11 results on '"Pérez-Mayorga M"'
Search Results
2. Comparison of plasma pigment epithelium-derived factor (PEDF), retinol binding protein 4 (RBP-4), chitinase-3-like protein 1 (YKL-40) and brain-derived neurotrophic factor (BDNF) for the identification of insulin resistance
- Author
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Toloza, F.J.K., primary, Pérez-Matos, M.C., additional, Ricardo-Silgado, M.L., additional, Morales-Álvarez, M.C., additional, Mantilla-Rivas, J.O., additional, Pinzón-Cortés, J.A., additional, Pérez-Mayorga, M., additional, Arévalo-García, M.L., additional, Tolosa-González, G., additional, and Mendivil, C.O., additional
- Published
- 2017
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3. Relationship between fish community and riparian vegetation cover in two hydrological periods (Coffee-growing region, Colombia) | Relación entre comunidad íctica y cobertura vegetal riparia en dos períodos hidrológicos (Eje Cafetero, Colombia)
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Pérez-Mayorga, M. A. and Saúl Prada-Pedreros
4. METADATO DE LA COLECCIÓN DE PECES DEL MUSEO JAVERIANO DE HISTORIA NATURAL LORENZO URIBE, S.J.
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Pérez Mayorga, M. A.; Laboratorio de Ictiología Unidad de Ecología y Sistemática (UNESIS) Departamento de Biología Facultad de Ciencias Pontificia Universidad Javeriana, Bogotá, Prada Pedreros, Saúl; Laboratorio de Ictiología Unidad de Ecología y Sistemática (UNESIS) Departamento de Biología Facultad de Ciencias Pontificia Universidad Javeriana, Bogotá, Pérez Mayorga, M. A.; Laboratorio de Ictiología Unidad de Ecología y Sistemática (UNESIS) Departamento de Biología Facultad de Ciencias Pontificia Universidad Javeriana, Bogotá, and Prada Pedreros, Saúl; Laboratorio de Ictiología Unidad de Ecología y Sistemática (UNESIS) Departamento de Biología Facultad de Ciencias Pontificia Universidad Javeriana, Bogotá
5. METADATO DE LA COLECCIÓN DE PECES DEL MUSEO JAVERIANO DE HISTORIA NATURAL LORENZO URIBE, S.J.
- Author
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Pérez Mayorga, M. A.; Laboratorio de Ictiología Unidad de Ecología y Sistemática (UNESIS) Departamento de Biología Facultad de Ciencias Pontificia Universidad Javeriana, Bogotá, Prada Pedreros, Saúl; Laboratorio de Ictiología Unidad de Ecología y Sistemática (UNESIS) Departamento de Biología Facultad de Ciencias Pontificia Universidad Javeriana, Bogotá, Pérez Mayorga, M. A.; Laboratorio de Ictiología Unidad de Ecología y Sistemática (UNESIS) Departamento de Biología Facultad de Ciencias Pontificia Universidad Javeriana, Bogotá, and Prada Pedreros, Saúl; Laboratorio de Ictiología Unidad de Ecología y Sistemática (UNESIS) Departamento de Biología Facultad de Ciencias Pontificia Universidad Javeriana, Bogotá
6. METADATO DE LA COLECCIÓN DE PECES DEL MUSEO JAVERIANO DE HISTORIA NATURAL LORENZO URIBE, S.J.
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Pérez Mayorga, M. A.; Laboratorio de Ictiología Unidad de Ecología y Sistemática (UNESIS) Departamento de Biología Facultad de Ciencias Pontificia Universidad Javeriana, Bogotá, Prada Pedreros, Saúl; Laboratorio de Ictiología Unidad de Ecología y Sistemática (UNESIS) Departamento de Biología Facultad de Ciencias Pontificia Universidad Javeriana, Bogotá, Pérez Mayorga, M. A.; Laboratorio de Ictiología Unidad de Ecología y Sistemática (UNESIS) Departamento de Biología Facultad de Ciencias Pontificia Universidad Javeriana, Bogotá, and Prada Pedreros, Saúl; Laboratorio de Ictiología Unidad de Ecología y Sistemática (UNESIS) Departamento de Biología Facultad de Ciencias Pontificia Universidad Javeriana, Bogotá
- Abstract
Gran parte de la información sobre biodiversidad se encuentra contenida en catálogos de Colecciones Biológicas. Con el objetivo de aumentar la divulgación de información surge la necesidad de buscar medios que permitan el intercambio de estos conjuntos de datos. El metadato de la base de datos de la Colección de Peces del Museo Javeriano de Historia Natural “Lorenzo Uribe, S.J.”, contribuye al conocimiento sobre la biodiversidad de peces de Colombia, constituyéndose en el cuarto metadato publicado sobre el tema para el país. Para su elaboración se realizó la digitación de la información contenida en el catálogo en una base de datos Access; la revisión del estándar de metadatos propuesto por el Sistema de Información sobre Biodiversidad de Colombia (SIB) y la utilización de la aplicación Multistandard, Multilingual, Metadata Cataloguing Tool (M3Cat) a través de un explorador web. Este metadato estará disponible para su consulta en la página Web del SIB.
7. Genetic variants in triglyceride metabolism genes among individuals with hypertriglyceridemia in Colombia.
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Puerto-Baracaldo K, Amaya-Montoya M, Parra-Serrano G, Prada-Robles DC, Serrano-Gómez S, Restrepo-Giraldo LM, Fragozo-Ramos MC, Tangarife V, Giraldo-González GC, Builes-Barrera CA, Naranjo-Vanegas MS, Gómez-Aldana A, Llano JP, Gil-Ochoa N, Nieves-Barreto LD, Gaete PV, Pérez-Mayorga M, and Mendivil CO
- Abstract
Background: The genetic substrate of severe hypertriglyceridemia (sHTG) in Latin America is insufficiently understood., Objective: To identify genetic variants in genes related to triglyceride (TG) metabolism among adults with sHTG from Colombia., Methods: In individuals with plasma TG≥880 mg/dL at least once in their lifetime, we amplified and sequenced all exons and intron/exon boundaries of the genes LPL, APOC2, APOA5, GPIHBP1 and LMF1. For each variant we ascertained its location, zygosity, allelic frequency and pathogenicity classification according to American College of Medical Genetics (ACMG) criteria., Results: The study included 166 participants (62 % male, mean age 50), peak TG levels ranged between 894 and 11,000 mg/dL. We identified 92 variants: 19 in LPL, 7 in APOC2, 11 in GPIHBP1, 38 in LMF1, and 17 in APOA5. Eighteen of these variants had not been reported. We identified a new pathogenic variant in LMF1 (c.41C>A; p.Ser14*), a new likely pathogenic variant in LMF1 (c.1527 C > T; p.Pro509=, also expressed as c.1447C>T; p.Gln483*), and a known pathogenic variant in LMF1 (c.779G>A; p.Trp260*). Four participants were heterozygous for variant c.953A>G; p.Asn318Ser in LPL, a known risk factor for hypertriglyceridemia. Participants with variants of unknown significance (VUS) in LMF1 had significantly higher peak TG than those with VUS in other genes. Peak TG were 4317 mg/dL in participants with a history of pancreatitis, and 1769 mg/dL in those without it (p = 0.001)., Conclusion: Our study identified variants associated with sHTG among Latinos, and showed that genetic variation in LMF1 may be frequently associated with sHTG in this population., Competing Interests: Declaration of competing interest This study was funded by PTC Therapeutics through an investigator-initiated grant, but the sponsor had no incidence in the design or execution of the study, or on the decision to publish., (Copyright © 2024. Published by Elsevier Inc.)
- Published
- 2024
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8. A randomized clinical trial of lipid metabolism modulation with fenofibrate for acute coronavirus disease 2019.
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Chirinos JA, Lopez-Jaramillo P, Giamarellos-Bourboulis EJ, Dávila-Del-Carpio GH, Bizri AR, Andrade-Villanueva JF, Salman O, Cure-Cure C, Rosado-Santander NR, Cornejo Giraldo MP, González-Hernández LA, Moghnieh R, Angeliki R, Cruz Saldarriaga ME, Pariona M, Medina C, Dimitroulis I, Vlachopoulos C, Gutierrez C, Rodriguez-Mori JE, Gomez-Laiton E, Cotrina Pereyra R, Ravelo Hernández JL, Arbañil H, Accini-Mendoza J, Pérez-Mayorga M, Milionis C, Poulakou G, Sánchez G, Valdivia-Vega R, Villavicencio-Carranza M, Ayala-García RJ, Castro-Callirgos CA, Alfaro Carrasco RM, Garrido Lecca Danos W, Sharkoski T, Greene K, Pourmussa B, Greczylo C, Ortega-Legaspi J, Jacoby D, Chittams J, Katsaounou P, Alexiou Z, Sympardi S, Sweitzer NK, Putt M, and Cohen JB
- Subjects
- Humans, Female, Adult, Middle Aged, Aged, Male, SARS-CoV-2, Lipid Metabolism, PPAR alpha, COVID-19, Fenofibrate therapeutic use
- Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) cytotoxicity may involve inhibition of peroxisome proliferator-activated receptor alpha. Fenofibrate activates peroxisome proliferator-activated receptor alpha and inhibits SARS-CoV-2 replication in vitro. Whether fenofibrate can be used to treat coronavirus disease 2019 (COVID-19) infection in humans remains unknown. Here, we randomly assigned inpatients and outpatients with COVID-19 within 14 d of symptom onset to 145 mg of oral fenofibrate nanocrystal formulation versus placebo for 10 d, in a double-blinded fashion. The primary endpoint was a severity score whereby participants were ranked across hierarchical tiers incorporating time to death, mechanical ventilation duration, oxygenation, hospitalization and symptom severity and duration. In total, 701 participants were randomized to fenofibrate (n = 351) or placebo (n = 350). The mean age of participants was 49 ± 16 years, 330 (47%) were female, mean body mass index was 28 ± 6 kg/m
2 and 102 (15%) had diabetes. Death occurred in 41 participants. Compared with placebo, fenofibrate had no effect on the primary endpoint. The median (interquartile range) rank in the placebo arm was 347 (172, 453) versus 345 (175, 453) in the fenofibrate arm (P = 0.819). There was no difference in secondary and exploratory endpoints, including all-cause death, across arms. There were 61 (17%) adverse events in the placebo arm compared with 46 (13%) in the fenofibrate arm, with slightly higher incidence of gastrointestinal side effects in the fenofibrate group. Overall, among patients with COVID-19, fenofibrate has no significant effect on various clinically relevant outcomes ( NCT04517396 )., (© 2022. The Author(s), under exclusive licence to Springer Nature Limited.)- Published
- 2022
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9. A Randomized Trial of Lipid Metabolism Modulation with Fenofibrate for Acute Coronavirus Disease 2019.
- Author
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Chirinos J, Lopez-Jaramillo P, Giamarellos-Bourboulis E, Dávila-Del-Carpio G, Bizri A, Andrade-Villanueva J, Salman O, Cure-Cure C, Rosado-Santander N, Giraldo MC, González-Hernández L, Moghnieh R, Angeliki R, Saldarriaga MC, Pariona M, Medina C, Dimitroulis I, Vlachopoulos C, Gutierrez C, Rodriguez-Mori J, Gomez-Laiton E, Pereyra R, Hernández JR, Arbañil H, Accini-Mendoza J, Pérez-Mayorga M, Milionis H, Poulakou G, Sánchez G, Valdivia-Vega R, Villavicencio-Carranza M, Ayala-Garcia R, Castro-Callirgos C, Carrasco RA, Danos WL, Sharkoski T, Greene K, Pourmussa B, Greczylo C, Chittams J, Katsaounou P, Alexiou Z, Sympardi S, Sweitzer N, Putt M, and Cohen J
- Abstract
Background Abnormal cellular lipid metabolism appears to underlie SARS-CoV-2 cytotoxicity and may involve inhibition of peroxisome proliferator activated receptor alpha (PPARα). Fenofibrate, a PPAR-α activator, modulates cellular lipid metabolism. Fenofibric acid has also been shown to affect the dimerization of angiotensin-converting enzyme 2, the cellular receptor for SARS-CoV-2. Fenofibrate and fenofibric acid have been shown to inhibit SARS-CoV-2 replication in cell culture systems in vitro . Methods We randomly assigned 701 participants with COVID-19 within 14 days of symptom onset to 145 mg of fenofibrate (nanocrystal formulation with dose adjustment for renal function or dose-equivalent preparations of micronized fenofibrate or fenofibric acid) vs. placebo for 10 days, in a double-blinded fashion. The primary endpoint was a ranked severity score in which participants were ranked across hierarchical tiers incorporating time to death, duration of mechanical ventilation, oxygenation parameters, subsequent hospitalizations and symptom severity and duration. ClinicalTrials.gov registration: NCT04517396. Findings: Mean age of participants was 49 ± 16 years, 330 (47%) were female, mean BMI was 28 ± 6 kg/m
2 , and 102 (15%) had diabetes mellitus. A total of 41 deaths occurred. Compared with placebo, fenofibrate administration had no effect on the primary endpoint. The median (interquartile range [IQR]) rank in the placebo arm was 347 (172, 453) vs. 345 (175, 453) in the fenofibrate arm (P = 0.819). There was no difference in various secondary and exploratory endpoints, including all-cause death, across randomization arms. These results were highly consistent across pre-specified sensitivity and subgroup analyses. Conclusion Among patients with COVID-19, fenofibrate has no significant effect on various clinically relevant outcomes.- Published
- 2022
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10. Insulin Resistance Markers to Detect Nonalcoholic Fatty Liver Disease in a Male Hispanic Population.
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Pérez-Mayorga M, Lopez-Lopez JP, Chacon-Manosalva MA, Castillo MG, Otero J, Martinez-Bello D, Gomez-Arbelaez D, Cohen DD, and Lopez-Jaramillo P
- Subjects
- Adult, Biomarkers, Cross-Sectional Studies, Glucose, Hispanic or Latino, Humans, Insulin, Male, Middle Aged, Triglycerides, Insulin Resistance, Non-alcoholic Fatty Liver Disease diagnosis
- Abstract
Background: Nonalcoholic fatty liver disease (NAFLD) is one of the leading causes of chronic liver disease and is closely associated with cardiometabolic disorders, being insulin resistance (IR) the common pathogenic mechanism. The triglycerides/glucose (TyG) index and triglycerides/HDL-c (TG/HDL) ratio are markers correlated with IR. We compared the capacity of these two indexes, alongside IR, to detect NAFLD., Methods: In a cross-sectional cohort study, we examined 263 active military personnel from the Colombian Air Force, aged between 29 and 54 years. Anthropometric measurements and biochemical determinations (glycemia, lipid profile, and insulin) were obtained, and ultrasound studies were performed to evaluate the presence of NAFLD. HOMA-IR index was calculated as (fasting insulin ( µ IU/mL) × fasting glucose (mmol/L)/22.5), the TyG index as Ln (triglycerides (mg/dL) × fasting glucose (mg/dL)/2), and the TG/HDL ratio as (triglycerides (mg/dL)/HDL-c (mg/dL))., Results: NAFLD ultrasound criteria were met in 70 individuals (26.6%). Subjects with NAFLD had significantly higher values of HOMA-IR (2.55 ± 1.36 vs. 1.51 ± 0.91), TyG (9.17 ± 0.53 vs. 8.7 ± 0.51), and TG/HDL (6.6 ± 4.54 vs. 3.52 ± 2.32) compared to those without NAFLD ( p < 0.001). A TyG cutoff point of 8.92 showed an AUC of 0.731, while cutoff points of 3.83 for TG/HDL and 1.68 for HOMA-IR showed an AUC of 0.766 and 0.781, respectively., Conclusion: Our study shows that novel and lower-cost markers of IR are useful for detecting NALFD, with a performance comparable to the HOMA-IR index. These markers should be used as the first step when screening patients for NAFLD., Competing Interests: The authors declare that there are no conflicts of interest., (Copyright © 2022 Maritza Pérez-Mayorga et al.)
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- 2022
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11. Plasma Levels of Myonectin But Not Myostatin or Fibroblast-Derived Growth Factor 21 Are Associated with Insulin Resistance in Adult Humans without Diabetes Mellitus.
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Toloza FJK, Mantilla-Rivas JO, Pérez-Matos MC, Ricardo-Silgado ML, Morales-Alvarez MC, Pinzón-Cortés JA, Pérez-Mayorga M, Arévalo-Garcia ML, Tolosa-González G, and Mendivil CO
- Abstract
Background: Myokines are a group of protein mediators produced by skeletal muscle under stress or physical exertion. Even though their discovery and effects in cell culture and animal models of disease have elicited great enthusiasm, very little is known about their role in human metabolism. We assessed whether plasma concentrations of three known myokines [myonectin, myostatin, and fibroblast-derived growth factor 21 (FGF-21)] would be associated with direct and indirect indicators of insulin resistance (IR) in individuals who did not have a diagnosis of diabetes., Methods: We studied 81 adults of both sexes comprising a wide range of body adiposity and insulin sensitivity. All participants underwent a thorough clinical assessment and a 5-point oral glucose tolerance test with calculation of multiple IR and insulin sensitivity indices. Twenty-one of them additionally underwent a hyperinsulinemic-euglycemic clamp with determination of steady-state whole-body insulin-stimulated glucose disposal ("M"). We compared plasma myokine concentrations across quartiles of IR indices and clinical IR surrogates, and explored the correlation of each myokine with the M -value., Results: Plasma myonectin levels increased monotonically across quartiles of the incremental area under the insulin curve (higher values indicate more IR) ( p -trend = 0.021) and decreased monotonically across quartiles of the insulin sensitivity index (ISI - higher values indicate less IR) ( p -trend = 0.012). After multivariate adjustment for other relevant determinants of IR (body mass index, age, and sex), the negative association of myonectin with ISI persisted (standardized beta = -0.235, p = 0.023). Myostatin was not associated with any clinical IR indicator or direct IR index measure. In multivariate analyses, FGF-21 showed a trend toward a positive correlation with glucose disposal that did not reach statistical significance (standardized beta = 0.476, p = 0.091)., Conclusion: The secretion of myonectin may constitute an attempt at a compensatory mechanism against IR in humans.
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- 2018
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