoL stack, a novel sample geometry for an in situ fatigue experiment using x-ray microscopy was developed. The x-ray microscope (ZEISS Xradia 800 Ultra) enables high-resolution imaging of the 3D-patterned sample structures and defects such as microcracks. The tailored sample geometry allows the application of a tensile load to a BEoL specimen by a lever mechanism. The feasibility of the sample design is shown by mode-I loading of a pure interconnect sample. Post-mortem analysis by scanning electron microscopy (SEM), confirming planar microcrack propagation from the notch through the dielectric layer with small deflections of the crack path near cone shaped copper vias. FEM simulations focusing on the stress-strain fields around a crack tip indicate the beginning of copper plasticity as major mechanism starting the redirection of cracks due to resulting material compression in front of the obstacle.
Scroogled E-mail users find Gmail isn't really free after all
[...]they read your email, pick up on themes and direct targeted ads to you as a result.
Privacy matters: Don't get Scroogled by Gmail
[...]88 percent of Americans disapprove of email providers scanning the content of your personal emails in order to target ads, according to Gfk Roper's recent poll.
Strain history dependence of the nonlinear stress response of fibrin and collagen networks
We show that the nonlinear mechanical response of networks formed from un-cross-linked fibrin or collagen type I continually changes in response to repeated large-strain loading. We demonstrate that this dynamic evolution of the mechanical response arises from a shift of a characteristic nonlinear stress-strain relationship to higher strains. Therefore, the imposed loading does not weaken the underlying matrices but instead delays the occurrence of the strain stiffening. Using confocal microscopy, we present direct evidence that this behavior results from persistent lengthening of individual fibers caused by an interplay between fiber stretching and fiber buckling when the networks are repeatedly strained. Moreover, we show that covalent cross-linking of fibrin or collagen inhibits the shift of the nonlinear material response, suggesting that the molecular origin of individual fiber lengthening may be slip of monomers within the fibers. Thus, a fibrous architecture in combination with constituents that exhibit internal plasticity creates a material whose mechanical response adapts to external loading conditions. This design principle may be useful to engineer novel materials with this capability.
Stress controls the mechanics of collagen networks
Collagen is the main structural and load-bearing element of various connective tissues, where it forms the extracellular matrix that supports cells. It has long been known that collagenous tissues exhibit a highly nonlinear stress–strain relationship, although the origins of this nonlinearity remain unknown. Here, we show that the nonlinear stiffening of reconstituted type I collagen networks is controlled by the applied stress and that the network stiffness becomes surprisingly insensitive to network concentration. We demonstrate how a simple model for networks of elastic fibers can quantitatively account for the mechanics of reconstituted collagen networks. Our model points to the important role of normal stresses in determining the nonlinear shear elastic response, which can explain the approximate exponential relationship between stress and strain reported for collagenous tissues. This further suggests principles for the design of synthetic fiber networks with collagen-like properties, as well as a mechanism for the control of the mechanics of such networks.
Dual-pathway inhibition for secondary and tertiary antithrombotic prevention in cardiovascular disease
Advances in antiplatelet therapies for patients with cardiovascular disease have improved patient outcomes over time, but the challenge of balancing the risks of ischaemia and bleeding remains substantial. Moreover, many patients with cardiovascular disease have a residual risk of ischaemic events despite receiving antiplatelet therapy. Therefore, novel strategies are needed to prevent clinical events through mechanisms beyond platelet inhibition and with an acceptable associated risk of bleeding. The advent of non-vitamin K antagonist oral anticoagulants, which attenuate fibrin formation by selective inhibition of factor Xa or thrombin, has renewed the interest in dual-pathway inhibition strategies that combine an antiplatelet agent with an anticoagulant drug. In this Review, we highlight the emerging pharmacological rationale and clinical development of dual-pathway inhibition strategies for the prevention of atherothrombotic events in patients with different manifestations of cardiovascular disease, such as coronary artery disease, cerebrovascular disease and peripheral artery disease.Many patients with cardiovascular disease have a residual risk of ischaemic events despite receiving antiplatelet therapy. In this Review, Angiolillo and colleagues discuss the pharmacological rationale and clinical development of dual-pathway inhibition strategies for the prevention of atherothrombotic events in patients with cardiovascular disease.
Physical limits to biomechanical sensing in disordered fibre networks
Cells actively probe and respond to the stiffness of their surroundings. Since mechanosensory cells in connective tissue are surrounded by a disordered network of biopolymers, their in vivo mechanical environment can be extremely heterogeneous. Here we investigate how this heterogeneity impacts mechanosensing by modelling the cell as an idealized local stiffness sensor inside a disordered fibre network. For all types of networks we study, including experimentally-imaged collagen and fibrin architectures, we find that measurements applied at different points yield a strikingly broad range of local stiffnesses, spanning roughly two decades. We verify via simulations and scaling arguments that this broad range of local stiffnesses is a generic property of disordered fibre networks. Finally, we show that to obtain optimal, reliable estimates of global tissue stiffness, a cell must adjust its size, shape, and position to integrate multiple stiffness measurements over extended regions of space. Cells in the connective tissue are surrounded by a heterogeneous network of biopolymers. Here, the authors investigate how such heterogeneity affects cellular mechanosensing by simulating the deformation response of experimental and modelled biopolymer networks to locally applied forces.
Formation of moiré interlayer excitons in space and time
Moiré superlattices in atomically thin van der Waals heterostructures hold great promise for extended control of electronic and valleytronic lifetimes 1 – 7 , the confinement of excitons in artificial moiré lattices 8 – 13 and the formation of exotic quantum phases 14 – 18 . Such moiré-induced emergent phenomena are particularly strong for interlayer excitons, where the hole and the electron are localized in different layers of the heterostructure 19 , 20 . To exploit the full potential of correlated moiré and exciton physics, a thorough understanding of the ultrafast interlayer exciton formation process and the real-space wavefunction confinement is indispensable. Here we show that femtosecond photoemission momentum microscopy provides quantitative access to these key properties of the moiré interlayer excitons. First, we elucidate that interlayer excitons are dominantly formed through femtosecond exciton–phonon scattering and subsequent charge transfer at the interlayer-hybridized Σ valleys. Second, we show that interlayer excitons exhibit a momentum fingerprint that is a direct hallmark of the superlattice moiré modification. Third, we reconstruct the wavefunction distribution of the electronic part of the exciton and compare the size with the real-space moiré superlattice. Our work provides direct access to interlayer exciton formation dynamics in space and time and reveals opportunities to study correlated moiré and exciton physics for the future realization of exotic quantum phases of matter. Multidimensional time- and angle-resolved photoelectron spectroscopy is used to determine the interlayer exciton formation process, reveal a direct hallmark of the superlattice moiré modification, and reconstruct the real-space wavefunction distribution.
Interleukin-3 amplifies acute inflammation and is a potential therapeutic target in sepsis
Sepsis is a frequently fatal condition characterized by an uncontrolled and harmful host reaction to microbial infection. Despite the prevalence and severity of sepsis, we lack a fundamental grasp of its pathophysiology. Here we report that the cytokine interleukin-3 (IL-3) potentiates inflammation in sepsis. Using a mouse model of abdominal sepsis, we showed that innate response activator B cells produce IL-3, which induces myelopoiesis of Ly-6Chigh monocytes and neutrophils and fuels a cytokine storm. IL-3 deficiency protects mice against sepsis. In humans with sepsis, high plasma IL-3 levels are associated with high mortality even after adjusting for prognostic indicators. This study deepens our understanding of immune activation, identifies IL-3 as an orchestrator of emergency myelopoiesis, and reveals a new therapeutic target for treating sepsis.