Browsing by Author "Godoy J., Iván"
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- ItemAssessment of Left Atrial Function in Hypertrophic Cardiomyopathy and Athlete's Heart: A Left Atrial Myocardial Deformation Study(2012) Gabrielli, Luigi; Enríquez, Andrés; Córdova Alvestegui, Samuel Edmundo; Yáñez, Fernando; Godoy J., Iván; Corbalán Herreros, Ramón
- ItemBlood Pressure After Recent Stroke : Baseline Findings From the Secondary Prevention of Small Subcortical Strokes Trial(2013) White, Carole; Pergola, Pablo E.; Szychowski, Jeff M.; Talbert, Robert; Cervantes-Arriaga, Amin; Clark, Heather D.; Del Brutto, Oscar.; Godoy J., Iván
- ItemBoldina disminuye la apoptosis miocárdica post isquemia reperfusión en la rata(2011) López Hernández, René Ramón.; Sáez, Juan Carlos; Godoy J., Iván; Ocaranza Jeraldino, M. Paz; López Hernández, René Ramón.; Sáez, Juan Carlos; Godoy J., Iván; Ocaranza, María Paz
- ItemIncreased Rho-Kinase Activity in Hypertensive Patients With Left Ventricular Hypertrophy(2014) Gabrielli, Luigi; Winter, J.; Godoy J., Iván; Mc-Nab Martin, Paul Andrew; Padilla Argote, Ivonne Evelyn; Cordova, Samuel; Rigotti, P.; Novoa, Ulises; Mora, I.; Garcia, L.; Ocaranza Jeraldino, M. Paz; Jalil Milad, Jorge; Gabrielli, Luigi; Winter, J.; Godoy J., Iván; Mc-Nab Martin, Paul Andrew; Padilla Argote, Ivonne Evelyn; Cordova, Samuel; Rigotti, P.; Novoa, Ulises; Mora, I.; Garcia, L.; Ocaranza, María Paz; Jalil Milad, Jorge
- ItemMetabolic syndrome and subclinical atherosclerosis in children(2011) Arnáiz Gómez, Pilar; Villarroel del Pino, Luis A.; Godoy J., Iván; Barja Y., Salesa; Castillo Valenzuela, Oscar; Farías Jofré, Marcelo Enrique; Domínguez de Landa, María Angélica; Mardones S., FranciscoAtherosclerosis begins in childhood in response to the clustering of metabolic syndrome (MS) risk components since early life. Carotid intima-media thickness (CIMT), a surrogate marker of subclinical atherosclerosis, has been strongly related with cardiovascular disease and Diabetes 2 in adulthood. We aimed to study the possible association of CIMT with the MS components in a population of Chilean children. A cross-sectional study of 304 children of low socio-economic strata from an urban area of Santiago was performed during 2009-2010. This sample was selected mainly considering the presence of one or more MS components and insulin resistance (IR). Anthropometry and systolic and diastolic blood pressure were assessed by trained personnel. While fasting, a blood sample was taken to determine lipids (enzymatic colorimetric tests), glycemia (hexoquinase), insulin (quimioluminiscence) and HOMA. CIMT was assessed using ultrasonography with automated software. Pearson correlation, chi-squared test and stepwise regression were used. Mean age was 11.5 ± 0.9 years old; 57% girls and 42% pre-pubertal; 64% overweight; and 25% had MS. MS components distribution was: 20% had 0, 29% had one, 26% had two and 25% had three or more. Pearson coefficients for CIMT medium and maximum with systolic blood pressure were: 0.206 (p 0.0003) and r: 0.213 (p 0.0002). Some MS components and IR had higher proportions of children over the 75th percentile of CIMT medium and maximum in the contingency tables: 1) the proportion of children with high CIMT medium was significantly higher for IR (0.035) and CHDL ≤ 40 mg/dL (p 0.039); 2) A tendency for significant differences was found for the proportions of children with high (>75th percentile) CIMT medium with waist circumference (p 0.052) and children with high (>75th percentile) CIMT maximum with CHDL ≤ 40 mg/dL (p 0.062). Multiple linear regression models for CIMT medium and maximum selected just systolic blood pressure in both; p values were 0.0003 and 0.0002. Univariate analyses showed that CIMT medium and maximum were directly associated with systolic blood pressure. Bivariate analyses showed that CIMT medium was significantly associated with IR and CHDL ≤ 40 mg/dL. However, multiple regression models for both CIMTs just selected systolic blood pressure, a fact that would make it a proxy for CIMTs. These results are the first reported in our country.
- ItemPleiotropic effects of atorvastatin in heart failure : role in oxidative stress, inflammation, endothelial function, and exercise capacity(2008) Castro Gálvez, Pablo Federico; Miranda, Rodrigo; Verdejo Pinochet, Hugo; Greig, Douglas; Gabrielli, Luigi; Alcaíno, Hernán; Chiong, Mario; Bustos, Carlos; García, Lorena; Mellado Suazo, Rosemarie; Vukasovic, José Luis; Godoy J., Iván; Lavandero, Sergio
- ItemPositive association between aldosterone-renin ratio and carotid intima-media thickness in hypertensive children(2013) Loureiro Pérez, Carolina Andrea; Campino Johnson, María del Carmen; Martínez Aguayo, Alejandro Gregorio; Godoy J., Iván; Aglony Imbarack, Marlene Elizabeth; Bancalari, R.; García Bruce, Hernán; Carvajal, C.; Fardella B., Carlos
- ItemRho kinase cascade activation in circulating leukocytes in patients with diabetes mellitus type 2(2020) Ocaranza Jeraldino, M. Paz; Moya López, Jackeline Trinidad.; Gabrielli, Luigi; Godoy J., Iván; Córdova, S.; MacNab, P.; Farías, Luis.; Jalil Milad, Jorge; Valderas Igor, Juan Patricio; García Nannig, Lorena.; Ocaranza, María Paz; Moya López, Jackeline Trinidad.; Gabrielli, Luigi; Godoy J., Iván; Córdova, S.; MacNab, P.; Farías, Luis.; Jalil Milad, Jorge; Valderas Igor, Juan Patricio; García Nannig, Lorena.Abstract Background The intracellular ROCK signaling pathway is an important modulator of blood pressure and of cardiovascular and renal remodeling when Rho-kinase activity is increased. Besides, in preclinical models of diabetes, ROCK activation has also a role in abnormal glucose metabolism as well as in subsequent vascular and myocardial dysfunction. In humans, there are a few data assessing ROCK activation in patients with type 2 diabetes mellitus (T2D) and no studies assessing upstream/downstream components of the ROCK pathway. We assessed here levels of ROCK activation and some of the RhoA/ROCK cascade molecules in peripheral blood mononuclear cells (PBMCs) in T2D patients under current treatment. Methods Cross-sectional observational study comparing 28 T2D patients under current antidiabetic treatment with 31 consecutive healthy subjects, matched by age and gender. Circulating levels of malondialdehyde, angiotensin II and inflammatory cytokines IL-6 and IL-8 were determined in all subjects. ROCK activation in PMBCs, upstream and downstream cascade proteins, and levels of the proinflammatory molecules VCAM, ICAM-1 and IL-8 were determined in their PMBCs by Western blot. Results Compared to healthy controls, ROCK activation in T2D patients measured by 2 direct ROCK targets in PBMCs was increased by 420 and 570% (p < 0001) and it correlated significantly with serum glucose levels. p38 MAPK phosphorylation (downstream from ROCK) and JAK-2 (upstream from ROCK) were significantly higher in the T2D patients by 580% and 220%, respectively. In T2D patients, significantly increased PBMC levels of the proinflammatory molecules VCAM-1, ICAM-1 and IL-8 were observed compared to control subjects (by 180%, 360% and 260%, respectively). Circulating levels of Ang II and MDA were significantly higher in T2D patients by 29 and 63%, respectively. Conclusions T2D patients under treatment with glucose-lowering drugs, antihypertensive treatment as well as with statins have significantly increased ROCK activation in their circulating leukocytes along with higher phosphorylation of downstream cascade proteins despite pharmacologic treatment, along with increased plasma angiotensin II and MDA levels. ROCK inhibition might have an additional role in the prevention and treatment of T2D.Abstract Background The intracellular ROCK signaling pathway is an important modulator of blood pressure and of cardiovascular and renal remodeling when Rho-kinase activity is increased. Besides, in preclinical models of diabetes, ROCK activation has also a role in abnormal glucose metabolism as well as in subsequent vascular and myocardial dysfunction. In humans, there are a few data assessing ROCK activation in patients with type 2 diabetes mellitus (T2D) and no studies assessing upstream/downstream components of the ROCK pathway. We assessed here levels of ROCK activation and some of the RhoA/ROCK cascade molecules in peripheral blood mononuclear cells (PBMCs) in T2D patients under current treatment. Methods Cross-sectional observational study comparing 28 T2D patients under current antidiabetic treatment with 31 consecutive healthy subjects, matched by age and gender. Circulating levels of malondialdehyde, angiotensin II and inflammatory cytokines IL-6 and IL-8 were determined in all subjects. ROCK activation in PMBCs, upstream and downstream cascade proteins, and levels of the proinflammatory molecules VCAM, ICAM-1 and IL-8 were determined in their PMBCs by Western blot. Results Compared to healthy controls, ROCK activation in T2D patients measured by 2 direct ROCK targets in PBMCs was increased by 420 and 570% (p < 0001) and it correlated significantly with serum glucose levels. p38 MAPK phosphorylation (downstream from ROCK) and JAK-2 (upstream from ROCK) were significantly higher in the T2D patients by 580% and 220%, respectively. In T2D patients, significantly increased PBMC levels of the proinflammatory molecules VCAM-1, ICAM-1 and IL-8 were observed compared to control subjects (by 180%, 360% and 260%, respectively). Circulating levels of Ang II and MDA were significantly higher in T2D patients by 29 and 63%, respectively. Conclusions T2D patients under treatment with glucose-lowering drugs, antihypertensive treatment as well as with statins have significantly increased ROCK activation in their circulating leukocytes along with higher phosphorylation of downstream cascade proteins despite pharmacologic treatment, along with increased plasma angiotensin II and MDA levels. ROCK inhibition might have an additional role in the prevention and treatment of T2D.Abstract Background The intracellular ROCK signaling pathway is an important modulator of blood pressure and of cardiovascular and renal remodeling when Rho-kinase activity is increased. Besides, in preclinical models of diabetes, ROCK activation has also a role in abnormal glucose metabolism as well as in subsequent vascular and myocardial dysfunction. In humans, there are a few data assessing ROCK activation in patients with type 2 diabetes mellitus (T2D) and no studies assessing upstream/downstream components of the ROCK pathway. We assessed here levels of ROCK activation and some of the RhoA/ROCK cascade molecules in peripheral blood mononuclear cells (PBMCs) in T2D patients under current treatment. Methods Cross-sectional observational study comparing 28 T2D patients under current antidiabetic treatment with 31 consecutive healthy subjects, matched by age and gender. Circulating levels of malondialdehyde, angiotensin II and inflammatory cytokines IL-6 and IL-8 were determined in all subjects. ROCK activation in PMBCs, upstream and downstream cascade proteins, and levels of the proinflammatory molecules VCAM, ICAM-1 and IL-8 were determined in their PMBCs by Western blot. Results Compared to healthy controls, ROCK activation in T2D patients measured by 2 direct ROCK targets in PBMCs was increased by 420 and 570% (p < 0001) and it correlated significantly with serum glucose levels. p38 MAPK phosphorylation (downstream from ROCK) and JAK-2 (upstream from ROCK) were significantly higher in the T2D patients by 580% and 220%, respectively. In T2D patients, significantly increased PBMC levels of the proinflammatory molecules VCAM-1, ICAM-1 and IL-8 were observed compared to control subjects (by 180%, 360% and 260%, respectively). Circulating levels of Ang II and MDA were significantly higher in T2D patients by 29 and 63%, respectively. Conclusions T2D patients under treatment with glucose-lowering drugs, antihypertensive treatment as well as with statins have significantly increased ROCK activation in their circulating leukocytes along with higher phosphorylation of downstream cascade proteins despite pharmacologic treatment, along with increased plasma angiotensin II and MDA levels. ROCK inhibition might have an additional role in the prevention and treatment of T2D.Abstract Background The intracellular ROCK signaling pathway is an important modulator of blood pressure and of cardiovascular and renal remodeling when Rho-kinase activity is increased. Besides, in preclinical models of diabetes, ROCK activation has also a role in abnormal glucose metabolism as well as in subsequent vascular and myocardial dysfunction. In humans, there are a few data assessing ROCK activation in patients with type 2 diabetes mellitus (T2D) and no studies assessing upstream/downstream components of the ROCK pathway. We assessed here levels of ROCK activation and some of the RhoA/ROCK cascade molecules in peripheral blood mononuclear cells (PBMCs) in T2D patients under current treatment. Methods Cross-sectional observational study comparing 28 T2D patients under current antidiabetic treatment with 31 consecutive healthy subjects, matched by age and gender. Circulating levels of malondialdehyde, angiotensin II and inflammatory cytokines IL-6 and IL-8 were determined in all subjects. ROCK activation in PMBCs, upstream and downstream cascade proteins, and levels of the proinflammatory molecules VCAM, ICAM-1 and IL-8 were determined in their PMBCs by Western blot. Results Compared to healthy controls, ROCK activation in T2D patients measured by 2 direct ROCK targets in PBMCs was increased by 420 and 570% (p < 0001) and it correlated significantly with serum glucose levels. p38 MAPK phosphorylation (downstream from ROCK) and JAK-2 (upstream from ROCK) were significantly higher in the T2D patients by 580% and 220%, respectively. In T2D patients, significantly increased PBMC levels of the proinflammatory molecules VCAM-1, ICAM-1 and IL-8 were observed compared to control subjects (by 180%, 360% and 260%, respectively). Circulating levels of Ang II and MDA were significantly higher in T2D patients by 29 and 63%, respectively. Conclusions T2D patients under treatment with glucose-lowering drugs, antihypertensive treatment as well as with statins have significantly increased ROCK activation in their circulating leukocytes along with higher phosphorylation of downstream cascade proteins despite pharmacologic treatment, along with increased plasma angiotensin II and MDA levels. ROCK inhibition might have an additional role in the prevention and treatment of T2D.Abstract Background The intracellular ROCK signaling pathway is an important modulator of blood pressure and of cardiovascular and renal remodeling when Rho-kinase activity is increased. Besides, in preclinical models of diabetes, ROCK activation has also a role in abnormal glucose metabolism as well as in subsequent vascular and myocardial dysfunction. In humans, there are a few data assessing ROCK activation in patients with type 2 diabetes mellitus (T2D) and no studies assessing upstream/downstream components of the ROCK pathway. We assessed here levels of ROCK activation and some of the RhoA/ROCK cascade molecules in peripheral blood mononuclear cells (PBMCs) in T2D patients under current treatment. Methods Cross-sectional observational study comparing 28 T2D patients under current antidiabetic treatment with 31 consecutive healthy subjects, matched by age and gender. Circulating levels of malondialdehyde, angiotensin II and inflammatory cytokines IL-6 and IL-8 were determined in all subjects. ROCK activation in PMBCs, upstream and downstream cascade proteins, and levels of the proinflammatory molecules VCAM, ICAM-1 and IL-8 were determined in their PMBCs by Western blot. Results Compared to healthy controls, ROCK activation in T2D patients measured by 2 direct ROCK targets in PBMCs was increased by 420 and 570% (p < 0001) and it correlated significantly with serum glucose levels. p38 MAPK phosphorylation (downstream from ROCK) and JAK-2 (upstream from ROCK) were significantly higher in the T2D patients by 580% and 220%, respectively. In T2D patients, significantly increased PBMC levels of the proinflammatory molecules VCAM-1, ICAM-1 and IL-8 were observed compared to control subjects (by 180%, 360% and 260%, respectively). Circulating levels of Ang II and MDA were significantly higher in T2D patients by 29 and 63%, respectively. Conclusions T2D patients under treatment with glucose-lowering drugs, antihypertensive treatment as well as with statins have significantly increased ROCK activation in their circulating leukocytes along with higher phosphorylation of downstream cascade proteins despite pharmacologic treatment, along with increased plasma angiotensin II and MDA levels. ROCK inhibition might have an additional role in the prevention and treatment of T2D.Abstract Background The intracellular ROCK signaling pathway is an important modulator of blood pressure and of cardiovascular and renal remodeling when Rho-kinase activity is increased. Besides, in preclinical models of diabetes, ROCK activation has also a role in abnormal glucose metabolism as well as in subsequent vascular and myocardial dysfunction. In humans, there are a few data assessing ROCK activation in patients with type 2 diabetes mellitus (T2D) and no studies assessing upstream/downstream components of the ROCK pathway. We assessed here levels of ROCK activation and some of the RhoA/ROCK cascade molecules in peripheral blood mononuclear cells (PBMCs) in T2D patients under current treatment. Methods Cross-sectional observational study comparing 28 T2D patients under current antidiabetic treatment with 31 consecutive healthy subjects, matched by age and gender. Circulating levels of malondialdehyde, angiotensin II and inflammatory cytokines IL-6 and IL-8 were determined in all subjects. ROCK activation in PMBCs, upstream and downstream cascade proteins, and levels of the proinflammatory molecules VCAM, ICAM-1 and IL-8 were determined in their PMBCs by Western blot. Results Compared to healthy controls, ROCK activation in T2D patients measured by 2 direct ROCK targets in PBMCs was increased by 420 and 570% (p < 0001) and it correlated significantly with serum glucose levels. p38 MAPK phosphorylation (downstream from ROCK) and JAK-2 (upstream from ROCK) were significantly higher in the T2D patients by 580% and 220%, respectively. In T2D patients, significantly increased PBMC levels of the proinflammatory molecules VCAM-1, ICAM-1 and IL-8 were observed compared to control subjects (by 180%, 360% and 260%, respectively). Circulating levels of Ang II and MDA were significantly higher in T2D patients by 29 and 63%, respectively. Conclusions T2D patients under treatment with glucose-lowering drugs, antihypertensive treatment as well as with statins have significantly increased ROCK activation in their circulating leukocytes along with higher phosphorylation of downstream cascade proteins despite pharmacologic treatment, along with increased plasma angiotensin II and MDA levels. ROCK inhibition might have an additional role in the prevention and treatment of T2D.Abstract Background The intracellular ROCK signaling pathway is an important modulator of blood pressure and of cardiovascular and renal remodeling when Rho-kinase activity is increased. Besides, in preclinical models of diabetes, ROCK activation has also a role in abnormal glucose metabolism as well as in subsequent vascular and myocardial dysfunction. In humans, there are a few data assessing ROCK activation in patients with type 2 diabetes mellitus (T2D) and no studies assessing upstream/downstream components of the ROCK pathway. We assessed here levels of ROCK activation and some of the RhoA/ROCK cascade molecules in peripheral blood mononuclear cells (PBMCs) in T2D patients under current treatment. Methods Cross-sectional observational study comparing 28 T2D patients under current antidiabetic treatment with 31 consecutive healthy subjects, matched by age and gender. Circulating levels of malondialdehyde, angiotensin II and inflammatory cytokines IL-6 and IL-8 were determined in all subjects. ROCK activation in PMBCs, upstream and downstream cascade proteins, and levels of the proinflammatory molecules VCAM, ICAM-1 and IL-8 were determined in their PMBCs by Western blot. Results Compared to healthy controls, ROCK activation in T2D patients measured by 2 direct ROCK targets in PBMCs was increased by 420 and 570% (p < 0001) and it correlated significantly with serum glucose levels. p38 MAPK phosphorylation (downstream from ROCK) and JAK-2 (upstream from ROCK) were significantly higher in the T2D patients by 580% and 220%, respectively. In T2D patients, significantly increased PBMC levels of the proinflammatory molecules VCAM-1, ICAM-1 and IL-8 were observed compared to control subjects (by 180%, 360% and 260%, respectively). Circulating levels of Ang II and MDA were significantly higher in T2D patients by 29 and 63%, respectively. Conclusions T2D patients under treatment with glucose-lowering drugs, antihypertensive treatment as well as with statins have significantly increased ROCK activation in their circulating leukocytes along with higher phosphorylation of downstream cascade proteins despite pharmacologic treatment, along with increased plasma angiotensin II and MDA levels. ROCK inhibition might have an additional role in the prevention and treatment of T2D.
- ItemRho-kinase pathway activation and apoptosis in circulating leucocytes in patients with heart failure with reduced ejection fraction(2020) Ocaranza, María Paz; Moya, J; Jalil Milad, Jorge; Lavandero, S; Kalergis Parra, Alexis Mikes; Molina, C; Gabrielli, Luigi; Godoy J., Iván; Cordova, Samuel; Castro Gálvez, Pablo Federico; Mac Nab, P; Rossel, V; Garcia, L; Gonzalez, J; Mancilla, C; Fierro, C; Farias, L
- ItemSerum uric acid correlates with extracellular superoxide dismutase activity in patients with chronic heart failure(2008) Alcaíno, Hernán; Greig, Douglas; Chiong, Mario; Verdejo Pinochet, Hugo; Miranda, Rodrigo; Concepcion, Roberto; Vukasovic, José Luis; Díaz-Araya, Guillermo; Mellado Suazo, Rosemarie; García, Lorena; Salas, Daniela; González, Leticia; Godoy J., Iván; Castro Gálvez, Pablo Federico; Lavandero, Sergio