Institution
Kettering University
Education•Flint, Michigan, United States•
About: Kettering University is a education organization based out in Flint, Michigan, United States. It is known for research contribution in the topics: Cancer & RNA. The organization has 6842 authors who have published 7689 publications receiving 337503 citations. The organization is also known as: GMI Engineering & Management Institute & General Motors Institute.
Topics: Cancer, RNA, Antigen, DNA, Population
Papers published on a yearly basis
Papers
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TL;DR: In this article, the authors present some models and their applications, in terms of reliability analyses, to situations where the system can have a whole range of states and all its components can also have a wide range of multiple states.
Abstract: An important problem in reliability theory is to determine the reliability of a complex system given the reliabilities of its components. In real life, the system and its components can be found in a range of states varying from perfect functioning through various levels of performance degradation to complete failure. This paper presents some models and their applications, in terms of reliability analyses, to situations where the system can have a whole range of states and all its components can also have a wide range of multiple states. Properties of the system structure function and computation and approximation of system state probabilities and system reliability measures are given.
91 citations
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TL;DR: A role is established for the phagocytic blood cells of Drosophila in detection of infection and activation of the humoral immune response, and a gene, psidin, is identified that encodes a lysosomal protein required in the blood cells for both degradation of engulfed bacteria andactivation of fat-body Defensin.
91 citations
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TL;DR: It is demonstrated that dense intestinal colonization with vancomycin-resistant Enterococcus faecium (VRE) does not reduce in vivo growth of carbapenem-resistant Klebsiella pneumoniae, and transplantation of a diverse fecal microbiota eliminates both VRE and K. pneumoniae from the gut.
Abstract: Antibiotic resistance among enterococci and γ-proteobacteria is an increasing problem in healthcare settings. Dense colonization of the gut by antibiotic-resistant bacteria facilitates their spread between patients and also leads to bloodstream and other systemic infections. Antibiotic-mediated destruction of the intestinal microbiota and consequent loss of colonization resistance are critical factors leading to persistence and spread of antibiotic-resistant bacteria. The mechanisms underlying microbiota-mediated colonization resistance remain incompletely defined and are likely distinct for different antibiotic-resistant bacterial species. It is unclear whether enterococci or γ-proteobacteria, upon expanding to high density in the gut, confer colonization resistance against competing bacterial species. Herein, we demonstrate that dense intestinal colonization with vancomycin-resistant Enterococcus faecium (VRE) does not reduce in vivo growth of carbapenem-resistant Klebsiella pneumoniae. Reciprocally, K. pneumoniae does not impair intestinal colonization by VRE. In contrast, transplantation of a diverse fecal microbiota eliminates both VRE and K. pneumoniae from the gut. Fluorescence in situ hybridization demonstrates that VRE and K. pneumoniae localize to the same regions in the colon but differ with respect to stimulation and invasion of the colonic mucus layer. While VRE and K. pneumoniae occupy the same three-dimensional space within the gut lumen, their independent growth and persistence in the gut suggests that they reside in distinct niches that satisfy their specific in vivo metabolic needs.
91 citations
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TL;DR: The importance of 2-hydroxyestrone as a product of the metabolism of estradiol in man is discussed and the substantial losses of this metabolite in the various stages of isolation from urine have been estimated.
Abstract: The importance of 2-hydroxyestrone as a product of the metabolism of estradiol in man is discussed. The substantial losses of this metabolite in the various stages of isolation from urine have been estimated.
91 citations
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TL;DR: The promoter structure, the proximal DNA sequences responsible for transcription of Fc gamma RIIIA in macrophages and the protein factors which interact with these sequences are reported and two cis‐acting elements have been identified and required for full promoter function.
Abstract: Expression of the low-affinity Fc receptor for IgG (murine Fc gamma RIIIA) is restricted to cells of myelomonocytic origin. We report here the promoter structure, the proximal DNA sequences responsible for transcription of Fc gamma RIIIA in macrophages and the protein factors which interact with these sequences. A 51 bp sequence, termed the myeloid restricted region (MRR), was both necessary and sufficient for conferring cell type-specific expression in macrophages. Reporter constructs containing mutations in this sequence result in the loss of MRR activity upon transfection into the macrophage cell line, RAW264.7. Two cis-acting elements have been identified and are required for full promoter function. These same elements analyzed by EMSA define two binding sites recognized by nuclear factors derived from macrophages. A 3' purine tract (-50 to -39) within the MRR binds the macrophage and B cell-specific factor, PU.1, and a second E box-like element, termed MyE, upstream of the PU.1 box (-88 to -78) binds the HLH factors TFE3 and USF. EMSA studies using RAW cell extracts suggest that both PU.1 and MyE factors may bind simultaneously to the MRR resulting in a ternary complex that is responsible, in part, for the myeloid-specific activity of the Fc gamma RIIIA promoter.
91 citations
Authors
Showing all 6853 results
Name | H-index | Papers | Citations |
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Joan Massagué | 189 | 408 | 149951 |
Chris Sander | 178 | 713 | 233287 |
Timothy A. Springer | 167 | 669 | 122421 |
Murray F. Brennan | 161 | 925 | 97087 |
Charles M. Rice | 154 | 561 | 83812 |
Lloyd J. Old | 152 | 775 | 101377 |
Howard I. Scher | 151 | 944 | 101737 |
Paul Tempst | 148 | 309 | 89225 |
Pier Paolo Pandolfi | 146 | 529 | 88334 |
Barton F. Haynes | 144 | 911 | 79014 |
Jedd D. Wolchok | 140 | 713 | 123336 |
James P. Allison | 137 | 483 | 83336 |
Harold E. Varmus | 137 | 496 | 76320 |
Scott W. Lowe | 134 | 396 | 89376 |
David S. Klimstra | 133 | 564 | 61682 |