Institution
Tufts University
Education•Medford, Massachusetts, United States•
About: Tufts University is a education organization based out in Medford, Massachusetts, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 32800 authors who have published 66881 publications receiving 3451152 citations. The organization is also known as: Tufts College & Universitatis Tuftensis.
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TL;DR: In vitro experiments demonstrated that CD11b+ macrophages alone were capable of forming tube-like structures that expressed markers of lymphatic endothelium such as LYVE-1 and podoplanin, which suggests a new mechanism of lymphangiogenesis.
Abstract: In the inflamed cornea, there is a parallel outgrowth of blood and lymphatic vessels into the normally avascular cornea. We tested whether adaptive and/or innate immune cells were actively involved in the genesis of new lymphatic vessels. Our results indicate that innate immune cells (CD11b+ macrophages, but not CD11c+ dendritic cells) physically contributed to lymphangiogenesis under pathological conditions and that bone marrow–derived CD11b+ macrophages expressed lymphatic endothelial markers such as LYVE-1 and Prox-1 under inflamed conditions in the corneal stromata of mice. Furthermore, blood vascular endothelial cells that expressed the Tie2 promoter did not contribute to newly formed lymphatic vessels under inflamed conditions. Our in vitro experiments demonstrated that CD11b+ macrophages alone were capable of forming tube-like structures that expressed markers of lymphatic endothelium such as LYVE-1 and podoplanin. The novel finding that CD11b+ macrophages are critical for the development of inflammation-dependent lymphangiogenesis in the eye suggests a new mechanism of lymphangiogenesis.
662 citations
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TL;DR: The notion that n-3 fatty acids may be beneficial in patients affected by diseases characterized by active inflammation is supported, as well as the fact that PUFAs were independently associated with lower levels of proinflammatory markers and higher levels of antiinflammatory markers independent of confounders.
Abstract: Aims: Persons with high intake of polyunsaturated fatty acids (PUFAs) have lower cardiovascular morbidity and mortality. The protective effect of PUFAs is mediated by multiple mechanisms, including their antiinflammatory properties. The association of physiological PUFA levels with pro- and antiinflammatory markers has not been established. Methods and Results: In 1123 persons (aged 20–98 yr), we examined the relationship between relative concentration of fatty acids in fasting plasma and level of inflammatory markers. Adjusting for age, sex, and major confounders, lower arachidonic and docosahexaenoic acids were associated with significantly higher IL-6 and IL-1ra and significantly lower TGF. Lower -linolenic acid was associated with higherC-reactiveproteinandIL-1ra,andlowereicosapentaenoicacid was associated with higher IL-6 and lower TGF. Lower docosahexaenoic acid was strongly associated with lower IL-10. Total n-3 fatty acids were associated with lower IL-6 (P 0.005), IL-1ra (P 0.004), and TNF (P 0.040) and higher soluble IL-6r (P 0.001), IL-10 (P 0.024), and TGF (P 0.0012). Lower n-6 fatty acid levels weresignificantlyassociatedwithhigherIL-1ra(P0.026)andlower TGF(P0.014).Then-6ton-3ratiowasastrong,negativecorrelate of IL-10. Findings were similar in participants free of cardiovascular diseases and after excluding lipids from covariates. Conclusions: In this community-based sample, PUFAs, and especially total n-3 fatty acids, were independently associated with lower levels of proinflammatory markers (IL-6, IL-1ra, TNF, C-reactive protein) and higher levels of antiinflammatory markers (soluble IL6r, IL-10, TGF) independent of confounders. Our findings support the notion that n-3 fatty acids may be beneficial in patients affected by diseases characterized by active inflammation. (J Clin Endocrinol Metab 91: 439–446, 2006)
660 citations
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The Racah Institute of Physics1, Imperial College London2, Northeastern University3, ETH Zurich4, Swiss Federal Institute of Aquatic Science and Technology5, Tufts University6, Uppsala University7, Princeton University8, University of Basel9, Wyss Institute for Biologically Inspired Engineering10, Massachusetts Institute of Technology11, Broad Institute12, Harvard University13, Pasteur Institute14, University of Groningen15, Emory University16, Katholieke Universiteit Leuven17, National Institutes of Health18, Genentech19, University of Tartu20, Université libre de Bruxelles21, University of Zurich22
TL;DR: Scientists working on the response of bacteria to antibiotics define antibiotic persistence and provide practical guidance on how to study bacterial persister cells, and provide a guide to measuring persistence.
Abstract: Increasing concerns about the rising rates of antibiotic therapy failure and advances in single-cell analyses have inspired a surge of research into antibiotic persistence. Bacterial persister cells represent a subpopulation of cells that can survive intensive antibiotic treatment without being resistant. Several approaches have emerged to define and measure persistence, and it is now time to agree on the basic definition of persistence and its relation to the other mechanisms by which bacteria survive exposure to bactericidal antibiotic treatments, such as antibiotic resistance, heteroresistance or tolerance. In this Consensus Statement, we provide definitions of persistence phenomena, distinguish between triggered and spontaneous persistence and provide a guide to measuring persistence. Antibiotic persistence is not only an interesting example of non-genetic single-cell heterogeneity, it may also have a role in the failure of antibiotic treatments. Therefore, it is our hope that the guidelines outlined in this article will pave the way for better characterization of antibiotic persistence and for understanding its relevance to clinical outcomes.
659 citations
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TL;DR: This review discusses current concepts of the pathogenesis, treatment, and prevention of sarcopenia, the loss of muscle mass and strength with age, which is becoming recognized as a major cause of disability and morbidity in the elderly population.
Abstract: Sarcopenia, the loss of muscle mass and strength with age, is becoming recognized as a major cause of disability and morbidity in the elderly population. Sarcopenia is part of normal aging and does not require a disease to occur, although muscle wasting is accelerated by chronic diseases. Sarcopenia is thought to have multiple causes, although the relative importance of each is not clear. Neurological, metabolic, hormonal, nutritional, and physical-activity-related changes with age are likely to contribute to the loss of muscle mass. In this review, we discuss current concepts of the pathogenesis, treatment, and prevention of sarcopenia.
659 citations
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TL;DR: These findings demonstrate that differentiating lymphocytes and neurons strictly require the XRCC4 and DNA ligase IV end-joining proteins and point to the general stage of neuronal development in which these proteins are necessary.
659 citations
Authors
Showing all 33110 results
Name | H-index | Papers | Citations |
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Walter C. Willett | 334 | 2399 | 413322 |
Frank B. Hu | 250 | 1675 | 253464 |
Ralph B. D'Agostino | 226 | 1287 | 229636 |
John Q. Trojanowski | 226 | 1467 | 213948 |
Peter Libby | 211 | 932 | 182724 |
David Baltimore | 203 | 876 | 162955 |
Eric B. Rimm | 196 | 988 | 147119 |
Lewis C. Cantley | 196 | 748 | 169037 |
Bernard Rosner | 190 | 1162 | 147661 |
Charles A. Dinarello | 190 | 1058 | 139668 |
William B. Kannel | 188 | 533 | 175659 |
Scott M. Grundy | 187 | 841 | 231821 |
John P. A. Ioannidis | 185 | 1311 | 193612 |
David H. Weinberg | 183 | 700 | 171424 |
Joel Schwartz | 183 | 1149 | 109985 |