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Institution

Universidade Federal de Minas Gerais

EducationBelo 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
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Journal ArticleDOI
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

Journal ArticleDOI
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

Journal ArticleDOI
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

Journal ArticleDOI
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

Proceedings ArticleDOI
04 Jul 2017
TL;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

NameH-indexPapersCitations
Michael Marmot1931147170338
Pulickel M. Ajayan1761223136241
Alan D. Lopez172863259291
Jens Nielsen1491752104005
Mildred S. Dresselhaus136762112525
Jing Kong12655372354
Mauricio Terrones11876061202
Michael Brammer11842446763
Terence G. Langdon117115861603
Caroline A. Sabin10869044233
Michael Brauer10648073664
Michael Bader10373537525
Michael S. Strano9848060141
Pablo Jarillo-Herrero9124539171
Riichiro Saito9150248869
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023111
2022624
20215,708
20205,955
20195,269
20185,020