Browsing by Author "Acevedo, M."
Now showing 1 - 4 of 4
Results Per Page
Sort Options
- ItemAchievement of treatment targets of cardiovascular risk factors in a pilot secondary prevention program in Chile(2008) Acevedo, M.; Kraemer, V.; Chamorro, G.; Krogh, G.; Munoz, A.; Corbalan, R.
- ItemAn inactivated SARS-CoV-2 vaccine is safe and induces humoral and cellular immunity against virus variants in healthy children and adolescents in Chile(2022) Soto, J.A.; Melo-González, F.; Gutierrez-Vera, C.; Schultz, B.M.; Berríos-Rojas, R.V.; Rivera-Pérez, D.; Piña-Iturbe, A.; Hoppe-Elsholz, G.; Duarte, L.F.; Vázquez, Y.; Moreno-Tapia, D.; Ríos, M.; Palacios, P.A.; Garcia-Betancourt, R.; Santibañez, Á.; Mendez, C.; Diethelm-Varela, B.; Astudillo, P.; Calvo, M.; Cárdenas, A.; González, M.; Goldsack, M.; Gutiérrez, V.; Potin, M.; Schilling, A.; Tapia, L.I.; Twele, L.; Villena, R.; Grifoni, A.; Sette, A.; Weiskopf, D.; Fasce, R.A.; Fernández, J.; Mora, J.; Ramírez, E.; Gaete-Argel, A.; Acevedo, M.; Valiente-Echeverría, F.; Soto-Rifo, R.; Retamal-Díaz, A.; Muñoz-Jofré, N.; Meng, X.; Xin, Q.; Alarcón-Bustamante, E.; González-Aramundiz, J.V.; Le Corre, N.; Álvarez, M.J.; González, P.A.; Abarca, K.; Perret, C.; Carreño, L.J.; Kalergis, A.M.; Bueno, S.M.
- ItemHumoral and cellular response induced by a second booster of an inactivated SARS-CoV-2 vaccine in adults(2022) Melo González, Felipe; Méndez, Constanza; Peñaloza, H.F.; Schultz, B.M.; Piña Iturbe, A.; Ríos, M.; Moreno Tapia, D.; Pereira Sánchez, P.; Leighton, D.; Orellana, C.; Covarrubias, C.; Gálvez, N.M.S.; Soto, J.A.; Duarte, L.F.; Rivera Pérez, D.; Vázquez, Y.; Cabrera, A.; Bustos, S.; Iturriaga, C.; Urzua, M.; Navarrete, M.S.; Rojas, Á.; Fasce, R.; Fernández, J.; Mora, J.; Ramírez, E.; Gaete Argel, A.; Acevedo, M.; Valiente Echeverría, F.; Soto Rifo, R.; Weiskopf, D.; Grifoni, A.; Sette, A.; Zeng, G.; Meng, W.; González Aramundiz, J.V.; González, P.A.; Abarca, K.; Bueno, S.M.; Kalergis, A.M.The SARS-CoV-2 Omicron variant has challenged the control of the COVID-19 pandemic even in highly vaccinated countries. While a second booster of mRNA vaccines improved the immunity against SARS-CoV-2, the humoral and cellular responses induced by a second booster of an inactivated SARS-CoV-2 vaccine have not been studied. In the context of a phase 3 clinical study, we report that a second booster of CoronaVac® increased the neutralizing response against the ancestral virus yet showed poor neutralization against the Omicron variant. Additionally, isolated PBMCs displayed equivalent activation of specific CD4+ T cells and IFN-γ production when stimulated with a mega-pool of peptides derived from the spike protein of the ancestral virus or the Omicron variant. In conclusion, a second booster dose of CoronaVac® does not improve the neutralizing response against the Omicron variant compared with the first booster dose, yet it helps maintaining a robust spike-specific CD4+ T cell response.
- ItemNew Mechanisms to Prevent Heart Failure with Preserved Ejection Fraction Using Glucagon-like Peptide-1 Receptor Agonism (GLP-1 RA) in Metabolic Syndrome and in Type 2 Diabetes: A Review(2024) Jalil Milad, Jorge Emilio; Gabrielli Nervi, Luigi Arnaldo; Ocaranza Jeraldino, María Paz; MacNab, P.; Fernandez R.; Grassi Corrales, Bruno; Jofré Mendoza, Paulina Eugenia; Verdejo, H.; Acevedo, M.; Cordova Alvestegui, Samuel Edmundo; Sanhueza, Luis; Greig Undurraga, Douglas PatrickThis review examines the impact of obesity on the pathophysiology of heart failure with preserved ejection fraction (HFpEF) and focuses on novel mechanisms for HFpEF prevention using a glucagon-like peptide-1 receptor agonism (GLP-1 RA). Obesity can lead to HFpEF through various mechanisms, including low-grade systemic inflammation, adipocyte dysfunction, accumulation of visceral adipose tissue, and increased pericardial/epicardial adipose tissue (contributing to an increase in myocardial fat content and interstitial fibrosis). Glucagon-like peptide 1 (GLP-1) is an incretin hormone that is released from the enteroendocrine L-cells in the gut. GLP-1 reduces blood glucose levels by stimulating insulin synthesis, suppressing islet α-cell function, and promoting the proliferation and differentiation of β-cells. GLP-1 regulates gastric emptying and appetite, and GLP-1 RA is currently indicated for treating type 2 diabetes (T2D), obesity, and metabolic syndrome (MS). Recent evidence indicates that GLP-1 RA may play a significant role in preventing HFpEF in patients with obesity, MS, or obese T2D. This effect may be due to activating cardioprotective mechanisms (the endogenous counter-regulatory renin angiotensin system and the AMPK/mTOR pathway) and by inhibiting deleterious remodeling mechanisms (the PKA/RhoA/ROCK pathway, aldosterone levels, and microinflammation). However, there is still a need for further research to validate the impact of these mechanisms on humans.
