6 results on '"Ulaf, Raisa G."'
Search Results
2. Evaluation of the efficacy and safety of icatibant and C1 esterase/kallikrein inhibitor in severe COVID-19: study protocol for a three-armed randomized controlled trial
- Author
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Mansour, Eli, Bueno, Flávia F., de Lima-Júnior, José C., Palma, Andre, Monfort-Pires, Milena, Bombassaro, Bruna, Araujo, Eliana P., Bernardes, Ana Flavia, Ulaf, Raisa G., Nunes, Thyago A., Ribeiro, Luciana C., Falcão, Antônio Luís E., Santos, Thiago Martins, Trabasso, Plinio, Dertkigil, Rachel P., Dertkigil, Sergio S., Maia, Rafael P., Benaglia, Tatiana, Moretti, Maria Luiza, and Velloso, Licio A.
- Published
- 2021
- Full Text
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3. Elevated Glucose Levels Favor SARS-CoV-2 Infection and Monocyte Response through a HIF-1α/Glycolysis-Dependent Axis
- Author
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Codo, Ana Campos, Davanzo, Gustavo Gastão, Monteiro, Lauar de Brito, de Souza, Gabriela Fabiano, Muraro, Stéfanie Primon, Virgilio-da-Silva, João Victor, Prodonoff, Juliana Silveira, Carregari, Victor Corasolla, de Biagi Junior, Carlos Alberto Oliveira, Crunfli, Fernanda, Jimenez Restrepo, Jeffersson Leandro, Vendramini, Pedro Henrique, Reis-de-Oliveira, Guilherme, Bispo dos Santos, Karina, Toledo-Teixeira, Daniel A., Parise, Pierina Lorencini, Martini, Matheus Cavalheiro, Marques, Rafael Elias, Carmo, Helison R., Borin, Alexandre, Coimbra, Laís Durço, Boldrini, Vinícius O., Brunetti, Natalia S., Vieira, Andre S., Mansour, Eli, Ulaf, Raisa G., Bernardes, Ana F., Nunes, Thyago A., Ribeiro, Luciana C., Palma, Andre C., Agrela, Marcus V., Moretti, Maria Luiza, Sposito, Andrei C., Pereira, Fabrício Bíscaro, Velloso, Licio Augusto, Vinolo, Marco Aurélio Ramirez, Damasio, André, Proença-Módena, José Luiz, Carvalho, Robson Francisco, Mori, Marcelo A., Martins-de-Souza, Daniel, Nakaya, Helder I., Farias, Alessandro S., and Moraes-Vieira, Pedro M.
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- 2020
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4. Safety and Outcomes Associated with the Pharmacological Inhibition of the Kinin–Kallikrein System in Severe COVID-19.
- Author
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Mansour, Eli, Palma, Andre C., Ulaf, Raisa G., Ribeiro, Luciana C., Bernardes, Ana Flavia, Nunes, Thyago A., Agrela, Marcus V., Bombassaro, Bruna, Monfort-Pires, Milena, Camargo, Rafael L., Araujo, Eliana P., Brunetti, Natalia S., Farias, Alessandro S., Falcão, Antônio Luís E., Santos, Thiago Martins, Trabasso, Plinio, Dertkigil, Rachel P., Dertkigil, Sergio S., Moretti, Maria Luiza, and Velloso, Licio A.
- Subjects
COVID-19 ,MIDDLE East respiratory syndrome ,ANGIOTENSIN converting enzyme ,SARS-CoV-2 - Abstract
Background: Coronavirus disease 19 (COVID-19) can develop into a severe respiratory syndrome that results in up to 40% mortality. Acute lung inflammatory edema is a major pathological finding in autopsies explaining O
2 diffusion failure and hypoxemia. Only dexamethasone has been shown to reduce mortality in severe cases, further supporting a role for inflammation in disease severity. SARS-CoV-2 enters cells employing angiotensin-converting enzyme 2 (ACE2) as a receptor, which is highly expressed in lung alveolar cells. ACE2 is one of the components of the cellular machinery that inactivates the potent inflammatory agent bradykinin, and SARS-CoV-2 infection could interfere with the catalytic activity of ACE2, leading to the accumulation of bradykinin. Methods: In this case control study, we tested two pharmacological inhibitors of the kinin–kallikrein system that are currently approved for the treatment of hereditary angioedema, icatibant, and inhibitor of C1 esterase/kallikrein, in a group of 30 patients with severe COVID-19. Results: Neither icatibant nor inhibitor of C1 esterase/kallikrein resulted in changes in time to clinical improvement. However, both compounds were safe and promoted the significant improvement of lung computed tomography scores and increased blood eosinophils, which are indicators of disease recovery. Conclusions: In this small cohort, we found evidence for safety and a beneficial role of pharmacological inhibition of the kinin–kallikrein system in two markers that indicate improved disease recovery. [ABSTRACT FROM AUTHOR]- Published
- 2021
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5. SARS-CoV-2 uses CD4 to infect T helper lymphocytes.
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Brunetti NS, Davanzo GG, de Moraes D, Ferrari AJR, Souza GF, Muraro SP, Knittel TL, Boldrini VO, Monteiro LB, Virgílio-da-Silva JV, Profeta GS, Wassano NS, Nunes Santos L, Carregari VC, Dias AHS, Veras FP, Tavares LA, Forato J, Castro IMS, Silva-Costa LC, Palma AC, Mansour E, Ulaf RG, Bernardes AF, Nunes TA, Ribeiro LC, Agrela MV, Moretti ML, Buscaratti LI, Crunfli F, Ludwig RG, Gerhardt JA, Munhoz-Alves N, Marques AM, Sesti-Costa R, Amorim MR, Toledo-Teixeira DA, Parise PL, Martini MC, Bispos-Dos-Santos K, Simeoni CL, Granja F, Silvestrini VC, de Oliveira EB, Faca VM, Carvalho M, Castelucci BG, Pereira AB, Coimbra LD, Dias MMG, Rodrigues PB, Gomes ABSP, Pereira FB, Santos LMB, Bloyet LM, Stumpf S, Pontelli MC, Whelan S, Sposito AC, Carvalho RF, Vieira AS, Vinolo MAR, Damasio A, Velloso L, Figueira ACM, da Silva LLP, Cunha TM, Nakaya HI, Marques-Souza H, Marques RE, Martins-de-Souza D, Skaf MS, Proenca-Modena JL, Moraes-Vieira PMM, Mori MA, and Farias AS
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- Humans, CD8-Positive T-Lymphocytes, T-Lymphocytes, Helper-Inducer, Lung, SARS-CoV-2, COVID-19
- Abstract
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the agent of a major global outbreak of respiratory tract disease known as Coronavirus Disease 2019 (COVID-19). SARS-CoV-2 infects mainly lungs and may cause several immune-related complications, such as lymphocytopenia and cytokine storm, which are associated with the severity of the disease and predict mortality. The mechanism by which SARS-CoV-2 infection may result in immune system dysfunction is still not fully understood. Here, we show that SARS-CoV-2 infects human CD4
+ T helper cells, but not CD8+ T cells, and is present in blood and bronchoalveolar lavage T helper cells of severe COVID-19 patients. We demonstrated that SARS-CoV-2 spike glycoprotein (S) directly binds to the CD4 molecule, which in turn mediates the entry of SARS- CoV-2 in T helper cells. This leads to impaired CD4 T cell function and may cause cell death. SARS-CoV-2-infected T helper cells express higher levels of IL-10, which is associated with viral persistence and disease severity. Thus, CD4-mediated SARS-CoV-2 infection of T helper cells may contribute to a poor immune response in COVID-19 patients., Competing Interests: NB, GD, Dd, AF, GS, SM, TK, VB, LM, JV, GP, NW, LN, VC, AD, FV, LT, JF, IC, LS, AP, EM, RU, AB, TN, LR, MA, MM, LB, FC, RL, JG, NM, AM, RS, MA, DT, PP, MM, KB, CS, FG, VS, Ed, VF, MC, BC, AP, LC, MD, PR, AG, FP, LS, LB, SS, MP, SW, AS, RC, AV, MV, AD, LV, AF, Ld, TC, HN, HM, RM, DM, MS, JP, PM, MM, AF No competing interests declared, (© 2023, Brunetti, Davanzo, de Moraes et al.)- Published
- 2023
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6. Plasma Angiotensin II Is Increased in Critical Coronavirus Disease 2019.
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Camargo RL, Bombassaro B, Monfort-Pires M, Mansour E, Palma AC, Ribeiro LC, Ulaf RG, Bernardes AF, Nunes TA, Agrela MV, Dertkigil RP, Dertkigil SS, Araujo EP, Nadruz W, Moretti ML, Velloso LA, and Sposito AC
- Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) employs angiotensin-converting enzyme 2 (ACE2) as its receptor for cell entrance, and studies have suggested that upon viral binding, ACE2 catalytic activity could be inhibited; therefore, impacting the regulation of the renin-angiotensin-aldosterone system (RAAS). To date, only few studies have evaluated the impact of SARS-CoV-2 infection on the blood levels of the components of the RAAS. The objective of this study was to determine the blood levels of ACE, ACE2, angiotensin-II, angiotensin (1-7), and angiotensin (1-9) at hospital admission and discharge in a group of patients presenting with severe or critical evolution of coronavirus disease 2019 (COVID-19). We showed that ACE, ACE2, angiotensin (1-7), and angiotensin (1-9) were similar in patients with critical and severe COVID-19. However, at admission, angiotensin-II levels were significantly higher in patients presenting as critical, compared to patients presenting with severe COVID-19. We conclude that blood levels of angiotensin-II are increased in hospitalized patients with COVID-19 presenting the critical outcome of the disease. We propose that early measurement of Ang-II could be a useful biomarker for identifying patients at higher risk for extremely severe progression of the disease., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Camargo, Bombassaro, Monfort-Pires, Mansour, Palma, Ribeiro, Ulaf, Bernardes, Nunes, Agrela, Dertkigil, Dertkigil, Araujo, Nadruz, Moretti, Velloso and Sposito.)
- Published
- 2022
- Full Text
- View/download PDF
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