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 & Context (language use). The organization has 41631 authors who have published 75688 publications receiving 1249905 citations.
Topics: Population, Context (language use), Medicine, Immune system, Health care
Papers published on a yearly basis
Papers
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TL;DR: Development in gene editing technology and novel gene delivery carriers make gene therapy a promising therapeutic modality for RP and other hereditary retinal dystrophies in the future.
273 citations
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25 Oct 2011-Materials Science and Engineering A-structural Materials Properties Microstructure and Processing
TL;DR: In this article, a finite element model was used to examine the flow processes in high pressure torsion (HPT) when using quasi-constrained conditions where disks are contained within depressions on the inner surfaces of the upper and lower anvils.
Abstract: Finite element modeling was used to examine the flow processes in high-pressure torsion (HPT) when using quasi-constrained conditions where disks are contained within depressions on the inner surfaces of the upper and lower anvils. Separate simulations were performed using applied pressures from 0.5 to 2.0 GPa, rotations up to 1.5 turns and friction coefficients from 0 to 1.0 outside of the depressions. The simulations demonstrate the distribution of effective strain within the depressions is comparable to the prediction by ideal torsion, and the applied pressure and the friction coefficient outside the depressions play only a minor role in the distribution of effective strain. The mean stresses during processing vary linearly with the distance from the center of the disk such that there are higher compressive stresses in the disk centers and lower stresses at the edges. The torque required for rotation of the anvil is strongly dependent upon the friction coefficient between the sample and the anvil outside the depressions.
273 citations
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TL;DR: Results indicate ECG analysis based on DNNs, previously studied in a single-lead setup, generalizes well to 12-lead exams, taking the technology closer to the standard clinical practice.
Abstract: The role of automatic electrocardiogram (ECG) analysis in clinical practice is limited by the accuracy of existing models. Deep Neural Networks (DNNs) are models composed of stacked transformations that learn tasks by examples. This technology has recently achieved striking success in a variety of task and there are great expectations on how it might improve clinical practice. Here we present a DNN model trained in a dataset with more than 2 million labeled exams analyzed by the Telehealth Network of Minas Gerais and collected under the scope of the CODE (Clinical Outcomes in Digital Electrocardiology) study. The DNN outperform cardiology resident medical doctors in recognizing 6 types of abnormalities in 12-lead ECG recordings, with F1 scores above 80% and specificity over 99%. These results indicate ECG analysis based on DNNs, previously studied in a single-lead setup, generalizes well to 12-lead exams, taking the technology closer to the standard clinical practice.
270 citations
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TL;DR: Netrin-1, a neuroimmune guidance cue, was secreted by macrophages in human and mouse atheroma, where it inactivated the migration of macrophage toward chemokines linked to their egress from plaques, establishing a causative role for negative regulators of leukocyte migration in chronic inflammation.
Abstract: Atherosclerotic plaque formation is fueled by the persistence of lipid-laden macrophages in the artery wall. The mechanisms by which these cells become trapped, thereby establishing chronic inflammation, remain unknown. Here we found that netrin-1, a neuroimmune guidance cue, was secreted by macrophages in human and mouse atheroma, where it inactivated the migration of macrophages toward chemokines linked to their egress from plaques. Acting via its receptor, UNC5b, netrin-1 inhibited the migration of macrophages directed by the chemokines CCL2 and CCL19, activation of the actin-remodeling GTPase Rac1 and actin polymerization. Targeted deletion of netrin-1 in macrophages resulted in much less atherosclerosis in mice deficient in the receptor for low-density lipoprotein and promoted the emigration of macrophages from plaques. Thus, netrin-1 promoted atherosclerosis by retaining macrophages in the artery wall. Our results establish a causative role for negative regulators of leukocyte migration in chronic inflammation.
270 citations
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TL;DR: It is demonstrated that BCG-induced lipid body formation is TLR2 mediated and these structures function as signaling platforms in inflammatory mediator production, because compartmentalization of substrate and key enzymes within lipid bodies has impact on the capacity of activated leukocytes to generate increased amounts of eicosanoids during experimental infection by BCG.
Abstract: Differentiation of macrophages into foamy (lipid-laden) macrophages is a common pathological observation in tuberculous granulomas both in experimental settings as well as in clinical conditions; however, the mechanisms that regulate intracellular lipid accumulation in the course of mycobacterial infection and their significance to pathophysiology of tuberculosis are not well understood. In this study, we investigated the mechanisms of formation and function of lipid-laden macrophages in a murine model of tuberculosis. Mycobacterium bovis bacillus Calmette-Guerin (BCG), but not Mycobacterium smegmatis, induced a dose- and time-dependent increase in lipid body-inducible nonmembrane-bound cytoplasmic lipid domain size and numbers. Lipid body formation was drastically inhibited in TLR2-, but not in TLR4-deficient mice, indicating a role for TLR2 in BCG recognition and signaling to form lipid bodies. Increase in lipid bodies during infection correlated with increased generation of PGE2 and localization of cyclooxygenase-2 within lipid bodies. Moreover, we demonstrated by intracellular immunofluorescent localization of newly formed eicosanoid that lipid bodies were the predominant sites of PGE2 synthesis in activated macrophages. Our findings demonstrated that BCG-induced lipid body formation is TLR2 mediated and these structures function as signaling platforms in inflammatory mediator production, because compartmentalization of substrate and key enzymes within lipid bodies has impact on the capacity of activated leukocytes to generate increased amounts of eicosanoids during experimental infection by BCG.
269 citations
Authors
Showing all 42077 results
Name | H-index | Papers | Citations |
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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 |