Search

Your search keyword '"Navarro, Alfonso"' showing total 481 results
Start Over Author "Navarro, Alfonso"
481 results on '"Navarro, Alfonso"'

2. Multiple beta cell-independent mechanisms drive hypoglycemia in Timothy syndrome

Author

Matsui, Maiko, Lynch, Lauren E., Distefano, Isabella, Galante, Allison, Gade, Aravind R., Wang, Hong-Gang, Gómez-Banoy, Nicolas, Towers, Patrick, Sinden, Daniel S., Wei, Eric Q., Barnett, Adam S., Johnson, Kenneth, Lima, Renan, Rubio-Navarro, Alfonso, Li, Ang K., Marx, Steven O., McGraw, Timothy E., Thornton, Paul S., Timothy, Katherine W., Lo, James C., and Pitt, Geoffrey S.

Published
2024
Full Text
View/download PDF

4. A beta cell subset with enhanced insulin secretion and glucose metabolism is reduced in type 2 diabetes.

Author

Rubio-Navarro, Alfonso, Gómez-Banoy, Nicolás, Stoll, Lisa, Dündar, Friederike, Mawla, Alex, Ma, Lunkun, Cortada, Eric, Zumbo, Paul, Li, Ang, Reiterer, Moritz, Montoya-Oviedo, Nathalia, Homan, Edwin, Imai, Norihiro, Gilani, Ankit, Liu, Chengyang, Naji, Ali, Yang, Boris, Chong, Angie, Cohen, David, Chen, Shuibing, Cao, Jingli, Pitt, Geoffrey, Betel, Doron, Lo, James, and Huising, Mark

Subjects
Humans, Mice, Animals, Diabetes Mellitus, Type 2, Insulin Secretion, Insulin, Diabetes Mellitus, Experimental, Insulin-Secreting Cells, Glucose
Abstract

The pancreatic islets are composed of discrete hormone-producing cells that orchestrate systemic glucose homeostasis. Here we identify subsets of beta cells using a single-cell transcriptomic approach. One subset of beta cells marked by high CD63 expression is enriched for the expression of mitochondrial metabolism genes and exhibits higher mitochondrial respiration compared with CD63lo beta cells. Human and murine pseudo-islets derived from CD63hi beta cells demonstrate enhanced glucose-stimulated insulin secretion compared with pseudo-islets from CD63lo beta cells. We show that CD63hi beta cells are diminished in mouse models of and in humans with type 2 diabetes. Finally, transplantation of pseudo-islets generated from CD63hi but not CD63lo beta cells into diabetic mice restores glucose homeostasis. These findings suggest that loss of a specific subset of beta cells may lead to diabetes. Strategies to reconstitute or maintain CD63hi beta cells may represent a potential anti-diabetic therapy.

Published
2023

13. Phase 2 Clinical Trial of Infusing Haploidentical K562-mb15-41BBL–Activated and Expanded Natural Killer Cells as Consolidation Therapy for Pediatric Acute Myeloblastic Leukemia

Author

Gómez García, Lara Maria, Escudero, Adela, Mestre, Carmen, Fuster Soler, Jose L., Martínez, Antonia Pascual, Vagace Valero, Jose M., Vela, María, Ruz, Beatriz, Navarro, Alfonso, Fernández, Lucia, Fernández, Adrián, Leivas, Alejandra, Martínez-López, Joaquin, Ferreras, Cristina, De Paz, Raquel, Blanquer, Miguel, Galán, Victor, González, Berta, Corral, Dolores, Sisinni, Luisa, Mirones, Isabel, Balas, Antonio, Vicario, José Luis, Valle, Paula, Borobia, Alberto M., and Pérez-Martínez, Antonio

Published
2021
Full Text
View/download PDF

14. Population Pharmacokinetic–Pharmacodynamic Analysis of a Reserpine-Induced Myalgia Model in Rats.

Author

Alfosea-Cuadrado, Gloria M., Zarzoso-Foj, Javier, Adell, Albert, Valverde-Navarro, Alfonso A., González-Soler, Eva M., Mangas-Sanjuán, Víctor, and Blasco-Serra, Arantxa

Subjects
LABORATORY rats, RESERPINE, CHRONIC pain, PREFRONTAL cortex, SPINAL cord
Abstract

(1) Background: Fibromyalgia syndrome (FMS) is a chronic pain condition with widespread pain and multiple comorbidities, for which conventional therapies offer limited benefits. The reserpine-induced myalgia (RIM) model is an efficient animal model of FMS in rodents. This study aimed to develop a pharmacokinetic–pharmacodynamic (PK–PD) model of reserpine in rats, linking to its impact on monoamines (MAs). (2) Methods: Reserpine was administered daily for three consecutive days at dose levels of 0.1, 0.5, and 1 mg/kg. A total of 120 rats were included, and 120 PK and 828 PD observations were collected from 48 to 96 h after the first dose of reserpine. Non-linear mixed-effect data analysis was applied for structural PK–PD model definition, variability characterization, and covariate analysis. (3) Results: A one-compartment model best described reserpine in rats (V = 1.3 mL/kg and CL = 4.5 × 10−1 mL/h/kg). A precursor-pool PK–PD model (kin = 6.1 × 10−3 mg/h, kp = 8.6 × 10−4 h−1 and kout = 2.7 × 10−2 h−1) with a parallel transit chain (k0 = 1.9 × 10−1 h−1) characterized the longitudinal levels of MA in the prefrontal cortex, spinal cord, and amygdala in rats. Reserpine stimulates the degradation of MA from the pool compartment (Slope1 = 1.1 × 10−1 h) and the elimination of MA (Slope2 = 1.25 h) through the transit chain. Regarding the reference dose (1 mg/kg) of the RIM model, the administration of 4 mg/kg would lead to a mean reduction of 65% (Cmax), 80% (Cmin), and 70% (AUC) of MA across the brain regions tested. (4) Conclusions: Regional brain variations in neurotransmitter depletion were identified, particularly in the amygdala, offering insights for therapeutic strategies and biomarker identification in FMS research. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

22. Adipsin preserves beta cells in diabetic mice and associates with protection from type 2 diabetes in humans

Author

Gómez-Banoy, Nicolás, Guseh, J. Sawalla, Li, Ge, Rubio-Navarro, Alfonso, Chen, Tong, Poirier, BreAnne, and Putzel, Gregory

Subjects
Pancreatic beta cells -- Research, Insulin -- Usage, Type 2 diabetes -- Complications and side effects -- Care and treatment, Hyperglycemia -- Risk factors, Biological sciences, Health
Abstract

Type 2 diabetes is characterized by insulin resistance and a gradual loss of pancreatic beta cell mass and function.sup.1,2. Currently, there are no therapies proven to prevent beta cell loss and some, namely insulin secretagogues, have been linked to accelerated beta cell failure, thereby limiting their use in type 2 diabetes.sup.3,4. The adipokine adipsin/complement factor D controls the alternative complement pathway and generation of complement component C3a, which acts to augment beta cell insulin secretion.sup.5. In contrast to other insulin secretagogues, we show that chronic replenishment of adipsin in diabetic db/db mice ameliorates hyperglycemia and increases insulin levels while preserving beta cells by blocking dedifferentiation and death. Mechanistically, we find that adipsin/C3a decreases the phosphatase Dusp26; forced expression of Dusp26 in beta cells decreases expression of core beta cell identity genes and sensitizes to cell death. In contrast, pharmacological inhibition of DUSP26 improves hyperglycemia in diabetic mice and protects human islet cells from cell death. Pertaining to human health, we show that higher concentrations of circulating adipsin are associated with a significantly lower risk of developing future diabetes among middle-aged adults after adjusting for body mass index (BMI). Collectively, these data suggest that adipsin/C3a and DUSP26-directed therapies may represent a novel approach to achieve beta cell health to treat and prevent type 2 diabetes. Targeting the adipokine adipsin and its downstream pathway may provide an approach for preservation of beta cell loss in type 2 diabetes., Author(s): Nicolás Gómez-Banoy [sup.1] , J. Sawalla Guseh [sup.2] , Ge Li [sup.3] , Alfonso Rubio-Navarro [sup.1] , Tong Chen [sup.1] , BreAnne Poirier [sup.1] , Gregory Putzel [sup.4] , [...]

Published
2019
Full Text
View/download PDF

31. Cross-species single-cell comparison of systemic and cardiac inflammatory responses after cardiac injury

Author

Cortada, Eric, primary, Yao, Jun, additional, Xia, Yu, additional, Dundar, Friederike, additional, Zumbo, Paul, additional, Yang, Boris, additional, Rubio-Navarro, Alfonso, additional, Perder, Bjorn, additional, Qiu, Miaoyan, additional, Pettinato, Anthony M, additional, Homan, Edwin A, additional, Stoll, Lisa, additional, Betel, Doron, additional, Cao, Jingli, additional, and Lo, James, additional

Published
2023
Full Text
View/download PDF

33. Familial CD45RA– T cells to treat severe refractory infections in immunocompromised patients

Author

Al-Akioui Sanz, Karima, primary, Echecopar Parente, Carlos, additional, Ferreras, Cristina, additional, Menéndez Ribes, Marta, additional, Navarro, Alfonso, additional, Mestre, Carmen, additional, Clares, Laura, additional, Vicario, José Luis, additional, Balas, Antonio, additional, De Paz, Raquel, additional, López Granados, Eduardo, additional, Sánchez Zapardiel, Elena, additional, Jiménez, Carlos, additional, López-Oliva, María, additional, Ramos, Esther, additional, Hernández-Oliveros, Francisco, additional, and Pérez-Martínez, Antonio, additional

Published
2023
Full Text
View/download PDF

38. Extracellular vesicles of human diabetic retinopathy retinal tissue and urine of diabetic retinopathy patients are enriched for the junction plakoglo bin protein

Author

Mighty, Jason, primary, Rubio-Navarro, Alfonso, additional, Shi, Cui, additional, Zhou, Jing, additional, Flores-Bellver, Miguel, additional, Heissel, Søren, additional, Onwumere, Onyekwere, additional, Einbond, Linda, additional, Gharbaran, Rajendra, additional, Casper, Daniel S., additional, Benito-Martin, Alberto, additional, and Redenti, Stephen, additional

Published
2023
Full Text
View/download PDF

39. TWEAK/Fn14 System is Involved in Rhabdomyolysis-Induced Acute Kidney Injury

Author

Guerrero-Hue, Melania, primary, Vallejo-Mudarra, Mercedes, additional, García-Caballero, Cristina, additional, Córdoba, Gina Marcela, additional, Palomino-Antolín, Alejandra, additional, Herencia, Carmen, additional, Vendrell-Casana, Beatriz, additional, Rubio-Navarro, Alfonso, additional, Egido, Jesús, additional, Blanco-Colio, Luis, additional, and Moreno, Juan Antonio, additional

Published
2023
Full Text
View/download PDF

45. Podocytes are new cellular targets of haemoglobin‐mediated renal damage

Author

Rubio‐Navarro, Alfonso, Sanchez‐Niño, Maria Dolores, Guerrero‐Hue, Melania, García‐Caballero, Cristina, Gutiérrez, Eduardo, Yuste, Claudia, Sevillano, Ángel, Praga, Manuel, Egea, Javier, Román, Elena, Cannata, Pablo, Ortega, Rosa, Cortegano, Isabel, de Andrés, Belén, Gaspar, María Luisa, Cadenas, Susana, Ortiz, Alberto, Egido, Jesús, and Moreno, Juan Antonio

Published
2018
Full Text
View/download PDF

46. Haematuria as a risk factor for chronic kidney disease progression in glomerular diseases: A review

Author

Moreno, Juan Antonio, Yuste, Claudia, Gutierrez, Eduardo, Sevillano, Ángel M., Rubio-Navarro, Alfonso, Amaro-Villalobos, Juan Manuel, Praga, Manuel, and Egido, Jesús

Subjects
Preventive medicine -- Research, Hematuria -- Research -- Development and progression -- Care and treatment -- Complications and side effects, Health
Abstract

Haematuria has long been considered to be a benign condition associated with glomerular diseases. However, new evidences suggest that haematuria has a pathogenic role in promoting kidney disease progression. An increased risk for end-stage renal disease has been reported in adolescents and young adults with persistent microscopic haematuria. A persistent impairment of renal function has been also reported following macroscopic haematuria-associated acute kidney injury in immunoglobulin A nephropathy. Haematuria-induced renal damage has been related to oxidant, cytotoxic and inflammatory effects induced by haemoglobin or haem released from red blood cells. The pathophysiological origin of haematuria may be due to a more fragile and easily ruptured glomerular filtration barrier, as reported in several glomerular diseases. In this review we describe a number of the key issues associated with the epidemiology and pathogenesis of haematuria-associated diseases, provide an update of recent knowledge on the role of haematuria on renal function outcome and discuss specific therapeutic approaches in this setting. Key summary points Glomerular haematuria is a common observation in a number of renal diseases that may lead to persistent renal injury. Haematuria in children differs from that in adults in specific aspects, particularly in the frequency of glomerular diseases and renal disease outcome. Regular follow-up of renal function in children with isolated microhaematuria may be recommended., Author(s): Juan Antonio Moreno[sup.1] , Claudia Yuste[sup.2] , Eduardo Gutierrez[sup.3] , Ángel M. Sevillano[sup.3] , Alfonso Rubio-Navarro[sup.1] , Juan Manuel Amaro-Villalobos[sup.1] , Manuel Praga[sup.3] , Jesús Egido[sup.1] [sup.4] Author Affiliations: [...]

Published
2016
Full Text
View/download PDF

47. Nuevo índice aterogénico para la predicción de aterosclerosis carotídea basado en la ratio proteína Creactiva no ultrasensible/HDL

Author

Fabregat-Andrés, Óscar, Pérez-de-Lucía, Pilar, Vallejo-García, Victor E., Vera-Ivars, Pablo, Valverde-Navarro, Alfonso A., and Tormos, José María

Abstract

La valoración del riesgo cardiovascular aparece en las guías clínicas como medida de prevención de enfermedades cardiovasculares, cuya etiología fundamental es la arteriosclerosis. Una de las herramientas que se utiliza para estimar el riesgo en práctica clínica son los índices aterogénicos (IA), cocientes entre fracciones lipídicas con rangos de referencia bien establecidos. A pesar de su uso extendido, existe todavía información limitada sobre su utilidad clínica. En los últimos años, algunas investigaciones han reforzado el papel de la inflamación en la etiología y cronicidad del proceso aterosclerótico. La inclusión de parámetros inflamatorios en el cálculo de IA podría mejorar su rendimiento diagnóstico en la detección de arteriosclerosis. Nos propusimos evaluar un nuevo IA en forma de ratio entre los valores de proteína C reactiva (PCR) no ultrasensible y las cifras de colesterol unido a lipoproteínas de alta densidad (HDL).

Published
2024
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results