JUAREZ ANTONIO SIMOES QUARESMA

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  • article 3 Citação(ões) na Scopus
    Identification of risk areas for arboviruses transmitted by Aedes aegypti in northern Brazil: A One Health analysis
    (2023) GOMES, Helierson; JESUS, Andrielly Gomes de; QUARESMA, Juarez Antonio Simoes
    Introduction: The complex and growing problem generated by the rapid expansion of unplanned urban areas includes high population density and increased infestation by vectors responsible for the transmission of several diseases. This requires interdisciplinary and intersectoral interventions due to the burden of diseases, especially those caused by arboviruses, which can present severe forms and generate significant pressure on health systems, especially in more vulnerable regions. The objective of this study was to analyze the spatial distribution of arboviruses transmitted by Aedes aegypti (dengue, Zika, and chikungunya) and assess their correlations with demographic, social, and environmental data from the state of Tocantins, Brazil.Methods: This was an ecological time series study of the dengue, Zika, and chikungunya arboviruses in the state of Tocantins. Local Moran's indices were used to observe the spatial autocorrelation of cases and to delimit clusters of high and low risks, correlating them with socioenvironmental indicators, in addition to analyses to detect case clusters.Results: The state reported a mean incidence of 591 annual cases of arbovirus infections per 100,000 inhabitants and a stationary trend with seasonal pattern. Female Pardo individuals aged 20-39 years, with an education level of below college education, were the most affected; Palmas and Araguaina, the two largest cities in the state in terms of economy and population, were the most affected.Conclusion: A better understanding of the interaction between social characteristics, the environment, and ecology of wild animals and vectors is important for the development of mechanisms to predict outbreaks as well as to develop strategies to reduce and/or mitigate recurring arboviral epidemics and other diseases.
  • article 1 Citação(ões) na Scopus
    New Insights into the Mechanism of Immune-Mediated Tissue Injury in Yellow Fever: The Role of Immunopathological and Endothelial Alterations in the Human Lung Parenchyma
    (2022) VASCONCELOS, Danielle Barbosa; FALCAO, Luiz Fabio Magno; PONTE, Lucas Coutinho Tuma Da; SILVA, Camilla Costa; MARTINS, Livia Caricio; NUNES, Bruno Tardelli Diniz; MARTINS FILHO, Arnaldo Jorge; FRANCO, Edna Cristina Santos; DUARTE, Maria Irma Seixas; SOUSA, Jorge Rodrigues De; VASCONCELOS, Pedro Fernando Da Costa; QUARESMA, Juarez Antonio Simoes
    Yellow fever (YF) may cause lesions in different organs. There are no studies regarding the in situ immune response in the human lung and investigating immunopathological aspects in fatal cases can help to better understand the evolution of the infection. Lung tissue samples were collected from 10 fatal cases of human yellow fever and three flavivirus-negative controls who died of other causes and whose lung parenchymal architecture was preserved. In YFV-positive fatal cases, the main histopathological changes included the massive presence of diffuse alveolar inflammatory infiltrate, in addition to congestion and severe hemorrhage. The immunohistochemical analysis of tissues in the lung parenchyma showed significantly higher expression of E-selectin, P-selectin, ICAM-1, VCAM-1 in addition to cytokines such as IL-4, IL-10, IL-13, TNF- alpha, IFN-gamma and TGF-beta compared to the negative control. The increase in immunoglobulins ICAM-1 and VCAM-1 results in strengthening of tissue transmigration signaling. E-selectin and P-selectin actively participate in this process of cell migration and formation of the inflammatory infiltrate. IFN-gamma and TNF-alpha participate in the process of cell injury and viral clearance. The cytokines IL-4 and TGF-beta, acting in synergism, participate in the process of tissue regeneration and breakdown. The anti-inflammatory cytokines IL-4, IL-10 and IL-13 also act in the reduction of inflammation and tissue repair. Our study indicates that the activation of the endothelium aggravates the inflammatory response by inducing the expression of adhesion molecules and cytokines that contribute to the rolling, recruitment, migration and eliciting of the inflammatory process in the lung parenchyma, contributing to the fatal outcome of the disease.
  • article 4 Citação(ões) na Scopus
    Endothelium Activation during Severe Yellow Fever Triggers an Intense Cytokine-Mediated Inflammatory Response in the Liver Parenchyma
    (2022) OLIMPIO, Fabio Alves; FALCAO, Luiz Fabio Magno; CARVALHO, Marcos Luiz Gaia; LOPES, Jeferson da Costa; MENDES, Caio Cesar Henriques; FILHO, Arnaldo Jorge Martins; SILVA, Carlos Augusto Moreira da; MIRANDA, Vanessa do Socorro Cabral; SANTOS, Lais Carneiro dos; VILACOERT, Fellipe Souza da Silva; CRUZ, Ana Cecilia Ribeiro; GALUCIO, Vanessa Costa Alves; AZEVEDO, Raimunda do Socorro da Silva; MARTINS, Livia Caricio; DUARTE, Maria Irma Seixas; SOUSA, Jorge Rodrigues de; VASCONCELOS, Pedro Fernando da Costa; QUARESMA, Juarez Antonio Simoes
    Yellow fever (YF) is a pansystemic disease caused by the yellow fever virus (YFV), the prototype species of the family Flaviviridae and genus Flavivirus, and has a highly complex host-pathogen relationship, in which endothelial dysfunction reflects viral disease tropism. In this study, the in situ endothelial response was evaluated. Liver tissue samples were collected from 21 YFV-positive patients who died due to the disease and five flavivirus-negative controls who died of other causes and whose hepatic parenchyma architecture was preserved. Immunohistochemical analysis of tissues in the hepatic parenchyma of YF cases showed significantly higher expression of E-selectin, P-selectin, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and very late antigen-4 in YFV-positive cases than in flavivirus-negative controls. These results indicate that endothelium activation aggravates the inflammatory response by inducing the expression of adhesion molecules that contribute to the rolling, recruitment, migration, and construction of the inflammatory process in the hepatic parenchyma in fatal YF cases.
  • article 0 Citação(ões) na Scopus
    Role of Th17 Cytokines in the Liver's Immune Response during Fatal Yellow Fever: Triggering Cell Damage Mechanisms
    (2022) CARVALHO, Marcos Luiz Gaia; FALCAO, Luiz Fabio Magno; LOPES, Jeferson da Costa; MENDES, Caio Cesar Henriques; OLIMPIO, Fabio Alves; MIRANDA, Vanessa do Socorro Cabral; SANTOS, Lais Carneiro dos; MORAES, Daniel Dias Pinheiro de; BERTONSIN FILHO, Marcos Virgilio; COSTA, Luccas Delgado da; AZEVEDO, Raimunda do Socorro da Silva; CRUZ, Ana Cecilia Ribeiro; GALUCIO, Vanessa Costa Alves; MARTINS, Livia Caricio; DUARTE, Maria Irma Seixas; MARTINS FILHO, Arnaldo Jorge; SOUSA, Jorge Rodrigues de; VASCONCELOS, Pedro Fernando da Costa; QUARESMA, Juarez Antonio Simoes
    Yellow fever (YF) is an infectious and acute viral haemorrhagic disease that triggers a cascade of host immune responses. We investigated the Th17 cytokine profile in the liver tissue of patients with fatal YF. Liver tissue samples were collected from 26 deceased patients, including 21 YF-positive and 5 flavivirus-negative patients, with preserved hepatic parenchyma architecture, who died of other causes. Histopathological and immunohistochemical analysis were performed on the liver samples to evaluate the Th17 profiles (ROR-gamma, STAT3, IL-6, TGF-beta, IL-17A, and IL-23). Substantial differences were found in the expression levels of these markers between the patients with fatal YF and controls. A predominant expression of Th17 cytokine markers was observed in the midzonal region of the YF cases, the most affected area in the liver acinus, compared with the controls. Histopathological changes in the hepatic parenchyma revealed cellular damage characterised mainly by the presence of inflammatory cell infiltrates, Councilman bodies (apoptotic cells), micro/macrovesicular steatosis, and lytic and coagulative necrosis. Hence, Th17 cytokines play a pivotal role in the immunopathogenesis of YF and contribute markedly to triggering cell damage in patients with fatal disease outcomes.
  • article 12 Citação(ões) na Scopus
    Endoplasmic Reticulum Stress Markers and Their Possible Implications in Leprosy's Pathogenesis
    (2018) HIRAI, Kelly Emi; SOUSA, Jorge Rodrigues de; SILVA, Luciana Mota; DIAS JUNIOR, Leonidas Braga; FURLANETO, Ismari Perini; CARNEIRO, Francisca Regina Oliveira; AARAO, Tinara Leila de Souza; SOTTO, Mirian Nacagami; QUARESMA, Juarez Antonio Simoes
    Mycobacterium leprae causes leprosy, a dermatoneurological disease which affects the skin and peripheral nerves. One of several cellular structures affected during M. leprae infection is the endoplasmic reticulum (ER). Infection by microorganisms can result in ER stress and lead to the accumulation of unfolded or poorly folded proteins. To restore homeostasis in the cell, the cell induces a series of signaling cascades known as the unfolded protein response called UPR (unfolded protein response). The present work is aimed at investigating the in situ expression of these markers in cutaneous lesions of clinical forms of leprosy and establish possible correlation expression patterns and types of lesion. A total of 43 samples from leprosy patients were analyzed by immunohistochemistry with monoclonal antibodies against GRP78/BiP, PERK, IRE1, and ATF6. A statistically significant difference between the indeterminate, tuberculoid, and lepromatous clinical forms was detected, with high expression of GRP78/BiP, PERK, IRE1, and ATF6 in tuberculoid forms (TT) when compared to lepromatous leprosy (LL) and indeterminate (I) leprosy. These results represent the first evidence of ER stress in samples of skin lesions from leprosy patients. We believe that they will provide better understanding of the complex pathogenesis of the disease and facilitate further characterization of the cascade of molecular events elicited during infection.
  • article 25 Citação(ões) na Scopus
    Functional aspects, phenotypic heterogeneity, and tissue immune response of macrophages in infectious diseases
    (2019) SOUSA, Jorge Rodrigues de; VASCONCELOS, Pedro Fernando Da Costa; QUARESMA, Juarez Antonio Simes
    Macrophages are a functionally heterogeneous group of cells with specialized functions depending not only on their subgroup but also on the function of the organ or tissue in which the cells are located. The concept of macrophage phenotypic heterogeneity has been investigated since the 1980s, and more recent studies have identified a diverse spectrum of phenotypic subpopulations. Several types of macrophages play a central role in the response to infectious agents and, along with other components of the immune system, determine the clinical outcome of major infectious diseases. Here, we review the functions of various macrophage phenotypic subpopulations, the concept of macrophage polarization, and the influence of these cells on the evolution of infections. In addition, we emphasize their role in the immune response in vivo and in situ, as well as the molecular effectors and signaling mechanisms used by these cells. Furthermore, we highlight the mechanisms of immune evasion triggered by infectious agents to counter the actions of macrophages and their consequences. Our aim here is to provide an overview of the role of macrophages in the pathogenesis of critical transmissible diseases and discuss how elucidation of this relationship could enhance our understanding of the host-pathogen association in organ-specific immune responses.
  • article 1 Citação(ões) na Scopus
    Th22 cytokines and yellow fever: Possible implications for the immunopathogenesis of human liver infection
    (2022) MENDES, Caio Cesar Henriques; SOUSA, Jorge Rodrigues de; OLIMPIO, Fabio Alves; FALCAO, Luiz Fabio Magno; CARVALHO, Marcos Luiz Gaia; LOPES, Jeferson da Costa; MARTINS FILHO, Arnaldo Jorge; MIRANDA, Vanessa do Socorro Cabral; SANTOS, Lais Carneiro dos; VILACOERT, Fellipe Souza da Silva; GALUCIO, Vanessa Costa Alves; AZEVEDO, Raimunda do Socorro da Silva; MARTINS, Livia Caricio; DUARTE, Maria Irma Seixas; VASCONCELOS, Pedro Fernando da Costa; QUARESMA, Juarez Antonio Simoes
    Yellow fever (YF) is an infectious disease considered a public health problem in tropical and subtropical areas. YF has many pathophysiological events that are correlated with the host immune response. In this study, the in situ Th22 cytokine profile was evaluated. Liver tissue samples were collected from 21 YFV-positive patients who died of the disease and five flavivirus-negative controls who died of other causes and whose hepatic parenchyma architecture was preserved. Immunohistochemical (IHC) analysis of tissues in the hepatic parenchyma of YF cases showed significantly higher expression of interleukin (IL)-22, IL-13, tumour necrosis factor-alpha, and FGF basic (FGF b) in YFV-positive cases than that in flavivirus-negative controls. These results indicate that the response of Th22 cytokines emerges as an alternative for a better understanding of adaptive immunity in the hepatic parenchyma, highlighting the role of cytokines in the repair and suppressive responses in the immunopathogenesis of YFV infection.
  • article 3 Citação(ões) na Scopus
    Dengue fever ophthalmic manifestations: A review and update
    (2023) LUCENA-NETO, Francisco Dias; FALCAO, Luiz Fabio Magno; MORAES, Evelly Christinne da Silva; DAVID, Joacy Pedro Franco; VIEIRA-JUNIOR, Adolfo de Souza; SILVA, Camilla Costa; SOUSA, Jorge Rodrigues de; DUARTE, Maria Irma Seixas; VASCONCELOS, Pedro Fernando da Costa; QUARESMA, Juarez Antonio Simoes
    Dengue fever, the most common arbovirus disease, affects an estimated 390 million people annually. Dengue virus (DENV) is an RNA virus of the Flaviviridae family with four different serotypes. Dengue haemorrhagic fever is the deadliest form of dengue infection and is characterised by thrombocytopaenia, hypotension, and the possibility of multi-system organ failure. The mechanism hypothesised for DENV viral replication is intrinsic antibody-dependent enhancement, which refers to Fc gamma receptor-mediated viral amplification. This hypothesis suggests that the internalisation of DENV through the Fc gamma receptor inhibits antiviral genes by suppressing type-1 interferon-mediated antiviral responses. DENV NS1 antibodies can promote the release of various inflammatory mediators in the nuclear transcription factor pathway (NF-kappa B-dependent), including monocyte chemoattractant protein (MCP)-1, interleukin (IL)-6, and IL-8. As a result, MCP-1 increases ICAM-1 expression and facilitates leukocyte transmigration. In addition, anti-DENV NS1 antibodies induce endothelial cell apoptosis via a nitric oxide-regulated pathway. A chain reaction involving pre-existing DENV heterotypic antibodies and innate immune cells causes dysfunction in complement system activity and contributes to the action of autoantibodies and anti-endothelial cells, resulting in endothelial cell dysfunction, blood-retinal barrier breakdown, haemorrhage, and plasma leakage. A spectrum of ocular diseases associated with DENV infection, ranging from haemorrhagic to inflammatory manifestations, has been reported in the literature. Although rare, ophthalmic manifestations can occur in both the anterior and posterior segments and are usually associated with thrombocytopenia. The most common ocular complication is haemorrhage. However, ophthalmic complications, such as anterior uveitis and vasculitis, suggest an immune-mediated pathogenesis.
  • article 1 Citação(ões) na Scopus
    Persistent olfactory dysfunction associated with poor sleep quality and anxiety in patients with long COVID
    (2023) PARANHOS, Alna Carolina Mendes; DIAS, Apio Ricardo Nazareth; BASTOS, Thalita da Rocha; RODRIGUES, Arthur Nascimento; SANTANA, Karem Harumy Yamamoto; DIAS, Lorena Henriete Araujo; SANTOS, Lidiane Palheta Miranda dos; CERASI, Antonio Jose; MENDES, Michely Caroline Nascimento; OLIVEIRA, Cleiziane Lima de; DOMINGUES, Mariangela Moreno; KOURY, Gisele Vieira Hennemann; VASCONCELOS, Pedro Fernando da Costa; SOUZA, Givago Silva; QUARESMA, Juarez Antonio Simoes; FALCAO, Luiz Fabio Magno
    IntroductionPoor sleep quality have been widely reported in patients with long COVID. Determining the characteristics, type, severity, and relationship of long COVID with other neurological symptoms is essential for the prognosis and management of poor sleep quality. MethodsThis cross-sectional study was conducted at a public university in the eastern Amazon region of Brazil between November 2020 and October 2022. The study involved 288 patients with long COVID with self-report neurological symptoms. One hundred thirty-one patients were evaluated by using standardised protocols: Pittsburgh sleep quality index (PSQI), Beck Anxiety Inventory, Chemosensory Clinical Research Center (CCRC), and Montreal Cognitive Assessment (MoCA). This study aimed to describe the sociodemographic and clinical characteristics of patients with long COVID with poor sleep quality and their relationship with other neurological symptoms (anxiety, cognitive impairment, and olfactory disorder). ResultsPatients with poor sleep quality were mainly women (76.3%), 44.04 +/- 12.73 years old, with >12 years of education (93.1%), and had monthly incomes of up to US $240.00 (54.2%). Anxiety and olfactory disorder were more common in patients with poor sleep quality. DiscussionMultivariate analysis shows that the prevalence of poor sleep quality was higher in patients with anxiety, and olfactory disorder is associated with poor sleep quality. In this cohort of patients with long COVID, the prevalence of poor sleep quality was highest in the group tested by PSQI and were associated with other neurological symptoms, such as anxiety and olfactory dysfunction. A previous study indicates a significant association between poor sleep quality and psychological disorders over time. Recent studies involving neuroimaging found functional and structural changes in Long COVID patients with persistent olfactory disfunction. Poor sleep quality are integral part of complex changes related to Long COVID and should be part of patient's clinical management.
  • article 5 Citação(ões) na Scopus
    Headache in long COVID as disabling condition: A clinical approach
    (2023) RODRIGUES, Arthur Nascimento; DIAS, Apio Ricardo Nazareth; PARANHOS, Alna Carolina Mendes; SILVA, Camilla Costa; BASTOS, Thalita da Rocha; BRITO, Barbara Barros de; SILVA, Nivia Monteiro da; SOUSA, Emanuel de Jesus Soares de; QUARESMA, Juarez Antonio Simoes; FALCAO, Luiz Fabio Magno
    Background and purposeSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can exacerbate previous headache disorders or change the type of pain experienced from headaches. This study aimed to investigate the clinical features of Long COVID headaches. MethodThis was a cross-sectional, descriptive, and analytical observational study that included 102 patients (with previous headache, n = 50; without previous headache, n = 52) with long COVID and headache complaints. The Migraine Disability Assessment Test and Visual Analog Pain Scale were used to collect participants' headache data according to a standardized protocol. ResultsThe patients in this study who reported experiencing headaches before COVID-19 had longer headache duration in the long COVID phase than that in the pre-long COVID phase (p = 0.031), exhibited partial improvement in headache symptoms with analgesics (p = 0.045), and had a duration of long COVID of <1 year (p = 0.030). Patients with moderate or severe disability and those classified as having severe headaches in the long COVID phase were highly likely to develop chronic headaches. Hospital admission [odds ratio (OR) = 3.0082; 95% confidence interval (95% CI): 1.10-8.26], back pain (OR = 4.0017; 95% CI: 1.13-14.17), insomnia (OR = 3.1339; 95% CI: 1.39-7.06), and paraesthesia (OR = 2.7600; 95% CI: 1.20-6.33) were associated with headache in these patients. ConclusionHeadache is a disabling condition in patients with long COVID-19, exacerbating the conditions of those with headaches prior to contracting COVID-19.