Institution
Universidade Federal de Minas Gerais
Education•Belo Horizonte, Minas Gerais, Brazil•
About: Universidade Federal de Minas Gerais is a education organization based out in Belo Horizonte, Minas Gerais, Brazil. It is known for research contribution in the topics: Population & Immune system. The organization has 41631 authors who have published 75688 publications receiving 1249905 citations.
Papers published on a yearly basis
Papers
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University of Colorado Boulder1, University of Strasbourg2, Universidade Federal de Minas Gerais3, National Health Service4, University of Pennsylvania5, Johns Hopkins University6, Tohoku University7, University of Hong Kong8, University of Southern Denmark9, Charité10, University of California, San Francisco11
TL;DR: In this article, the authors showed that optic neuritis in NMO typically results in more severe retinal nerve fiber layer (RNFL) and ganglion cell layer thinning and more frequent development of microcystic macular edema than in MS.
Abstract: Neuromyelitis optica (NMO) is an inflammatory autoimmune disease of the central nervous system that preferentially targets the optic nerves and spinal cord. The clinical presentation may suggest multiple sclerosis (MS), but a highly specific serum autoantibody against the astrocytic water channel aquaporin-4 present in up to 80% of NMO patients enables distinction from MS. Optic neuritis may occur in either condition resulting in neuro-anatomical retinal changes. Optical coherence tomography (OCT) has become a useful tool for analyzing retinal damage both in MS and NMO. Numerous studies showed that optic neuritis in NMO typically results in more severe retinal nerve fiber layer (RNFL) and ganglion cell layer thinning and more frequent development of microcystic macular edema than in MS. Furthermore, while patients' RNFL thinning also occurs in the absence of optic neuritis in MS, subclinical damage seems to be rare in NMO. Thus, OCT might be useful in differentiating NMO from MS and serve as an outcome parameter in clinical studies.
210 citations
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TL;DR: It is shown that diabetes causes a shift in oral bacterial composition and, by transfer to germ-free mice, that the oral microbiota of diabetic mice is more pathogenic, and treatment with IL-17 antibody decreases the pathogenicity of the oral microbiome in diabetic mice.
210 citations
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TL;DR: The results corroborate the literature regarding the involvement of BDNF in PD and hypothesize that lower BDNF levels in early stages of the disease may be associated with pathogenic mechanisms of PD, and the increase ofBDNF levels with the progression of the Disease may be a compensatory mechanism in more advanced stages of PD.
Abstract: The brain-derived neurotrophic factor (BDNF) is a potent inhibitor of apoptosis-mediated cell death and neurotoxin-induced degeneration of dopaminergic neurons. There is a growing body of evidence implicating BDNF in the pathogenesis of Parkinson’s disease (PD), suggesting it may eventually be used in the development of neuroprotective therapies for PD. The serum BDNF of 47 PD patients and of 23 control subjects was assessed, and serum BNDF levels were significantly decreased in PD patients when compared with controls (p = 0.046). Interestingly enough, BDNF correlated positively with a longer time span of the disease, as well as with the severity of the PD symptoms and with more advanced stages of the disease. Additionally, higher BDNF levels also correlated with poor balance as assessed by the Berg Balance Scale, more time spent at the Timed Up & Go Test, reduced speed of gait and shorter distance walked during the Six-Minute Walk Test. Our results corroborate the literature regarding the involvement of BDNF in PD. We hypothesize that lower BDNF levels in early stages of the disease may be associated with pathogenic mechanisms of PD. The increase of BDNF levels with the progression of the disease may be a compensatory mechanism in more advanced stages of PD.
210 citations
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TL;DR: The role of the NLRP3 inflammasome is revealed in mediating MSU crystal-induced inflammation and dysfunction of the joints, and the previously unrecognized role of LTB(4) is highlighted in driving NLRP 3 inflammaome activation in response to MSU crystals, both in vitro and in vivo.
Abstract: Objective
Deposition of monosodium urate monohydrate (MSU) crystals in the joints promotes an intense inflammatory response and joint dysfunction. This study evaluated the role of the NLRP3 inflammasome and 5-lipoxygenase (5-LOX)–derived leukotriene B4 (LTB4) in driving tissue inflammation and hypernociception in a murine model of gout.
Methods
Gout was induced by injecting MSU crystals into the joints of mice. Wild-type mice and mice deficient in NLRP3, ASC, caspase 1, interleukin-1β (IL-1β), IL-1 receptor type I (IL-1RI), IL-18R, myeloid differentiation factor 88 (MyD88), or 5-LOX were used. Evaluations were performed to assess neutrophil influx, LTB4 activity, cytokine (IL-1β, CXCL1) production (by enzyme-linked immunosorbent assay), synovial microvasculature cell adhesion (by intravital microscopy), and hypernociception. Cleaved caspase 1 and production of reactive oxygen species (ROS) were analyzed in macrophages by Western blotting and fluorometric assay, respectively.
Results
Injection of MSU crystals into the knee joints of mice induced neutrophil influx and neutrophil-dependent hypernociception. MSU crystal–induced neutrophil influx was CXCR2-dependent and relied on the induction of CXCL1 in an NLRP3/ASC/caspase 1/IL-1β/MyD88–dependent manner. LTB4 was produced rapidly after injection of MSU crystals, and this was necessary for caspase 1–dependent IL-1β production and consequent release of CXCR2-acting chemokines in vivo. In vitro, macrophages produced LTB4 after MSU crystal injection, and LTB4 was relevant in the MSU crystal–induced maturation of IL-1β. Mechanistically, LTB4 drove MSU crystal–induced production of ROS and ROS-dependent activation of the NLRP3 inflammasome.
Conclusion
These results reveal the role of the NLRP3 inflammasome in mediating MSU crystal–induced inflammation and dysfunction of the joints, and highlight a previously unrecognized role of LTB4 in driving NLRP3 inflammasome activation in response to MSU crystals, both in vitro and in vivo.
210 citations
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04 Jul 2017TL;DR: The results identify hate speech forms and unveil a set of important patterns, providing not only a broader understanding of online hate speech, but also offering directions for detection and prevention approaches.
Abstract: Social media platforms provide an inexpensive communication medium that allows anyone to quickly reach millions of users. Consequently, in these platforms anyone can publish content and anyone interested in the content can obtain it, representing a transformative revolution in our society. However, this same potential of social media systems brings together an important challenge---these systems provide space for discourses that are harmful to certain groups of people. This challenge manifests itself with a number of variations, including bullying, offensive content, and hate speech. Specifically, authorities of many countries today are rapidly recognizing hate speech as a serious problem, specially because it is hard to create barriers on the Internet to prevent the dissemination of hate across countries or minorities. In this paper, we provide the first of a kind systematic large scale measurement and analysis study of hate speech in online social media. We aim to understand the abundance of hate speech in online social media, the most common hate expressions, the effect of anonymity on hate speech and the most hated groups across regions. In order to achieve our objectives, we gather traces from two social media systems: Whisper and Twitter. We then develop and validate a methodology to identify hate speech on both of these systems. Our results identify hate speech forms and unveil a set of important patterns, providing not only a broader understanding of online hate speech, but also offering directions for detection and prevention approaches.
210 citations
Authors
Showing all 42077 results
Name | H-index | Papers | Citations |
---|---|---|---|
Michael Marmot | 193 | 1147 | 170338 |
Pulickel M. Ajayan | 176 | 1223 | 136241 |
Alan D. Lopez | 172 | 863 | 259291 |
Jens Nielsen | 149 | 1752 | 104005 |
Mildred S. Dresselhaus | 136 | 762 | 112525 |
Jing Kong | 126 | 553 | 72354 |
Mauricio Terrones | 118 | 760 | 61202 |
Michael Brammer | 118 | 424 | 46763 |
Terence G. Langdon | 117 | 1158 | 61603 |
Caroline A. Sabin | 108 | 690 | 44233 |
Michael Brauer | 106 | 480 | 73664 |
Michael Bader | 103 | 735 | 37525 |
Michael S. Strano | 98 | 480 | 60141 |
Pablo Jarillo-Herrero | 91 | 245 | 39171 |
Riichiro Saito | 91 | 502 | 48869 |