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  1. Home
  2. Browse by Author

Browsing by Author "Morales, M."

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    Analysis of genetic diversity in Argentinian heterotic maize populations using molecular markers.
    (2010) Morales, M.; Decker, Viviana.; Ornella, Leonardo.
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    Development and assessment of the disposition index based on the oral glucose tolerance test in subjects with different glycaemic status
    (2016) Santos Martín, José Luis; Yévenes, I.; Cataldo Bascuñan, Luis Rodrigo; Morales, M.; Galgani Fuentes, José; Arancibia, C.; Vega, J.; Olmos Coelho, Pablo Roberto; Flores, M.; Valderas Igor, Juan Patricio; Pollak, F.
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    Epithelial Inclusion Cyst in Conjunctival Melanoma
    (2016) Esposito, E; Zoroquiain Vélez, José Pablo; Mastromonaco, C.; Morales, M.; Neto, R.; Burnier, M.
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    Inhibition of the angiotensin-converting enzyme decreases skeletal muscle fibrosis in dystrophic mice by a diminution in the expression and activity of connective tissue growth factor (CTGF/CCN-2)
    (2013) Morales, M.; Cabrera García, Daniel Alejandro; Céspedes Fierro, Carlos Mauricio.; Vio Lagos, Carlos P.
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    Preschoolers with recurrent wheezing have a high prevalence of sleep disordered breathing
    (2020) Rivera, N.; Flores, Juan Carlos; Morales, M.; Padilla Pérez, Oslando; Causade, S.; Brockmann Veloso, Pablo Edmundo; Castro Rodríguez, José Antonio
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    Regiones polimórficas del gen 11β-hidroxiesteroide deshidrogenasa tipo 1 (11βHSD1) en hipertensión arterial esencial: Posible rol etiopatogénico
    (2008) Morales, M.; Carvajal, C.; Ortiz, E.; Mosso, L.; Artigas, R.; Fardella, C.; Owen, G.; Morales, M.; Fardella, C.
    Background: Cortisol has been implicated in hypertension and lately reported to be regulated at the pre-receptor level by the 11βHSD1 enzyme, which converts cortisone (E) to cortisol (F). Over expression of this enzyme in adipose tissue could determine an increase in available cortisol that interacts with the mineralocorticoid receptor (MR) in renal, brain and heart tissue, leading to similar hypertensive effects as in 11βHSD2 impaired patients. Several polymorphisms have been reported in HSD11B1 gene (CA15, CA19 and InsA83557), which could modify HSD11B1 gene expression or activity. Aim: To determine the distribution and prevalence of CA15, CA19 and InsA83557 in the HSD11B1 gene, and to correlate these results with biochemical parameters in cortisol/ACTH (HPA) and renin-angiotensin-aldosterone (RAA) axis in patients with essential hypertension (EH). Patients and Methods: We studied 113 EH patients (76 non-obese and 37 obese, with a body mass index >30 kg/m 2) and 30 normotensive adults (NT). In each patient, we measured serum levels of F, E, serum aldosterone (SA), plasma renin activity (PRA), adrenocorticotrophic hormone (ACTH), the urinary free cortisol/creatinine (UFF/Cr), F/ACTH and SA/PRA ratios. Each polymorphism was studied by PCR and 8% polyacrylamide gel electrophoresis. Statistical associations were evaluated by Pearson correlations and the genetic equilibrium by the Hardy-Weinberg (H-W) equation. Results: We found all three polymorphisms in the EH and the NT group, both in genetic equilibrium. In obese essential hypertensives, the CA15 polymorphism showed association with SA/PRA ratio (r =0.189, p =0.012) and F/ACTH (r =0.301, p 0.048); CA19 also showed correlation with F/ACTH in obese EH (r =-0.220, p 0.009). The InsA83557 polymorphism correlated with UFF/Cr in both EH (r =0.206; p =0.03), and in obese EH (r =0.354; p =0.05). Conclusions: The CA15 and CA19 polymorphism correlated with changes in biochemical parameters in HPA and RAA axis of obese essential hypertensives. These changes may result of modifications in the expression of 11βHSD1, leading to increased cortisol and aldosterone levels independent of ACTH and renin control, respectively.
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    Urinary leukotriene and Bcl I polymorphism of glucocorticoid receptor gene in preschoolers with recurrent wheezing and high risk of asthma
    (2016) Morales, M.; Flores, C.; Pino, Karla; Angulo, J.; López Lastra, Marcelo Andrés; Castro Rodríguez, José Antonio

Bibliotecas - Pontificia Universidad Católica de Chile- Dirección oficinas centrales: Av. Vicuña Mackenna 4860. Santiago de Chile.

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