Institution
California Institute of Technology
Education•Pasadena, California, United States•
About: California Institute of Technology is a education organization based out in Pasadena, California, United States. It is known for research contribution in the topics: Galaxy & Redshift. The organization has 57649 authors who have published 146691 publications receiving 8620287 citations. The organization is also known as: Caltech & Cal Tech.
Topics: Galaxy, Redshift, Population, Star formation, Stars
Papers published on a yearly basis
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11 Oct 2017TL;DR: This work seeks to provide a theoretical framework for how to design controllers that are decomposed across timescales in this way, and exhibits a design, named Multi-timescale Reflexive Predictive Control (MRPC), which maintains a per-timestep cost within a constant factor of the offline optimal in an adversarial setting.
Abstract: Many real-world control systems, such as the smart grid and software defined networks, have decentralized components that react quickly using local information and centralized components that react slowly using a more global view. This work seeks to provide a theoretical framework for how to design controllers that are decomposed across timescales in this way. The framework is analogous to how the network utility maximization framework uses optimization decomposition to distribute a global control problem across independent controllers, each of which solves a local problem; except our goal is to decompose a global problem temporally, extracting a timescale separation. Our results highlight that decomposition of a multi-timescale controller into a fast timescale, reactive controller and a slow timescale, predictive controller can be near-optimal in a strong sense. In particular, we exhibit such a design, named Multi-timescale Reflexive Predictive Control (MRPC), which maintains a per-timestep cost within a constant factor of the offline optimal in an adversarial setting.
1,777 citations
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TL;DR: A more complete understanding of how to target DNA sites with specificity will lead not only to novel chemotherapeutics but also to a greatly expanded ability for chemists to probe DNA and to develop highly sensitive diagnostic agents.
Abstract: The design of small complexes that bind and react at specific sequences of DNA becomes important as we begin to delineate, on a molecular level, how genetic information is expressed. A more complete understanding of how to target DNA sites with specificity will lead not only to novel chemotherapeutics but also to a greatly expanded ability for chemists to probe DNA and to develop highly sensitive diagnostic agents.
1,769 citations
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TL;DR: This study uses microarray technology to identify miRNAs induced in primary murine macrophages after exposure to polyriboinosinic:polyribocytidylic acid or the cytokine IFN-β and characterize miR-155 as a common target of a broad range of inflammatory mediators.
Abstract: The mammalian inflammatory response to infection involves the induction of several hundred genes, a process that must be carefully regulated to achieve pathogen clearance and prevent the consequences of unregulated expression, such as cancer. Recently, microRNAs (miRNAs) have emerged as a class of gene expression regulators that has also been linked to cancer. However, the relationship between inflammation, innate immunity, and miRNA expression is just beginning to be explored. In the present study, we use microarray technology to identify miRNAs induced in primary murine macrophages after exposure to polyriboinosinic:polyribocytidylic acid or the cytokine IFN-β. miR-155 was the only miRNA of those tested that was substantially up-regulated by both stimuli. It also was induced by several Toll-like receptor ligands through myeloid differentiation factor 88- or TRIF-dependent pathways, whereas up-regulation by IFNs was shown to involve TNF-α autocrine signaling. Pharmacological inhibition of the kinase JNK blocked induction of miR-155 in response to either polyriboinosinic:polyribocytidylic acid or TNF-α, suggesting that miR-155-inducing signals use the JNK pathway. Together, these findings characterize miR-155 as a common target of a broad range of inflammatory mediators. Importantly, because miR-155 is known to function as an oncogene, these observations identify a potential link between inflammation and cancer.
1,769 citations
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01 Jan 2003TL;DR: Spacetime and Geometry as discussed by the authors is an introductory textbook on general relativity specifically aimed at students, which covers the foundations of the theory and mathematical formalism, providing an approachable introduction to what can often be an intimidating subject.
Abstract: Spacetime and Geometry is an introductory textbook on general relativity, specifically aimed at students. Using a lucid style, Carroll first covers the foundations of the theory and mathematical formalism, providing an approachable introduction to what can often be an intimidating subject. Three major applications of general relativity are then discussed: black holes, perturbation theory and gravitational waves, and cosmology. Students will learn the origin of how spacetime curves (the Einstein equation) and how matter moves through it (the geodesic equation). They will learn what black holes really are, how gravitational waves are generated and detected, and the modern view of the expansion of the universe. A brief introduction to quantum field theory in curved spacetime is also included. A student familiar with this book will be ready to tackle research-level problems in gravitational physics.
1,763 citations
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TL;DR: A computational model is presented that describes the temporal control of NF-κB activation by the coordinated degradation and synthesis of IκB proteins and demonstrates that IπκBα is responsible for strong negative feedback that allows for a fast turn-off of the NF-σB response.
Abstract: Nuclear localization of the transcriptional activator NF-κB (nuclear factor κB) is controlled in mammalian cells by three isoforms of NF-κB inhibitor protein: IκBα, -β, and -ɛ Based on simplifying reductions of the IκB–NF-κB signaling module in knockout cell lines, we present a computational model that describes the temporal control of NF-κB activation by the coordinated degradation and synthesis of IκB proteins The model demonstrates that IκBα is responsible for strong negative feedback that allows for a fast turn-off of the NF-κB response, whereas IκBβ and -ɛ function to reduce the system's oscillatory potential and stabilize NF-κB responses during longer stimulations Bimodal signal-processing characteristics with respect to stimulus duration are revealed by the model and are shown to generate specificity in gene expression
1,760 citations
Authors
Showing all 58155 results
Name | H-index | Papers | Citations |
---|---|---|---|
Eric S. Lander | 301 | 826 | 525976 |
Donald P. Schneider | 242 | 1622 | 263641 |
George M. Whitesides | 240 | 1739 | 269833 |
Yi Chen | 217 | 4342 | 293080 |
David Baltimore | 203 | 876 | 162955 |
Edward Witten | 202 | 602 | 204199 |
George Efstathiou | 187 | 637 | 156228 |
Michael A. Strauss | 185 | 1688 | 208506 |
Jing Wang | 184 | 4046 | 202769 |
Ruedi Aebersold | 182 | 879 | 141881 |
Douglas Scott | 178 | 1111 | 185229 |
Hyun-Chul Kim | 176 | 4076 | 183227 |
Phillip A. Sharp | 172 | 614 | 117126 |
Timothy M. Heckman | 170 | 754 | 141237 |
Zhenan Bao | 169 | 865 | 106571 |