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Optimización de la gestión de medicamentos en un centro de salud familiar para potenciar la figura del químico farmacéutico
(Universidad de Chile, 2017)
(SBOR): Corresponde a un cuadro
clínico de 3 o más episodios de obstrucción bronquial durante los dos primeros años de
vida [12].
ii. Asma (mayores y menores de 15 años): Inflamación crónica de las vías aéreas
generando episodios de obstrucción...
. Trabajo de título Daniel Amigo Díaz Página 8 Tabla 3 Canasta de medicamentos pertenecientes al Programa Ministerial de IRA/ERA [9]. Medicamento Observación Disponibilidad en CESFAM Bromuro de Ipratropio 20mcg/dosis INH Asma > 15 años, EPOC, NAC >65...
. Trabajo de título Daniel Amigo Díaz Página 8 Tabla 3 Canasta de medicamentos pertenecientes al Programa Ministerial de IRA/ERA [9]. Medicamento Observación Disponibilidad en CESFAM Bromuro de Ipratropio 20mcg/dosis INH Asma > 15 años, EPOC, NAC >65...
Effects of platelet-rich and -poor plasma on the reparative response of gingival fibroblasts
(2012)
are
differentiated into myofibroblasts character-
ized by the expression of the actin isoform
a-smooth muscle actin (a-SMA) (Hinz 2007).
An extensive remodeling of the actin cyto-
skeleton is observed during myofibroblastic
differentiation (Hinz 2007). Actin...
the differentiation of myofi- broblasts by inducing the expression of the actin isoform a-SMA that plays a key role in extracellular matrix (ECM) remodeling and wound contraction (Arora & McCulloch 1994; Hinz 2007). TGF-b1 may also promote cell migration...
the differentiation of myofi- broblasts by inducing the expression of the actin isoform a-SMA that plays a key role in extracellular matrix (ECM) remodeling and wound contraction (Arora & McCulloch 1994; Hinz 2007). TGF-b1 may also promote cell migration...
Effects of cigarette smoke and nicotine on cell viability, migration and myofibroblastic differentiation
(John Wiley & Sons A/S, 2012-02-04)
the
differentiation of myofibroblasts (25).
These cells are characterized by the
expression of the actin isoform
a-smooth muscle actin (a-SMA), which
renders a more contractile phenotype
that stimulates tissue remodeling
(26,27). Previous studies have explored...
to polyvinylidene difluoride transfer membrane (Thermo Scientific, Rockford, IL, USA). Membranes were exposed to primary commercial anti- bodies against a-SMA, clone 1A4, diluted 1:1000 (Sigma) and b-actin (Sigma), clone AC-74, diluted 1:5000. Afterwards, secondary...
to polyvinylidene difluoride transfer membrane (Thermo Scientific, Rockford, IL, USA). Membranes were exposed to primary commercial anti- bodies against a-SMA, clone 1A4, diluted 1:1000 (Sigma) and b-actin (Sigma), clone AC-74, diluted 1:5000. Afterwards, secondary...
Efecto de la exposición al MP2.5 proveniente de relaves mineros en la función pulmonar en escolares de Chañaral, III región, Chile
(Universidad de Chile, 2014)
respiratorias o cardiacas,
11
frecuencia cardiaca irregular, ataques cardiacos no fatales, agravamiento del
asma, disminución de la función pulmonar y aumento de síntomas
respiratorios (2). Las personas sanas pueden experimentar síntomas
temporales frente...
La infección primaria por pneumocystis carinii se asocia a estimulación del sistema neuroendocrino pulmonar en ratas inmunocompetentes
(Universidad de Chile, 2015)
enfermedades crónicas, como EPOC o Asma
Bronquial. Sin embargo, los mecanismos que explican estos cambios patológicos
durante la infección no se conocen con claridad. En este sentido, el sistema
neuroendocrino pulmonar podría contribuir a estos cambios.
El...
Pneumocystis is a fungus that causes an infection in immunocompetent individuals during their first months of life. This infection has been related to pathological changes in the airway, and they could be associated with severity or pathogeny of chronic diseases, such as COPD or asthma. However, mechanisms that underlie these pathological changes in the infection have not been described. Thus, Pulmonary Neuroendocrine System may be part of the infection pathogeny. The pulmonary neuroendocrine system is a group of innervated epitelial cells in the airway which have functions as chemoreceptors, stem cells reservoirs and hyperreactivity, inflammation, and tissue remodelling mediators. Several pulmonary diseases have been associated with morphological changes in neuroendocrine cells, that have been related to hypoxic response and an increase of amine and peptide levels, such as CGRP and GRP. These peptides have been described as inflammation, bronchoconstriction and remodelling factors, because of what they could contribute to the pathologic response in the airway for some respiratory diseases, eventually through the Pneumocystis primary infection. Therefore, we aimed to demostrate that the Pneumocystis carinii primary infection is related to pulmonary neuroendocrine system stimulation, expressed as PNEC/NEBs hyperplasia and hypertrophy, an increase in innervation of NEBs, increase in CGRP, GRP and GRPR gene expression and an increase in CGRP and GRP peptide levels. To demostrate this hypothesis, we used lungs of a P. carinii primary infection model in immnunocompetent rats. Morphological changes in PNEC/NEBs, nerves, and CGRP levels were determined by immnunohistochemisty, GRP concentration was measured by ELISA and CGRP, GRP and GRPR gene expression were determined using RT-PCR and qRT-PCR. We observed a significant increase in density of clusters of CGRP immunorreactive cells which indicate NEBs, on day 75 of the infection with respect to the control group, in small airway (less than 250 μm) and in total airway. No changes were observed in the NEBs density in the major airway nor in the PNECs density, independently of the day of infection. The NEBs size significanly increased on day 60 of the infection compared to the control group. Nerves were not seen with the techniques used in this thesis. The GRP concentration did not change throughout the infection. mRNA levels of CGRP and GRPR on day 75 of the infection were significantly higher than in the control group. In addition, we observed that a higher percentage of infected rats expressed GRP mRNA compared to control rats. These findings show that Pneumocystis primary infection in an immunocompetent rats model is associated with pulmonary neuroendocrine system stimulation, expressed as hyperplasia and hypertrohy of CGRP innmunorreactive cells which indicates NEBs, and an increase in CGRP, GRP and GRPR gene expression. This suggests that pulmonary neuroendocrine cells, especially CGRP could constitute part of the pathogeny in the Pneumocystis carinii primary infection in immunocompetent individuals, as a factor in the hypoxic response or contributing to airway inflammation, bronchoconstriction and remodelling. Additionally, GRPR may also participate in these functions. Nevertheless, more studies are needed to describe the participation of neuroendocrine cells, their neuropeptides and their receptors along the infection. Thus, CGRP and GRPR could become therapeutic targets in respiratory infections....
Pneumocystis is a fungus that causes an infection in immunocompetent individuals during their first months of life. This infection has been related to pathological changes in the airway, and they could be associated with severity or pathogeny of chronic diseases, such as COPD or asthma. However, mechanisms that underlie these pathological changes in the infection have not been described. Thus, Pulmonary Neuroendocrine System may be part of the infection pathogeny. The pulmonary neuroendocrine system is a group of innervated epitelial cells in the airway which have functions as chemoreceptors, stem cells reservoirs and hyperreactivity, inflammation, and tissue remodelling mediators. Several pulmonary diseases have been associated with morphological changes in neuroendocrine cells, that have been related to hypoxic response and an increase of amine and peptide levels, such as CGRP and GRP. These peptides have been described as inflammation, bronchoconstriction and remodelling factors, because of what they could contribute to the pathologic response in the airway for some respiratory diseases, eventually through the Pneumocystis primary infection. Therefore, we aimed to demostrate that the Pneumocystis carinii primary infection is related to pulmonary neuroendocrine system stimulation, expressed as PNEC/NEBs hyperplasia and hypertrophy, an increase in innervation of NEBs, increase in CGRP, GRP and GRPR gene expression and an increase in CGRP and GRP peptide levels. To demostrate this hypothesis, we used lungs of a P. carinii primary infection model in immnunocompetent rats. Morphological changes in PNEC/NEBs, nerves, and CGRP levels were determined by immnunohistochemisty, GRP concentration was measured by ELISA and CGRP, GRP and GRPR gene expression were determined using RT-PCR and qRT-PCR. We observed a significant increase in density of clusters of CGRP immunorreactive cells which indicate NEBs, on day 75 of the infection with respect to the control group, in small airway (less than 250 μm) and in total airway. No changes were observed in the NEBs density in the major airway nor in the PNECs density, independently of the day of infection. The NEBs size significanly increased on day 60 of the infection compared to the control group. Nerves were not seen with the techniques used in this thesis. The GRP concentration did not change throughout the infection. mRNA levels of CGRP and GRPR on day 75 of the infection were significantly higher than in the control group. In addition, we observed that a higher percentage of infected rats expressed GRP mRNA compared to control rats. These findings show that Pneumocystis primary infection in an immunocompetent rats model is associated with pulmonary neuroendocrine system stimulation, expressed as hyperplasia and hypertrohy of CGRP innmunorreactive cells which indicates NEBs, and an increase in CGRP, GRP and GRPR gene expression. This suggests that pulmonary neuroendocrine cells, especially CGRP could constitute part of the pathogeny in the Pneumocystis carinii primary infection in immunocompetent individuals, as a factor in the hypoxic response or contributing to airway inflammation, bronchoconstriction and remodelling. Additionally, GRPR may also participate in these functions. Nevertheless, more studies are needed to describe the participation of neuroendocrine cells, their neuropeptides and their receptors along the infection. Thus, CGRP and GRPR could become therapeutic targets in respiratory infections....
Sintomatología respiratoria aguda en niños según exposición a humo de tabaco ambiental
(Universidad de Chile, 2016)
,83
(1,38-2,42)
Dong et al.
(2007) [26]
Niños 1 a 6
años
6053
≥ 10 cigarros
al día en fin
de semana
Sibilancias OR 1,69
(1,29-2,23)
Transversal Exposición a
HTA durante
niñez
Asma OR 1,1
(0,9-1,4)
Gilliland et
al. (2001)
[21]
Mayoría de
los...
Niños 5 a 11 años 425 Niveles de cotinina en saliva Asma y síntomas respiratorios OR 1,8 (1,4-2,5) Transversal ≥ 20 cigarros al día en el hogar Diagnóstico de asma OR 2,1 (1,2-3,5) Gergen et al. (1998) [23] Niños 3 a 5 años 7680 ≥ 20...
Niños 5 a 11 años 425 Niveles de cotinina en saliva Asma y síntomas respiratorios OR 1,8 (1,4-2,5) Transversal ≥ 20 cigarros al día en el hogar Diagnóstico de asma OR 2,1 (1,2-3,5) Gergen et al. (1998) [23] Niños 3 a 5 años 7680 ≥ 20...
Sintomatología respiratoria aguda en niños según exposición a humo de tabaco ambiental
(Universidad de Chile, 2016)
,83
(1,38-2,42)
Dong et al.
(2007) [26]
Niños 1 a 6
años
6053
≥ 10 cigarros
al día en fin
de semana
Sibilancias OR 1,69
(1,29-2,23)
Transversal Exposición a
HTA durante
niñez
Asma OR 1,1
(0,9-1,4)
Gilliland et
al. (2001)
[21]
Mayoría de
los...
Niños 5 a 11 años 425 Niveles de cotinina en saliva Asma y síntomas respiratorios OR 1,8 (1,4-2,5) Transversal ≥ 20 cigarros al día en el hogar Diagnóstico de asma OR 2,1 (1,2-3,5) Gergen et al. (1998) [23] Niños 3 a 5 años 7680 ≥ 20...
Niños 5 a 11 años 425 Niveles de cotinina en saliva Asma y síntomas respiratorios OR 1,8 (1,4-2,5) Transversal ≥ 20 cigarros al día en el hogar Diagnóstico de asma OR 2,1 (1,2-3,5) Gergen et al. (1998) [23] Niños 3 a 5 años 7680 ≥ 20...
Características psicoambientales asociadas al inicio, curso y desarrollo de patologías alérgicas: una revisión general del fenómeno
(Hospital Clínico Universidad de Chile, 2012)
entre facto-
res genéticos y el desarrollo de patologías alérgicas.
Ambos usaron cohortes en estudios prospectivos.
Koeppen-Schomerus(25) estudió el rol de factores
genéticos y ambientales en el desarrollo de asma
tabla 1. criterios de exclusión de...
patología asmática entre gemelos. En este sentido plantean razonable creer que alérgenos ambienta- les ocupan un rol importante en el desarrollo de asma. Dicho ambiente si es compartido, debiese tener similar influencia en niños de una misma familia. El...
patología asmática entre gemelos. En este sentido plantean razonable creer que alérgenos ambienta- les ocupan un rol importante en el desarrollo de asma. Dicho ambiente si es compartido, debiese tener similar influencia en niños de una misma familia. El...
Espirometría amigable. Dispositivo médico para el diagnóstico de la función pulmonar de niños preescolares
(Universidad de Chile, 2015)
ejemplo, el asma que, según la OMS, es la en-
fermedad crónica más frecuente en los niños, siendo el 80% de los casos entre los 3 y 4 años de
edad y, por otra parte la mayor pérdida de función pulmonar ocurre antes de que los asmáticos
cumplan 6 años...
(Castro, 2013) . A menudo el asma no se diagnostica correctamente ni recibe el tratamiento adecuado, creando así una importante carga para los pacientes y sus familias, y pu- diendo limitar la actividad del paciente durante toda su vida. La OMS estima que...
(Castro, 2013) . A menudo el asma no se diagnostica correctamente ni recibe el tratamiento adecuado, creando así una importante carga para los pacientes y sus familias, y pu- diendo limitar la actividad del paciente durante toda su vida. La OMS estima que...