Institution
University of Florence
Education•Florence, Toscana, Italy•
About: University of Florence is a education organization based out in Florence, Toscana, Italy. It is known for research contribution in the topics: Population & Carbonic anhydrase. The organization has 27292 authors who have published 79599 publications receiving 2341684 citations. The organization is also known as: Università degli studi di Firenze & Universita degli studi di Firenze.
Papers published on a yearly basis
Papers
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TL;DR: The benefits, challenges, and potential solutions associated with cellular networks that incorporate millimeter-wave communications, arrays with a massive number of antennas, and small cell geometries are outlined.
Abstract: The combination of millimeter-wave communications, arrays with a massive number of antennas, and small cell geometries is a symbiotic convergence of technologies that has the potential to dramatically improve wireless access and throughput. This article outlines the benefits, challenges, and potential solutions associated with cellular networks that incorporate these technologies.
732 citations
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TL;DR: The aim is to present a framework for understanding questions of incremental stability fully compatible with the well-known input-to-state stability approach.
Abstract: Deals with several notions of incremental stability. In other words, the focus is on stability of trajectories with respect to one another, rather than with respect to some attractor. The aim is to present a framework for understanding such questions fully compatible with the well-known input-to-state stability approach. Applications of the newly introduced stability notions are also discussed.
731 citations
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TL;DR: Three new genome-wide significant nonsynonymous variants associated with Alzheimer's disease are observed, providing additional evidence that the microglia-mediated innate immune response contributes directly to the development of Alzheimer's Disease.
Abstract: We identified rare coding variants associated with Alzheimer's disease in a three-stage case–control study of 85,133 subjects. In stage 1, we genotyped 34,174 samples using a whole-exome microarray. In stage 2, we tested associated variants (P < 1 × 10−4) in 35,962 independent samples using de novo genotyping and imputed genotypes. In stage 3, we used an additional 14,997 samples to test the most significant stage 2 associations (P < 5 × 10−8) using imputed genotypes. We observed three new genome-wide significant nonsynonymous variants associated with Alzheimer's disease: a protective variant in PLCG2 (rs72824905: p.Pro522Arg, P = 5.38 × 10−10, odds ratio (OR) = 0.68, minor allele frequency (MAF)cases = 0.0059, MAFcontrols = 0.0093), a risk variant in ABI3 (rs616338: p.Ser209Phe, P = 4.56 × 10−10, OR = 1.43, MAFcases = 0.011, MAFcontrols = 0.008), and a new genome-wide significant variant in TREM2 (rs143332484: p.Arg62His, P = 1.55 × 10−14, OR = 1.67, MAFcases = 0.0143, MAFcontrols = 0.0089), a known susceptibility gene for Alzheimer's disease. These protein-altering changes are in genes highly expressed in microglia and highlight an immune-related protein–protein interaction network enriched for previously identified risk genes in Alzheimer's disease. These genetic findings provide additional evidence that the microglia-mediated innate immune response contributes directly to the development of Alzheimer's disease.
730 citations
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TL;DR: Results indicate that P can favor the development of Th cells producing Th2-type cytokines and is an inducer of both transient IL-4 production and CD30 expression in established Th1 cells.
Abstract: The effect of progesterone (P) on the cytokine production profile of Ag-specific human CD4+ T cell lines and clones was investigated. T cell lines specific for purified protein derivative or streptokinase (SK) derived in the presence of P exhibited significant increased ability to produce IL-5 in comparison with T cell lines derived in the absence of P. Moreover, IL-4 was significantly increased in SK-specific T cell lines derived in the presence of P in comparison with SK-specific T cell lines derived in the absence of this hormone. In addition, SK-specific T cell lines generated in the presence of P developed into T cell clones showing a Th0-, instead of Th1-like, cytokine profile. Furthermore, SK-specific T cell clones with an established Th1 profile of cytokine secretion did express mRNA for, and produced detectable amounts of, IL-4 when stimulated with P in combination with insoluble anti-CD3 mAb. Combined stimulation with P and insoluble anti-CD3 mAb also enabled Th1 clones to express CD30 on their surface membrane. These results indicate that P can favor the development of Th cells producing Th2-type cytokines and is an inducer of both transient IL-4 production and CD30 expression in established Th1 cells. Thus, P production at the placental level may be responsible, at least in part, for increased production of Th2-type cytokines which have been implied in fetal allograft survival and maintenance of successful pregnancy.
728 citations
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TL;DR: The International Consultation Committee for Sexual Medicine on Definitions/Epidemiology/Risk Factors for Sexual Dysfunction as mentioned in this paper provided a general overview of the definitions of sexual dysfunction for men and women, the incidence and prevalence rates, and a description of the risk factors identified in large population-based studies.
722 citations
Authors
Showing all 27699 results
Name | H-index | Papers | Citations |
---|---|---|---|
Charles A. Dinarello | 190 | 1058 | 139668 |
D. M. Strom | 176 | 3167 | 194314 |
Gregory Y.H. Lip | 169 | 3159 | 171742 |
Christopher M. Dobson | 150 | 1008 | 105475 |
Dirk Inzé | 149 | 647 | 74468 |
Thomas Hebbeker | 148 | 1984 | 114004 |
Marco Zanetti | 145 | 1439 | 104610 |
Richard B. Devereux | 144 | 962 | 116403 |
Gunther Roland | 141 | 1471 | 100681 |
Markus Klute | 139 | 1447 | 104196 |
Tariq Aziz | 138 | 1646 | 96586 |
Guido Tonelli | 138 | 1458 | 97248 |
Giorgio Trinchieri | 138 | 433 | 78028 |
Christof Roland | 137 | 1308 | 96632 |
Christoph Paus | 137 | 1585 | 100801 |