AMARO NUNES DUARTE NETO
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Patologia, Faculdade de Medicina - Docente
LIM/05 - Laboratório de Poluição Atmosférica Experimental, Hospital das Clínicas, Faculdade de Medicina
LIM/06 - Laboratório de Imunopatologia da Esquistossomose e outras Parasitoses, Hospital das Clínicas, Faculdade de Medicina
LIM/05 - Laboratório de Poluição Atmosférica Experimental, Hospital das Clínicas, Faculdade de Medicina
LIM/06 - Laboratório de Imunopatologia da Esquistossomose e outras Parasitoses, Hospital das Clínicas, Faculdade de Medicina
96 resultados
Resultados de Busca
Agora exibindo 1 - 10 de 96
conferenceObject ELEVATED ROS LEVELS AND DNA FRAGMENTATION IN SPERM FROM CONVALESCENT MEN IN SARS-COV-2 INFECTION(2022) HALLAK, Jorge; BERNARDES, Felipe; TEIXEIRA, Thiago Afonso Carvalho Celestino; SALDIVA, Paulo Hilario Nascimento; KALLAS, Esper Georges; CALDINI, Elia Tamaso Espin Garcia; DUARTE NETO, Amaro Nunes; FAQUINETI, Heloisa; JESUS, Vinicius Luiz Menezes; GUTIERREZ, Raul Segundo Sanchez; DREVET, Joel R.- TREATMENT WITH HUMAN UMBILICAL CORD-DERIVED MESENCHYMAL STEM CELLS IN A PIG MODEL OF SEPSIS-INDUCED ACUTE KIDNEY INJURY: EFFECTS ON MICROVASCULAR ENDOTHELIAL CELLS AND TUBULAR CELLS IN THE KIDNEY(2023) MAIA, Debora Rothstein Ramos; OTSUKI, Denise Aya; RODRIGUES, Camila Eleuterio; ZBORIL, Sabrina; SANCHES, Talita Rojas; NETO, Amaro Nunes Duarte; ANDRADE, Lucia; AULER, Jose Otavio CostaBackground: Approximately 50% of patients with sepsis develop acute kidney injury (AKI), which is predictive of poor outcomes, with mortality rates of up to 70%. The endothelium is a major target for treatments aimed at preventing the complications of sepsis. We hypothesized that human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) could attenuate tubular and endothelial injury in a porcine model of sepsis-induced AKI. Methods: Anesthetized pigs were induced to fecal peritonitis, resulting in septic shock, and were randomized to treatment with fluids, vasopressors, and antibiotics (sepsis group; n = 11) or to that same treatment plus infusion of 1 x 106 cells/kg of hUC-MSCs (sepsis+MSC group; n = 11). Results: At 24 h after sepsis induction, changes in serum creatinine and mean arterial pressure were comparable between the two groups, as was mortality. However, the sepsis+MSC group showed some significant differences in comparison with the sepsis group: lower fractional excretions of sodium and potassium; greater epithelial sodium channel protein expression; and lower protein expression of the Na-K-2Cl cotransporter and aquaporin 2 in the renal medulla. Expression of P-selectin, thrombomodulin, and vascular endothelial growth factor was significantly lower in the sepsis+MSC group than in the sepsis group, whereas that of Toll-like receptor 4 (TLR4) and nuclear factor-kappa B (NF-kappa B) was lower in the former. Conclusion: Treatment with hUC-MSCs seems to protect endothelial and tubular cells in sepsis-induced AKI, possibly via the TLR4/NF-kappa B signaling pathway. Therefore, it might be an effective treatment for sepsis-induced AKI.
- Understanding Sabia virus infections (Brazilian mammarenavirus)(2022) NASTRI, Ana Catharina; DUARTE-NETO, Amaro Nunes; CASADIO, Luciana Vilas Boas; SOUZA, William Marciel de; CLARO, Ingra M.; MANULI, Erika R.; SELEGATTO, Gloria; SALOMA, Matias C.; FIALKOVITZ, Gabriel; TABORDA, Mariane; ALMEIDA, Bianca Leal de; MAGRI, Marcello C.; GUEDES, Ana Rubia; NETO, Laura Vieira Perdigao; SATAKI, Fatima Mitie; GUIMARAES, Thais; MENDES-CORREA, Maria Cassia; TOZETTO-MENDOZA, Tania R.; FUMAGALLI, Marcilio Jorge; HO, Yeh-Li; SILVA, Camila ALves Maia da; COLETTI, Thais M.; JESUS, Jacqueline Goes de; ROMANO, Camila M.; HILL, Sarah C.; PYBUS, Oliver; PINHO, Joao Renato Rebello; LEDESMA, Felipe Lourenco; CASAL, Yuri R.; KANAMURA, Cristina; ARAUJO, Leonardo Jose Tadeu de; FERREIRA, Camila Santos da Silva; GUERRA, Juliana Mariotti; FIGUEIREDO, Luiz Tadeu Moraes; DOLHNIKOFF, Marisa; FARIA, Nuno R.; SABINO, Ester C.; AVANCINI, Venacio; ALVES, Ferreira; LEVIN, Anna S.Background: Only two naturally occurring human Sabi ' a virus (SABV) infections have been reported, and those occurred over 20 years ago. Methods: We diagnosed two new cases of SABV infection using metagenomics in patients thought to have severe yellow fever and described new features of histopathological findings. Results: We characterized clinical manifestations, histopathology and analyzed possible nosocomial transmission. Patients presented with hepatitis, bleeding, neurological alterations and died. We traced twenty-nine hospital contacts and evaluated them clinically and by RT-PCR and neutralizing antibodies. Autopsies uncovered unique features on electron microscopy, such as hepatocyte ""pinewood knot"" lesions. Although previous reports with similar New-World arenavirus had nosocomial transmission, our data did not find any case in contact tracing. Conclusions: Although an apparent by rare, Brazilian mammarenavirus infection is an etiology for acute hemorrhagic fever syndrome. The two fatal cases had peculiar histopathological findings not previously described. The virological diagnosis was possible only by contemporary techniques such as metagenomic assays. We found no subsequent infections when we used serological and molecular tests to evaluate close contacts.
bookPart Infecção pelo HIV e SIDA(2021) BRANDãO NETO, Rodrigo Antonio; DUARTE NETO, Amaro Nunes- Trichosporon inkin as an Emergent Pathogen in Patients With Severe Pemphigus(2015) ALMEIDA JUNIOR, Joao Nobrega de; OLIVEIRA, Renata Buccheri de; DUARTE, Amaro; MOTTA, Adriana Lopes; ROSSI, Flavia; FIGUEIREDO, Dulce Sachiko Yamamoto de; NEGRO, Gilda Maria Barbaro Del; AOKI, Valeria; MARUTA, Celina Wakisaka; SANTI, Claudia Giuli; BENARD, GilIMPORTANCE To our knowledge, these are the first reports of bloodstream infections by Trichosporon inkin in patients with pemphigus. OBSERVATIONS Trichosporon inkin, a novel organism causing bloodstream infection, was detected in 2 patients with pemphigus. An elderly man with pemphigus foliaceus died despite treatment with liposomal amphotericin B, 3mg/kg/d, and a young girl with pemphigus vulgaris responded to treatment with voriconazole, 8mg/kg/d, for 24 days. One of the T inkin isolates had a minimal inhibitory concentration of 2mg/L against amphotericin B, suggesting resistance to the drug. CONCLUSIONS AND RELEVANCE Delayed suspicion of invasive infection by T inkin may result in a poor outcome in patients with severe forms of pemphigus. This opportunistic infection is highly refractory to conventional potent antifungal treatment.
- Severe Leptospirosis Features in the Spleen Indicate Cellular Immunosuppression Similar to That Found in Septic Shock(2019) DUARTE-NETO, Amaro Nunes; CRODA, Julio; PAGLIARI, Carla; SORIANO, Francisco Garcia; NICODEMO, Antonio Carlos; DUARTE, Maria Irma SeixasObjectives: To compare microscopic and immunologic features in the spleens of patients who died of pulmonary hemorrhage and shock caused by leptospirosis (11 cases) or Gram-positive/-negative bacterial septic shock (10 cases) to those from control spleens (12 cases from splenectomy). Methodology: Histological features in the red pulp and white pulp were analyzed using archived samples by a semi quantitative score. Immunohistochemistry was used for the recognition of immune cell markers, cytokines, caspase-3 and Leptospira antigens. Results: The control group differed significantly from the leptospirosis and septic shock patients which demonstrate strong similarities: diffuse congestion in the red pulp with a moderate to intense infiltration of plasma cells and polymorphonuclear cells; follicles with marked atrophy; high density of CD20(+) cells; low density of NK, TCD4(+) and active caspase-3 positive cells and strong expression of IL-10; leptospirosis patients had higher S100 and TNF-alpha positive cells in the spleen than the other groups. Conclusion: The results suggest that an immunosuppressive state develops at the terminal stage of severe leptospirosis with pulmonary hemorrhage and shock similar to that of patients with septic shock, with diffuse endothelial activation in the spleen, splenitis, and signs of disturbance in the innate and adaptive immunity in the spleen. The presence of leptospiral antigens in 73% of the spleens of the leptospirosis patients suggests the etiological agent contributes directly to the pathogenesis of the lesions. Our results support therapeutic approaches involving antibiotic and immunomodulatory treatments for leptospirosis patients and suggest that leptospirosis patients, which are usually young men with no co-morbidities, form a good group for studying sepsis and septic shock.
- 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
- Terlipressin combined with conservative fluid management attenuates hemorrhagic shock-induced acute kidney injury in rats(2022) CASTRO, Leticia Urbano Cardoso; OTSUKI, Denise Aya; SANCHES, Talita Rojas; SOUZA, Felipe Lima; SANTINHO, Mirela Aparecida Rodrigues; SILVA, Cleonice da; NORONHA, Irene de Lourdes; DUARTE-NETO, Amaro Nunes; GOMES, Samirah Abreu; MALBOUISSON, Luiz-Marcelo Sa; ANDRADE, LuciaHemorrhagic shock (HS), a major cause of trauma-related mortality, is mainly treated by crystalloid fluid administration, typically with lactated Ringer's (LR). Despite beneficial hemodynamic effects, such as the restoration of mean arterial pressure (MAP), LR administration has major side effects, including organ damage due to edema. One strategy to avoid such effects is pre-hospitalization intravenous administration of the potent vasoconstrictor terlipressin, which can restore hemodynamic stability/homeostasis and has anti-inflammatory effects. Wistar rats were subjected to HS for 60 min, at a target MAP of 30-40 mmHg, thereafter being allocated to receive LR infusion at 3 times the volume of the blood withdrawn (liberal fluid management); at 2 times the volume (conservative fluid management), plus terlipressin (10 mu g/100 g body weight); and at an equal volume (conservative fluid management), plus terlipressin (10 mu g/100 g body weight). A control group comprised rats not subjected to HS and receiving no fluid resuscitation or treatment. At 15 min after fluid resuscitation/treatment, the blood previously withdrawn was reinfused. At 24 h after HS, MAP was higher among the terlipressin-treated animals. Terlipressin also improved post-HS survival and provided significant improvements in glomerular/tubular function (creatinine clearance), neutrophil gelatinase-associated lipocalin expression, fractional excretion of sodium, aquaporin 2 expression, tubular injury, macrophage infiltration, interleukin 6 levels, interleukin 18 levels, and nuclear factor kappa B expression. In terlipressin-treated animals, there was also significantly higher angiotensin II type 1 receptor expression and normalization of arginine vasopressin 1a receptor expression. Terlipressin associated with conservative fluid management could be a viable therapy for HS-induced acute kidney injury, likely attenuating such injury by modulating the inflammatory response via the arginine vasopressin 1a receptor.
- Consumptive coagulopathy of severe yellow fever occurs independently of hepatocellular tropism and massive hepatic injury(2020) BAILEY, Adam L.; I, Liang- Kang; ZANELLA, Luiz Gonzaga Francisco de Assis Barros D'Elia; SILVEIRA, Cassia G. T.; HO, Yeh-Li; FOQUET, Lander; BIAL, Greg; MCCUNE, Broc T.; DUARTE-NETO, Amaro Nunes; THOMAS, Archana; RAUE, Hans-Peter; BYRNES, Kathleen; KALLAS, Esper G.; SLIFKA, Mark K.; DIAMOND, Michael S.Yellow fever (YF) is a mosquito-transmitted viral disease that causes tens of thousands of deaths each year despite the long-standing deployment of an effective vaccine. In its most severe form, YF manifests as a hemorrhagic fever that causes severe damage to visceral organs. Although coagulopathy is a defining feature of severe YF in humans, the mechanism by which it develops remains uncertain. Hepatocytes are a major target of yellow fever virus (YFV) infection, and the coagulopathy in severe YF has long been attributed to massive hepatocyte infection and destruction that results in a defect in clotting factor synthesis. However, when we analyzed blood from Brazilian patients with severe YF, we found high concentrations of plasma D-dimer, a fibrin split product, suggestive of a concurrent consumptive process. To define the relationship between coagulopathy and hepatocellular tropism, we compared infection and disease in Fah(-/-), Rag2(-/-), and Il2r gamma(-/-) mice engrafted with human hepatocytes (hFRG mice) and rhesus macaques using a highly pathogenic African YFV strain. YFV infection of macaques and hFRG mice caused substantial hepatocyte infection, liver damage, and coagulopathy as defined by virological, clinical, and pathological criteria. However, only macaques developed a consumptive coagulopathy whereas YFV-infected hFRG mice did not. Thus, infection of cell types other than hepatocytes likely contributes to the consumptive coagulopathy associated with severe YF in primates and humans. These findings expand our understanding of viral hemorrhagic disease and associated coagulopathy and suggest directions for clinical management of severe YF cases.
- Acute petrified myocardium associated with meningococcal sepsis in childhood-onset systemic lupus erythematous: a fatal case(2019) SANTOS, Ana Carolina Etrusco Zaroni; LUGLIO, Michele; DELGADO, Artur Figueiredo; SCHUWARTZ, Constance Dell Santo Vieira; MARQUES, Heloisa Helena Sousa; VALOES, Clarissa Carvalho de Miranda; DOMINGUEZ, Maria Andreina Cabrera; CARVALHO, Werther Brunow de; SILVA, Clovis Artur; DUARTE-NETO, Amaro NunesAcute petrified myocardium associated with septic shock, diagnosed by autopsy has rarely been described. A 15-year-old adolescent male was diagnosed with childhood-onset systemic lupus erythematosus. One year later, he was hospitalized with fever, myalgia, headache, arthritis, vomiting, dyspnea and was diagnosed with sepsis secondary to bronchopneumonia and meningitis. Blood culture identified Neisseria meningitidis serogroup Y. Despite antibiotics and intensive therapeutic measures, he died after 29 days of hospitalization. The autopsy revealed necrotic cardiomyocytes with dystrophic calcification and interstitial fibrosis.