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Patrones alimentarios y riesgo de un primer infarto cerebral en adultos mayores de 45 años en el Hospital Herminda Martín de Chillan, Región de Ñuble: Estudio de caso y control
(Universidad de Chile, 2019)
calculó el riesgo atribuible poblacional de la hipertensión arterial, diabetes mellitus, PAS ≥140 mmhg y consumo de alcohol para la población de Ñuble. Para determinar la asociación entre la adherencia a la dieta mediterránea y la probabilidad de un primer...
Infosura en equinos
(Universidad de Chile, 2011)
vasoconstricción de las anastomosis
arteriovenosas en la base de las láminas y perpetúa el
insulto isquémico. Además, las catecolaminas
contribuyen con el desarrollo de hipertensión
sistémica durante la presentación del cuadro. La
desviación de los líquidos de...
los compartimentos en la microcirculación da lugar a un edema digital. Si estos cambios son importantes la isquemia puede progresar hasta llegar a la necrosis laminar (Godoy., 1983). La hipertensión con que cursa el cuadro de infosura está...
los compartimentos en la microcirculación da lugar a un edema digital. Si estos cambios son importantes la isquemia puede progresar hasta llegar a la necrosis laminar (Godoy., 1983). La hipertensión con que cursa el cuadro de infosura está...
Comparación de prevalencia de xerostomía entre pacientes diabéticos tipo 2 compensados y descompensados metabólicamente
(Universidad de Chile, 2016)
...……………………………………………………………..……….... 2
1.4 Alteraciones salivales en sujetos con Diabetes mellitus y xerostomía ...……….....3
1.5 Diabetes, hipertensión arterial y xerostomía……………………………………........5
1.6 Calidad de vida, xerostomía y alcances de este estudio……………………..…......6
2...
control metabólico de esta enfermedad, a alteraciones salivales descritas en la misma o con la prescripción de fármacos asociados a enfermedades como la hipertensión, altamente relacionada con DM2 (McLean A y Le Couteur D 2004). 3 Si bien la...
control metabólico de esta enfermedad, a alteraciones salivales descritas en la misma o con la prescripción de fármacos asociados a enfermedades como la hipertensión, altamente relacionada con DM2 (McLean A y Le Couteur D 2004). 3 Si bien la...
Craneosinostosis, una perspectiva pediátrica
(Sociedad Chilena de Pediatría, 2020)
de otras malformaciones. Suele diagnosticarse y derivarse de forma tardía, lo que se asocia
a complicaciones como hipertensión endocraneana y alteración del desarrollo encefálico. La cirugía
precoz tiene menor comorbilidad y mejores resultados...
provoca una hipoplasia del tejido cerebral subyacente30. La hipertensión endocraneana es frecuente y una complicación esperada en las craneosinostosis sindro- máticas (hasta un 60%)31, en los pacientes con solo una sutura afectada, puede variar entre 4...
provoca una hipoplasia del tejido cerebral subyacente30. La hipertensión endocraneana es frecuente y una complicación esperada en las craneosinostosis sindro- máticas (hasta un 60%)31, en los pacientes con solo una sutura afectada, puede variar entre 4...
Prevalence of type 2 diabetes and obesity in two Chilean aboriginal populations living in urban zones
(SOC MEDICA SANTIAGO, 2004-10)
la acumulación de
un exceso de grasa en el cuerpo, que provoca
efectos adversos severos1. Al grave daño sobre la
salud que produce por sí misma, se suma la
asociación con patologías graves como la diabetes
tipo 2, la hipertensión, las complicaciones...
sentado y en reposo y se consideró el promedio de dos mediciones, una realizada al ingreso y otra una vez finalizada la prueba de tolerancia. Para la clasificación de hipertensión arterial (HTA: PS ≥140 mmHg y/o PD ≥90 mmHg) se utilizaron las cifras...
sentado y en reposo y se consideró el promedio de dos mediciones, una realizada al ingreso y otra una vez finalizada la prueba de tolerancia. Para la clasificación de hipertensión arterial (HTA: PS ≥140 mmHg y/o PD ≥90 mmHg) se utilizaron las cifras...
Estudio comparativo de algunas características demográficas y epidemiológicas, de los pacientes adultos mayores desdentados totales atendidos en la clínica de prótesis totales de la Facultad de Odontología Universidad de Chile y en el Centro de Referencia Maruri durante el año 2006
(Universidad de Chile, 2007)
presencia de espículas óseas que producen dolor al contacto con la
prótesis, el uso de ellas en estos pacientes es muy complicado (33, 34)
2.5.3.- Hipertensión
Se considera hipertenso a todo individuo que mantenga cifras de presión arterial...
que los hombres. A medida que la edad aumenta, hay mayor prevalencia de hipertensión, en los ≤ 65 años alcanza un 78,8% para ambos sexos. (31) 2.5.4.- Depresión La depresión es más frecuente en las edades medias (25 a 65 años) y en las mujeres...
que los hombres. A medida que la edad aumenta, hay mayor prevalencia de hipertensión, en los ≤ 65 años alcanza un 78,8% para ambos sexos. (31) 2.5.4.- Depresión La depresión es más frecuente en las edades medias (25 a 65 años) y en las mujeres...
Regulación de la autofagia por angiotensina II en células musculares lisas vasculares
(Universidad de Chile, 2018)
Las enfermedades cardiovasculares (ECV) son la principal causa de
muerte a nivel mundial. Dentro de los principales factores de riesgo para el
desarrollo de ECV, se encuentra la hipertensión arterial (HTA). Esta patología
presenta una elevada...
Cardiovascular diseases (CVD) are the leading cause of death worldwide. One of the principal risk factor for the development of CVD is high blood pressure (HBP) or hypertension. HBP is a disease with high morbidity and mortality. Its pathophysiology is characterized by an increase in blood pressure and development of cardiovascular remodeling. This pathology is associated with increased plasma levels of angiotensin II (Ang II). This peptide exerts its action by activating the Angiotensin type 1 receptor (AT1R). The AT1R is a G protein- coupled receptor whose activation regulates cell proliferation, migration, production of reactive oxygen species (ROS) and vascular smooth muscle cells (VSMCs) hypertrophy. Part of these effects are explained by the activation of the RhoA / ROCK pathway. This signaling pathway is activated downstream of the AT1R. ROCK is a serine-threonine kinase that plays an important role in cardiovascular remodeling. In pathologies such HBP, ROCK, facilitates the hypercontractile state of VSMCs and regulates a large part of the processes described above. However, the mechanism by which Ang II can affects VSMCs remain unclear. In this context, autophagy recently has been described to regulate vascular integrity, regulating the phenotype switch of VSMCs. In pathologies such as atherosclerosis, activation of autophagy induces change in VSMCs phenotype, from contractile to synthetic phenotype, which is relevant for this pathology. However, the effect of autophagy in pathologies such as hypertension is unknown. The hypothesis of this work was "Angiotensin II activates autophagy through an AT1R / ROCK-dependent mechanism, increasing contractile proteins in vascular smooth muscle cells". The general aim was "To evaluate the role of Ang II / AT1R / ROCK signaling pathway in the induction of autophagy and the control of contractile proteins". To answer this hypothesis, the following specific aims were proposed: (1) To determine if Ang II induces autophagy through AT1R activation in VSMCs. (2) To Evaluate the effect of ROCK in Ang II/AT1R- dependent autophagy in VSMCs. (3) To determine the role of Ang II / AT1R / ROCK-dependent autophagy in the control of contractile proteins in VSMCs. The working model was; The A7r5 cell line, derived from embryonic rat aorta, and the primary culture, prepared by removing the thoracic aorta from Sprague-Dawley rats (RASMs). These cells were cultured in DMEM medium with 10% fetal bovine serum (A7r5 cells) and 10% calf serum (RASMs cells). Once cells were confluent, the cells were maintained in DMEM medium 2% fetal bovine serum, A7r5 cells and 2% calf serum for RASMs for 24 h. Then, cells were treated with Ang II 100 nM for 24 h and pretreated with the different treatments, 1 h before the stimulus. Autophagy was determined by Western blot, measuring protein levels of LC3 II, LC3 I, total levels of LC3, Beclin1, phosphorylation of Beclin1, class III phosphatidylinositol 3-kinase (PI3KCIII/Vps34), Atg12–Atg5, Atg7, Atg4 and Bag3. Autophagic flux were determined in the presence or absence of chloroquine (CQ) 30 μM. The formation of autophagic punctae was determined by overexpression of LC3 with an Ad-LC3-GFP adenovirus and confocal microscopy, in the presence or absence of CQ. The ROCK activation levels were determined by measuring the phosphorylation levels of MYPT1 in threonine 853 (Thr853) by Western Blot. The levels of contractile proteins were determined by Western blot. The cells stimulated with Ang II showed higher levels of LC3 II, which was confirmed by an increase in the autophagic flux in the cells treated with Ang II and CQ. The use of the Ad-LC3-GFP, showed an increase in the number of autophagic vesicles after treatment with Ang II. This increase was enhanced by incubating the VSMCs for the last 4 hours with CQ. The treatment with Ang II increased the protein levels of Beclin-1, PI3KCIII, Atg-12–Atg5, Atg4 and Atg7, and the phosphorylation of Beclin 1. These results suggest that Ang II induces autophagy by activating the initiation/nucleation and the elongation of the phagophore. On the other hand, it was found that Ang II also increases the total LC3 levels. Using the transcription inhibitor (actinomycin D) and translation inhibitor (cycloheximide) it was determined that, Ang II regulates LC3 levels by a translational mechanism. Previously, we have described that Bag3, a cochaperone, regulates the translation of LC3 mRNA. Our results showed that, Ang II significantly increases Bag3 levels, suggesting that this cochaperone could be responsible for the control of total LC3 levels by Ang II. The pharmacological antagonism of AT1R, using Losartan (LOS), significantly decreased autophagy activation. This was evidentiated by a decrease in LC3 II levels and the autophagic punctae. LOS also blocked the increase of Beclin-1, PI3KCIII, Atg-12-Atg5, Atg4 and Atg7, protein levels as well as the phosphorylation of Beclin 1. These results suggest that, initiation/nucleation and the elongation of the phagophore in Ang II-dependent autophagy, occurs by activation of the AT1R. In addition, LOS also prevented the increase of Bag3 and total LC3 levels, induced by Ang II. The same result was observed using the chemical inhibitor of ROCK, Y27632. These results suggest that the control of autophagy in the VSMCs depends of the AT1R / ROCK signaling pathway. The treatment of VSMCs with Ang II significantly increased the levels of alpha-smooth muscle actin, (alpha-SMA), calponin and SM22, key proteins of the contractile phenotype. The inhibition of Ang II-dependent autophagy, by silencing Beclin 1, decreased the increase of these contractile proteins. Interestingly, the induction of autophagy due a mTORc1 inhibition mechanism with rapamycin, did not increase the levels of contractile proteins in the VSMC. In addition, Ang II increased phosphorylation of proteins downstream of the mTOR pathway. These results suggest that Ang II activates mTOR and the mTOR-independent autophagy may be responsible for the control of contractile proteins in VSMCs. In summary, Ang II induces autophagy through an Ang II / AT1R / ROCK, which in turn, promotes the increase of contractile proteins in VSMCs, however the mTORc1 dependent autophagy does not increased the levels of these proteins in VSMCs, suggesting that this autophagy is not involved in the regulation of contractile proteins. Thus, regulation of Ang II-dependent autophagy could be a new therapeutic target in the prevention of vascular damage induced by Ang II in hypertension....
Cardiovascular diseases (CVD) are the leading cause of death worldwide. One of the principal risk factor for the development of CVD is high blood pressure (HBP) or hypertension. HBP is a disease with high morbidity and mortality. Its pathophysiology is characterized by an increase in blood pressure and development of cardiovascular remodeling. This pathology is associated with increased plasma levels of angiotensin II (Ang II). This peptide exerts its action by activating the Angiotensin type 1 receptor (AT1R). The AT1R is a G protein- coupled receptor whose activation regulates cell proliferation, migration, production of reactive oxygen species (ROS) and vascular smooth muscle cells (VSMCs) hypertrophy. Part of these effects are explained by the activation of the RhoA / ROCK pathway. This signaling pathway is activated downstream of the AT1R. ROCK is a serine-threonine kinase that plays an important role in cardiovascular remodeling. In pathologies such HBP, ROCK, facilitates the hypercontractile state of VSMCs and regulates a large part of the processes described above. However, the mechanism by which Ang II can affects VSMCs remain unclear. In this context, autophagy recently has been described to regulate vascular integrity, regulating the phenotype switch of VSMCs. In pathologies such as atherosclerosis, activation of autophagy induces change in VSMCs phenotype, from contractile to synthetic phenotype, which is relevant for this pathology. However, the effect of autophagy in pathologies such as hypertension is unknown. The hypothesis of this work was "Angiotensin II activates autophagy through an AT1R / ROCK-dependent mechanism, increasing contractile proteins in vascular smooth muscle cells". The general aim was "To evaluate the role of Ang II / AT1R / ROCK signaling pathway in the induction of autophagy and the control of contractile proteins". To answer this hypothesis, the following specific aims were proposed: (1) To determine if Ang II induces autophagy through AT1R activation in VSMCs. (2) To Evaluate the effect of ROCK in Ang II/AT1R- dependent autophagy in VSMCs. (3) To determine the role of Ang II / AT1R / ROCK-dependent autophagy in the control of contractile proteins in VSMCs. The working model was; The A7r5 cell line, derived from embryonic rat aorta, and the primary culture, prepared by removing the thoracic aorta from Sprague-Dawley rats (RASMs). These cells were cultured in DMEM medium with 10% fetal bovine serum (A7r5 cells) and 10% calf serum (RASMs cells). Once cells were confluent, the cells were maintained in DMEM medium 2% fetal bovine serum, A7r5 cells and 2% calf serum for RASMs for 24 h. Then, cells were treated with Ang II 100 nM for 24 h and pretreated with the different treatments, 1 h before the stimulus. Autophagy was determined by Western blot, measuring protein levels of LC3 II, LC3 I, total levels of LC3, Beclin1, phosphorylation of Beclin1, class III phosphatidylinositol 3-kinase (PI3KCIII/Vps34), Atg12–Atg5, Atg7, Atg4 and Bag3. Autophagic flux were determined in the presence or absence of chloroquine (CQ) 30 μM. The formation of autophagic punctae was determined by overexpression of LC3 with an Ad-LC3-GFP adenovirus and confocal microscopy, in the presence or absence of CQ. The ROCK activation levels were determined by measuring the phosphorylation levels of MYPT1 in threonine 853 (Thr853) by Western Blot. The levels of contractile proteins were determined by Western blot. The cells stimulated with Ang II showed higher levels of LC3 II, which was confirmed by an increase in the autophagic flux in the cells treated with Ang II and CQ. The use of the Ad-LC3-GFP, showed an increase in the number of autophagic vesicles after treatment with Ang II. This increase was enhanced by incubating the VSMCs for the last 4 hours with CQ. The treatment with Ang II increased the protein levels of Beclin-1, PI3KCIII, Atg-12–Atg5, Atg4 and Atg7, and the phosphorylation of Beclin 1. These results suggest that Ang II induces autophagy by activating the initiation/nucleation and the elongation of the phagophore. On the other hand, it was found that Ang II also increases the total LC3 levels. Using the transcription inhibitor (actinomycin D) and translation inhibitor (cycloheximide) it was determined that, Ang II regulates LC3 levels by a translational mechanism. Previously, we have described that Bag3, a cochaperone, regulates the translation of LC3 mRNA. Our results showed that, Ang II significantly increases Bag3 levels, suggesting that this cochaperone could be responsible for the control of total LC3 levels by Ang II. The pharmacological antagonism of AT1R, using Losartan (LOS), significantly decreased autophagy activation. This was evidentiated by a decrease in LC3 II levels and the autophagic punctae. LOS also blocked the increase of Beclin-1, PI3KCIII, Atg-12-Atg5, Atg4 and Atg7, protein levels as well as the phosphorylation of Beclin 1. These results suggest that, initiation/nucleation and the elongation of the phagophore in Ang II-dependent autophagy, occurs by activation of the AT1R. In addition, LOS also prevented the increase of Bag3 and total LC3 levels, induced by Ang II. The same result was observed using the chemical inhibitor of ROCK, Y27632. These results suggest that the control of autophagy in the VSMCs depends of the AT1R / ROCK signaling pathway. The treatment of VSMCs with Ang II significantly increased the levels of alpha-smooth muscle actin, (alpha-SMA), calponin and SM22, key proteins of the contractile phenotype. The inhibition of Ang II-dependent autophagy, by silencing Beclin 1, decreased the increase of these contractile proteins. Interestingly, the induction of autophagy due a mTORc1 inhibition mechanism with rapamycin, did not increase the levels of contractile proteins in the VSMC. In addition, Ang II increased phosphorylation of proteins downstream of the mTOR pathway. These results suggest that Ang II activates mTOR and the mTOR-independent autophagy may be responsible for the control of contractile proteins in VSMCs. In summary, Ang II induces autophagy through an Ang II / AT1R / ROCK, which in turn, promotes the increase of contractile proteins in VSMCs, however the mTORc1 dependent autophagy does not increased the levels of these proteins in VSMCs, suggesting that this autophagy is not involved in the regulation of contractile proteins. Thus, regulation of Ang II-dependent autophagy could be a new therapeutic target in the prevention of vascular damage induced by Ang II in hypertension....
Rol inmunomodulador de la activación del receptor mineralocorticoides por corticosterona
(Universidad de Chile, 2014)
y su rol en el desarrollo de hipertensión. ................... 30
1.6
Efectos de la activación de MR y la expresión de HO-1. ....................................... 32
1.7
Respuestas no genómicas en la vías de señalización de los...
antiinflamatorios postulados, en pacientes que presentan un exceso de GCs han sido observados efectos adversos como hipertensión y daño cardiovascular. En estos casos, se ha propuesto que un exceso de GCs podría promover la excesiva activación MR, aumentando la...
antiinflamatorios postulados, en pacientes que presentan un exceso de GCs han sido observados efectos adversos como hipertensión y daño cardiovascular. En estos casos, se ha propuesto que un exceso de GCs podría promover la excesiva activación MR, aumentando la...
Caracterización epidemiológica ll de usuarios asistentes a la Clínica de Prótesis Fija de la Facultad de Odontología de la Universidad de Chile
(Universidad de Chile, 2013)
(44,72%) y
consumo de alcohol (30,69%). Se registraron 171 usuarios (34,8%) con alguna
enfermedad sistémica, donde las más prevalentes fueron: Hipertensión Arterial
(20,73%), Diabetes Mellitus (7,32%) e Hipotiroidismo (7,32%). Los dientes más...
un promedio nacional de 38,5%, del cual un 39% afecta a hombres y un 38,1% a mujeres. Con mayor prevalencia en el grupo de 45 – 64 años de edad (58,9%). - Hipertensión Arterial: con un promedio nacional de 26,9%, del cual un 28,7% afecta a...
un promedio nacional de 38,5%, del cual un 39% afecta a hombres y un 38,1% a mujeres. Con mayor prevalencia en el grupo de 45 – 64 años de edad (58,9%). - Hipertensión Arterial: con un promedio nacional de 26,9%, del cual un 28,7% afecta a...
Gastritis varioliforme y daño hepático crónico: Una inesperada asociación
(SOC MEDICA SANTIAGO, 2010-08)
los pacientes con GV, se realizó una
entrevista consultando por la presencia de comor-
bilidad (hipertensión arterial, diabetes mellitus,
insuficiencia cardíaca, insuficiencia renal), ingesta
de antiinflamatorios no esteroidales, aspirina,
tabaco y...
prospectivo (OR = 9,32 y 3,38 respectivamente). Pensando que esta asociación podría deberse a la presencia de hipertensión portal, evaluamos la correlación entre presencia de GV y presencia o ausencia de várices esofágicas. No observamos correlación...
prospectivo (OR = 9,32 y 3,38 respectivamente). Pensando que esta asociación podría deberse a la presencia de hipertensión portal, evaluamos la correlación entre presencia de GV y presencia o ausencia de várices esofágicas. No observamos correlación...