Institution
Universidade Estadual de Londrina
Education•Londrina, Brazil•
About: Universidade Estadual de Londrina is a education organization based out in Londrina, Brazil. It is known for research contribution in the topics: Population & Toxoplasma gondii. The organization has 13052 authors who have published 19291 publications receiving 212123 citations.
Topics: Population, Toxoplasma gondii, Oxidative stress, Starch, Germination
Papers published on a yearly basis
Papers
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TL;DR: Based on the available evidence, it appears unlikely that rigorous and prolonged exercise results in an oxidative stress level that is detrimental to human health.
216 citations
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TL;DR: Together, the genetic and molecular analysis suggested multiple alleles or closely linked genes that govern SBR resistance in soybean.
Abstract: Soybean production in South and North America has recently been threatened by the widespread dissemination of soybean rust (SBR) caused by the fungus Phakopsora pachyrhizi. Currently, chemical spray containing fungicides is the only effective method to control the disease. This strategy increases production costs and exposes the environment to higher levels of fungicides. As a first step towards the development of SBR resistant cultivars, we studied the genetic basis of SBR resistance in five F2 populations derived from crossing the Brazilian-adapted susceptible cultivar CD 208 to each of five different plant introductions (PI 200487, PI 200526, PI 230970, PI 459025, PI 471904) carrying SBR-resistant genes (Rpp). Molecular mapping of SBR-resistance genes was performed in three of these PIs (PI 459025, PI 200526, PI 471904), and also in two other PIs (PI 200456 and 224270). The strategy mapped two genes present in PI 230970 and PI 459025, the original sources of Rpp2 and Rpp4, to linkage groups (LG) J and G, respectively. A new SBR resistance locus, rpp5 was mapped in the LG-N. Together, the genetic and molecular analysis suggested multiple alleles or closely linked genes that govern SBR resistance in soybean.
215 citations
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Oswaldo Cruz Foundation1, Federal University of Ceará2, Universidade Federal de Minas Gerais3, Universidade Federal de Goiás4, University of São Paulo5, State University of Campinas6, Universidade de Pernambuco7, Universidade Estadual de Londrina8, Federal University of Rio de Janeiro9, University of Brasília10
TL;DR: The evidence is presented that resulted in the Brazilian Consensus on Chagas Disease, which was to review and standardize strategies for diagnosis, treatment, prevention, and control of the disease in the country, based on the available scientific evidence.
Abstract: Chagas disease is a neglected chronic condition with a high burden of morbidity and mortality. It has considerable psychological, social, and economic impacts. The disease represents a significant public health issue in Brazil, with different regional patterns. This document presents the evidence that resulted in the Brazilian Consensus on Chagas Disease. The objective was to review and standardize strategies for diagnosis, treatment, prevention, and control of Chagas disease in the country, based on the available scientific evidence. The consensus is based on the articulation and strategic contribution of renowned Brazilian experts with knowledge and experience on various aspects of the disease. It is the result of a close collaboration between the Brazilian Society of Tropical Medicine and the Ministry of Health. It is hoped that this document will strengthen the development of integrated actions against Chagas disease in the country, focusing on epidemiology, management, comprehensive care (including families and communities), communication, information, education, and research .
214 citations
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TL;DR: Delineating the specific mechanisms by which metals alter redox homeostasis is essential to understand the pathophysiology of AD, PD, and MS and may provide possible new targets for their prevention and treatment of the patients affected by these NDDs.
Abstract: Metals are involved in different pathophysiological mechanisms associated with neurodegenerative diseases (NDDs), including Alzheimer's disease (AD), Parkinson's disease (PD) and multiple sclerosis (MS). The aim of this study was to review the effects of the essential metals zinc (Zn), copper (Cu), manganese (Mn) and iron (Fe) on the central nervous system (CNS), as well as the mechanisms involved in their neurotoxicity. Low levels of Zn as well as high levels of Cu, Mn, and Fe participate in the activation of signaling pathways of the inflammatory, oxidative and nitrosative stress (ION however, at high levels, the binding of Zn to β-amyloid may enhance formation of fibrillar β-amyloid aggregation, leading to neurodegeneration. High levels of Cu, Mn and Fe participate in the formation α-synuclein aggregates in intracellular inclusions, called Lewy Body, that result in synaptic dysfunction and interruption of axonal transport. In PD, there is focal accumulation of Fe in the substantia nigra, while in AD a diffuse accumulation of Fe occurs in various regions, such as cortex and hippocampus, with Fe marginally increased in the senile plaques. Zn deficiency induces an imbalance between T helper (Th)1 and Th2 cell functions and a failure of Th17 down-regulation, contributing to the pathogenesis of MS. In MS, elevated levels of Fe occur in certain brain regions, such as thalamus and striatum, which may be due to inflammatory processes disrupting the blood-brain barrier and attracting Fe-rich macrophages. Delineating the specific mechanisms by which metals alter redox homeostasis is essential to understand the pathophysiology of AD, PD, and MS and may provide possible new targets for their prevention and treatment of the patients affected by these NDDs.
212 citations
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TL;DR: This review will focus on current studies related to mechanisms underlying Mn import and export, primarily the Mn transporters, and their function and roles in Mn‐induced neurotoxicity.
Abstract: Manganese (Mn) is an essential heavy metal that is naturally found in the environment. Daily intake through dietary sources provides the necessary amount required for several key physiological processes, including antioxidant defense, energy metabolism, immune function and others. However, overexposure from environmental sources can result in a condition known as manganism that features symptomatology similar to Parkinson's disease (PD). This disorder presents with debilitating motor and cognitive deficits that arise from a neurodegenerative process. In order to maintain a balance between its essentiality and neurotoxicity, several mechanisms exist to properly buffer cellular Mn levels. These include transporters involved in Mn uptake, and newly discovered Mn efflux mechanisms. This review will focus on current studies related to mechanisms underlying Mn import and export, primarily the Mn transporters, and their function and roles in Mn-induced neurotoxicity. Though and essential metal, overexposure to manganese may result in neurodegenerative disease analogous to Parkinson's disease. Manganese homeostasis is tightly regulated by transporters, including transmembrane importers (divalent metal transporter 1, transferrin and its receptor, zinc transporters ZIP8 and Zip14, dopamine transporter, calcium channels, choline transporters and citrate transporters) and exporters (ferroportin and SLC30A10), as well as the intracellular trafficking proteins (SPCA1 and ATP12A2). A manganese-specific sensor, GPP130, has been identified, which affords means for monitoring intracellular levels of this metal.
210 citations
Authors
Showing all 13138 results
Name | H-index | Papers | Citations |
---|---|---|---|
Michael Maes | 115 | 807 | 52050 |
Fernando Q. Cunha | 88 | 682 | 31501 |
Mariangela Hungria | 67 | 389 | 15219 |
Petar Popovski | 59 | 756 | 21009 |
Waldiceu A. Verri | 54 | 249 | 10311 |
Thiago M. Cunha | 54 | 268 | 9519 |
Emerson Franchini | 52 | 402 | 9620 |
Celso Vataru Nakamura | 51 | 418 | 10908 |
Diego Augusto Santos Silva | 51 | 389 | 53077 |
Susan M. Tarlo | 50 | 263 | 10850 |
Paulo Caramelli | 45 | 366 | 9666 |
Fabio Pitta | 44 | 213 | 11925 |
Joaquim Gama-Rodrigues | 43 | 225 | 8380 |
Ricardo Almeida | 43 | 250 | 7304 |
Hamilton Roschel | 43 | 235 | 5894 |