GABRIEL RIBEIRO DOS SANTOS JUNIOR

(Fonte: Lattes)
Índice h a partir de 2011
3
Projetos de Pesquisa
Unidades Organizacionais
Instituto Central, Hospital das Clínicas, Faculdade de Medicina

Resultados de Busca

Agora exibindo 1 - 9 de 9
  • bookPart
    Sexualidade
    (2019) BAUTISTA, Michele Melo; JúNIOR, Gabriel Ribeiro dos Santos
  • conferenceObject
    Lung ECM composition, its influence factors and transcriptomics in the lungs of severe COVID-19.
    (2023) COSTA, Natalia de Souza Xavier; RIBEIRO JUNIOR, Gabriel; NASCIMENTO, Ellen Toledo Do; BRITO, Jose Mara De; MONTEIRO, Jhonatas Sirino; SETUBAL, Joao Carlos; PINHO, Joao Renato Rebello; PEREIRA, Roberta Verciano; MONTEIRO, Renata Aparecida De Almeida; DUARTE NETO, Amaro Nunes; SALDIVA, Paulo Hilario Nascimento; SILVA, Luiz Fernando Ferraz Da; DOLHNIKOFF, Marisa; MAUAD, Thais
  • bookPart
    Quedas e instabilidade postural
    (2021) JúNIOR, Gabriel Ribeiro dos Santos
  • article 10 Citação(ões) na Scopus
    Air pollution impairs recovery and tissue remodeling in a murine model of acute lung injury
    (2020) COSTA, Natalia de Souza Xavier; RIBEIRO JUNIOR, Gabriel; ALEMANY, Adair Aparecida dos Santos; BELOTTI, Luciano; SCHALCH, Alexandre Santos; CAVALCANTE, Marcela Frota; RIBEIRO, Susan; VERAS, Mariana Matera; KALLAS, Esper Georges; SALDIVA, Paulo Hilario Nascimento; DOLHNIKOFF, Marisa; SILVA, Luiz Fernando Ferraz da
    Evidence regarding the impact of air pollution on acute respiratory distress syndrome (ARDS) is limited, and most studies focus on ARDS onset. Our study aimed to evaluate whether exposure to fine particulate matter interferes with lung recovery and remodeling in a murine model of acute lung injury. Forty-eight mice received nebulized LPS or the vehicle (controls). Blood, BALF, lungs and spleen were collected after 5 weeks of exposure to either PM2.5 (PM and LPS+PM group) or filtered air (control and LPS5w groups). Inflammatory cells and cytokines were assessed in the blood, BALF, lungs and spleen. Stereological analyses and remodeling assessments were performed by histology. The LPS+PM group showed increased BALF leukocytes, characterized by increased macrophages, increased IL-1 beta and IL-6 levels, anemia and thrombocytopenia. Moreover, we also observed septal thickening, decreased alveolar air space total volume and, septa surface density. Finally, regarding tissue remodeling, we observed elastosis of the lung parenchyma, and unlike in the LPS5w group, we did not observe fibrosis in the LPS+PM group. In conclusion, the delayed inflammation resolution due to subchronic exposure to PM2.5 could be influenced by low systemic and local lymphocyte counts, which lead to impaired lung injury recovery and tissue remodeling.
  • article 380 Citação(ões) na Scopus
    Presence of airborne microplastics in human lung tissue
    (2021) AMATO-LOURENCO, Luis Fernando; CARVALHO-OLIVEIRA, Regiani; RIBEIRO JUNIOR, Gabriel; GALVAO, Luciana dos Santos; ANDO, Romulo Augusto; MAUAD, Thais
    Plastics are ubiquitously used by societies, but most of the plastic waste is deposited in landfills and in the natural environment. Their degradation into submillimetre fragments, called microplastics, is a growing concern due to potential adverse effects on the environment and human health. Microplastics are present in the air and may be inhaled by humans, but whether they have deleterious effects on the respiratory system remain unknown. In this study, we determined the presence of microplastics in human lung tissues obtained at autopsies. Polymeric particles (n = 33) and fibres (n = 4) were observed in 13 of 20 tissue samples. All polymeric particles were smaller than 5.5 mu m in size, and fibres ranged from 8.12 to 16.8 mu m. The most frequently determined polymers were polyethylene and polypropylene. Deleterious health outcomes may be related to the heterogeneous characteristics of these contaminants in the respiratory system following inhalation.
  • article 14 Citação(ões) na Scopus
    Diesel exhaust exposure intensifies inflammatory and structural changes associated with lung aging in mice
    (2019) RIBEIRO JUNIOR, Gabriel; COSTA, Natalia de Souza Xavier; BELOTTI, Luciano; ALEMANY, Adair Aparecida dos Santos; AMATO-LOURENCO, Luis Fernando; CUNHA, Paula Gabriela da; DURO, Stephanie de Oliveira; RIBEIRO, Susan Pereira; VERAS, Mariana Matera; LOPES, Fernanda Degobbi Tenorio Quirino dos Santos; MARCOURAKIS, Tania; SALDIVA, Paulo Hilario Nascimento; FARSKY, Sandra Helena Poliselli; MAUAD, Thais
    Life expectancy is increasing worldwide. Lung aging is a process marked by changes in multiple morphological, physiological and age-related biomarkers (e.g., sirtuins) and is influenced by external factors, such as air pollution. Hence, the elderly are considered more vulnerable to the air pollution hazards. We hypothesized that diesel exhaust (DE) exposure intensifies changes in lung inflammatory and structural parameters in aging subjects. Two- and fifteen-month-old mice were exposed to DE for 30 days. Lung function was measured using the forced oscillation method. The inflammatory profile was evaluated in the bronchoalveolar lavage fluid (BALF) and blood, and lung volumes were estimated by stereology. Antioxidant enzyme activity was evaluated by spectrophotometry, sirtuin 1 (SIRT1), sirtuin 2 (SIRT2) and sirtuin 6 (SIRT6) expression was assessed by reverse transcription polymerase chain reaction (RT-PCR), and levels of the sirtuin proteins were evaluated by immunohistochemical staining in lung tissues. Older mice presented decreased pulmonary resistance and elastance, increased macrophage infiltration and decreased tumor necrosis factor (TNF) and interleukin 10 (IL-10) levels in the BALF, reduced activities of the antioxidant enzymes glutathione peroxidase (GPx) and glutathione reductase (GR), and increased activity glutathione S-transferase (GST); increased lung volumes with decreased elastic fiber and increased airway collagen content. SIRT1 gene expression was decreased in older animals, but protein levels were increased. DE exposure increased macrophage infiltration and oxidative stress in the lungs of animals of both ages. SIRT6 gene expression was decreased by DE exposure, with increased protein levels. In older animals, DE affected lung structure and collagen content. Lung aging features, such as decreased antioxidant reserves, lower IL-10 expression, and decreased SIRT1 levels may predispose subjects to exacerbated responses after DE exposure. Our data support the hypothesis that strategies designed to reduce ambient air pollution are an important step towards healthy aging.
  • article 2 Citação(ões) na Scopus
    LPS Response Is Impaired by Urban Fine Particulate Matter
    (2022) COSTA, Natalia de Souza Xavier; RIBEIRO JUNIOR, Gabriel; ALEMANY, Adair Aparecida dos Santos; BELOTTI, Luciano; CAVALCANTE, Marcela Frota; RIBEIRO, Susan; VERAS, Mariana Matera; KALLAS, Esper Georges; SALDIVA, Paulo Hilario Nascimento; DOLHNIKOFF, Marisa; SILVA, Luiz Fernando Ferraz da
    Fine particulate matter (PM2.5) is a complex mixture of components with diverse chemical and physical characteristics associated with increased respiratory and cardiovascular diseases mortality. Our study aimed to investigate the effects of exposure to concentrated PM2.5 on LPS-induced lung injury onset. BALB/c male mice were exposed to either filtered air or ambient fine PM2.5 in an ambient particle concentrator for 5 weeks. Then, an acute lung injury was induced with nebulized LPS. The animals were euthanized 24 h after the nebulization to either LPS or saline. Inflammatory cells and cytokines (IL-1 beta, IL-4, IL-5, IL-6, IL-10, IL-17, TNF) were assessed in the blood, bronchoalveolar lavage fluid (BALF), and lung tissue. In addition, lung morphology was assessed by stereological methods. Our results showed that the PM+LPS group showed histological evidence of injury, leukocytosis with increased neutrophils and macrophages, and a mixed inflammatory response profile, with increased KC, IL-6, IL-1 beta, IL-4, and IL-17. Our analysis shows that there is an interaction between the LPS nebulization and PM2.5 exposure, differently modulating the inflammatory response, with a distinct response pattern as compared to LPS or PM2.5 exposure alone. Further studies are required to explain the mechanism of immune modulation caused by PM2.5 exposure.
  • bookPart
    Transporte do paciente crítico
    (2023) JúNIOR, Gabriel Ribeiro dos Santos
  • bookPart
    Transporte do paciente crítico
    (2015) JúNIOR, Gabriel Ribeiro dos Santos