Dra. Cecilia Grierson, ejemplo luchadora y militante feminista

Fil: Prado, Natalia Jorgelina. Universidad Nacional de Cuyo. Facultad de Ciencias MédicasFil: Diez, Emiliano Raúl. Universidad Nacional de Cuyo. Facultad de Ciencias Médica

Las médicas descalzas : comprometidas y picantes que ocupen las alpargatas rojas para servir al pueblo

Fil: Diez, Emiliano Raúl. Universidad Nacional de Cuyo. Facultad de Ciencias MédicasFil: Prado, Natalia Jorgelina. Universidad Nacional de Cuyo. Facultad de Ciencias Médica

Melatonin for a Healthy Heart Rhythm

Melatonin is a promising cardioprotective agent. Its increase during the night is associated with healthy cardiovascular function. On the other hand, reduced levels of melatonin are related to diseases. Aging and chronodisruptors reduce melatonin levels. Pharmacological supplementation reduces the deleterious effects of cardiovascular risk factors and improves the myocardial response to ischemia/reperfusion injury and other proarrhythmic conditions. The protective mechanisms of melatonin involve its antioxidant properties as well as receptor-mediated actions. Signaling pathways include membrane responses, cytoplasmic modulation of kinases, nuclear receptor interactions, and improvement of mitochondrial functions. This chapter focuses on the electrophysiological and the antiarrhythmic properties of melatonin. The acute and chronic protective mechanisms of melatonin will be analyzed with an emphasis on transmembrane potentials and intercellular communication. An outstanding antifibrillatory effect makes melatonin a novel antiarrhythmic agent worthy of further exploration in the path to clinical applications

Efecto del poscondicionamiento isquémico sobre las arritmias de reperfusión en un modelo de hipertrofia miocárdica

Introducción El poscondicionamiento isquémico (PCI) es una estrategia cardioprotectora con propiedades antiarrítmicas. La hipertrofia cardíaca secundaria a hipertensión arterial se aumenta el riesgo de sufrir arritmias y, además, reduce la respuesta a algunos tratamientos. Objetivo Determinar si el efecto antiarrítmico del PCI se mantenía en corazones hipertróficos. Métodos Los corazones aislados de ratas Wistar Kyoto (WKY) y de ratas espontáneamente hipertensas (SHR) de la misma edad, fueron perfundidos según la técnica de Langendorff y sometidos a 15 min de isquemia regional. Al momento de la reperfusión se dividieron en: a) WKY, b) WKY-PCI, c) SHR, d) SHR-PCI (n=13 por grupo). El PCI consistió en 3 ciclos de 30 seg de reperfusión y 30 seg de isquemia. Se clasificaron las arritmias ventriculares observadas en el ECG. Se estimó la hipertrofia por el peso cardíaco relativo. Resultados La hipertensión arterial en las ratas SHR provocó hipertrofia miocárdica. Todos los corazones sufrieron una alta incidencia de fibrilación ventricular (SHR 92.3% y WKY 77%, ns). El PCI restituyó el ritmo sinusal en los corazones de las ratas normotensas (WKY-PCI 61,5% vs WKY 23,1%, p=0,0236 por test del χ2) y en los de las SHR (SHR-PCI 69,2% vs SHR 15,4%, p=0,0016 test del χ2). Conclusión El PCI es capaz de restituir a ritmo sinusal la mayoría de los corazones que presentaron arritmias ventriculares de reperfusión y el efecto antiarrítmico se mantiene en corazones hipertróficos provenientes de ratas SHR.Introduction: ischemic postconditioning (IPC) is a protective strategy against reperfusion injury with antiarrhythmic properties. Cardiac hypertrophy secondary to hypertension increases the risk of arrhythmias and also reduces the response to some treatments. Objective: to determine whether the antiarrhythmic effect of IPC was maintained in hypertrophic hearts. Methods: isolated rat hearts from Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) of the same age, were perfused according to Langendorff technique and subjected to 15 min regional ischemia. At the moment of reperfusion, hearts were divided into: a) WKY, b) WKY-IPC, c) SHR, d) SHR-IPC (each group, n= 13). The IPC consisted of 3 cycles of 30 s of reperfusion and 30 s of ischemia at the onset of reperfusion. Ventricular arrhythmias were diagnosed using ECG records. Hypertrophy was estimated by relative heart weight. Results: hypertension in SHR induce myocardial hypertrophy. All hearts underwent a high incidence of ventricular fibrillation (SHR 92,3% and WKY 77%, ns). IPC restored sinus rhythm in the hearts of normotensive rats (WKY-PCI 61,5% versus WKY 23,1%, p = 0,0236 by C2 test) and in those from SHR (SHR-PCI 69% versus SHR 15,4%, p = 0,0016 C2 test). Conclusion: IPC is able to restore sinus rhythm from most of the hearts that developed reperfusion ventricular arrhythmias and the antiarrhythmic effect remains in hypertrophic hearts from SHR rats.Fil: Diez, Emiliano Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Prado, Natalia Jorgelina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo; ArgentinaFil: Ponce Zumino, Amira Zulma. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Miatello, Roberto Miguel. Universidad Nacional de Cuyo; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentin

New proposal involving nanoformulated melatonin targeted to the mitochondria as a potential COVID-19 treatment

Melatonin may be a powerful auxiliary therapy in the prevention and treatment of viral infections, such as coronavirus disease 2019 (COVID-19). Casually, the so-called ‘super immunity’ of bats and the usually high levels of melatonin in children could contribute to their high resistance to the SARS-CoV-2 virus. Melatonin seems to play a key role in suppressing COVID-19 infections. This endogenous antioxidant inhibits cell apoptosis, blocks the inflammasomes that mediate lung inflammation, reduces blood vessel permeability which limits alveolar edema, improves anxiety and sleeps habits that stimulate general immunity and prevents lung fibrosis. These complications, which are usually the main consequences of COVID-19, may be significantly attenuated by melatonin...Fil: Martín Giménez, Virna Margarita. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - San Juan; Argentina. Universidad Católica de Cuyo. Facultad de Ciencias Químicas y Tecnológicas; ArgentinaFil: Prado, Natalia Jorgelina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Departamento de Patología; ArgentinaFil: Diez, Emiliano Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Fisiología; ArgentinaFil: Manucha, Walter Ariel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Fisiología; ArgentinaFil: Reiter, Russel. University of Texas at San Antonio; Estados Unido

Cardiac connexin-43 hemichannels and pannexin1 channels: Provocative antiarrhythmic targets

Cardiac connexin-43 (Cx43) creates gap junction channels (GJCs) at intercellular contacts and hemi-channels (HCs) at the peri-junctional plasma membrane and sarcolemmal caveolae/rafts compartments. GJCs are fundamental for the direct cardiac cell-to-cell transmission of electrical and molecular signals which ensures synchronous myocardial contraction. The HCs and structurally similar pannexin1 (Panx1) channels are active in stressful conditions. These channels are essential for paracrine and autocrine communication through the release of ions and signaling molecules to the extracellular environment, or for uptake from it. The HCs and Panx1 channel-opening profoundly affects intracellular ionic homeostasis and redox status and facilitates via purinergic signaling pro-inflammatory and pro-fibrotic processes. These conditions promote cardiac arrhythmogenesis due to the impairment of the GJCs and selective ion channel function. Crosstalk between GJCs and HCs/Panx1 channels could be crucial in the development of arrhythmogenic substrates, including fibrosis. Despite the knowledge gap in the regulation of these channels, current evidence indicates that HCs and Panx1 channel activation can enhance the risk of cardiac arrhythmias. It is extremely challenging to target HCs and Panx1 channels by inhibitory agents to hamper development of cardiac rhythm disorders. Progress in this field may contribute to novel therapeutic approaches for patients prone to develop atrial or ventricular fibrillation.Fil: Andelova, Katarina. Slovak Academy of Sciences. Institute for Heart Research; EslovaquiaFil: Benova, Tamara Egan. Slovak Academy of Sciences. Institute for Heart Research; EslovaquiaFil: Bacova, Barbara Szeiffova. Slovak Academy of Sciences. Institute for Heart Research; EslovaquiaFil: Sykora, Matus. Slovak Academy of Sciences. Institute for Heart Research; EslovaquiaFil: Prado, Natalia Jorgelina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Diez, Emiliano Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Hlivak, Peter. National Institute Of Cardiovascular Diseases; EslovaquiaFil: Tribulova, Narcis. Slovak Academy of Sciences. Institute for Heart Research; Eslovaqui

Ischemic Postconditioning Reduces Reperfusion arrhythmias by Adenosine Receptors and Protein Kinase C Activation but Is Independent of KATP Channels or Connexin 43

Ischemic postconditioning (IPoC) reduces reperfusion arrhythmias but the antiarrhythmic mechanisms remain unknown. The aim of this study was to analyze IPoC electrophysiological effects and the role played by adenosine A1, A2A and A3 receptors, protein kinase C, ATP-dependent potassium (KATP) channels, and connexin 43. IPoC reduced reperfusion arrhythmias (mainly sustained ventricular fibrillation) in isolated rat hearts, an effect associated with a transient delay in epicardial electrical activation, and with action potential shortening. Electrical impedance measurements and Lucifer-Yellow diffusion assays agreed with such activation delay. However, this delay persisted during IPoC in isolated mouse hearts in which connexin 43 was replaced by connexin 32 and in mice with conditional deletion of connexin 43. Adenosine A1, A2A and A3 receptor blockade antagonized the antiarrhythmic effect of IPoC and the associated action potential shortening, whereas exogenous adenosine reduced reperfusion arrhythmias and shortened action potential duration. Protein kinase C inhibition by chelerythrine abolished the protective effect of IPoC but did not modify the effects on action potential duration. On the other hand, glibenclamide, a KATP inhibitor, antagonized the action potential shortening but did not interfere with the antiarrhythmic effect. The antiarrhythmic mechanisms of IPoC involve adenosine receptor activation and are associated with action potential shortening. However, this action potential shortening is not essential for protection, as it persisted during protein kinase C inhibition, a maneuver that abolished IPoC protection. Furthermore, glibenclamide induced the opposite effects. In addition, IPoC delays electrical activation and electrical impedance recovery during reperfusion, but these effects are independent of connexin 43.Fil: Diez, Emiliano Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; ArgentinaFil: Sánchez, Jose Antonio. Centro de Investigación Biomédica en Red sobre Enfermedades Cardiovasculares; España. Universidad Autonoma de Barcelona. Hospital Vall D' Hebron. Instituto de Investigación Vall D'hebron. Serv.de Cardiología,laboratorio de Cardiología Experimenta; EspañaFil: Prado, Natalia Jorgelina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; ArgentinaFil: Ponce Zumino, Amira Zulma. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: García-Dorado, David. Universidad Autonoma de Barcelona. Hospital Vall D' Hebron. Instituto de Investigación Vall D'hebron. Serv.de Cardiología,laboratorio de Cardiología Experimenta; España. Centro de Investigación Biomédica en Red sobre Enfermedades Cardiovasculares; EspañaFil: Miatello, Roberto Miguel. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Rodríguez-Sinovas, Antonio. Centro de Investigación Biomédica en Red sobre Enfermedades Cardiovasculares; España. Universidad Autonoma de Barcelona. Hospital Vall D' Hebron. Instituto de Investigación Vall D'hebron. Serv.de Cardiología,laboratorio de Cardiología Experimenta; Españ

Anti-inflammatory, antioxidant, antihypertensive, and antiarrhythmic effect of indole-3-carbinol, a phytochemical derived from cruciferous vegetables

Background: Cardiovascular inflammation and oxidative stress are determining factors in high blood pressure and arrhythmias. Indole-3-carbinol is a cruciferous-derived phytochemical with potential anti-inflammatory and antioxidant effects. However, its implications on the modulation of cardiovascular inflammatory-oxidative markers are unknown. Objectives: To establish the effects of indole-3-carbinol on the oxidative-inflammatory-proarrhythmic conditions associated with hypertension. Materials: Histological, biochemical, molecular, and functional aspects were evaluated in 1) Culture of mouse BV-2 glial cells subjected to oxidative-inflammatory damage by lipopolysaccharides (100 ng/mL) in the presence or absence of 40 μM indole-3-carbinol (n = 5); 2) Male spontaneously hypertensive rats (SHR) and Wistar Kyoto rats receiving indole-3-carbinol (2000 ppm/day, orally) during the first 8 weeks of life (n = 15); 3) Isolated rat hearts were submitted to 10 min regional ischemia and 10 min reperfusion. Results: 1) lipopolysaccharides induced oxidative stress and increased inflammatory markers; indole-3-carbinol reversed both conditions (interleukin 6, tumor necrosis factor α, the activity of nicotinamide adenine dinucleotide phosphate oxidase, nitric oxide, inducible nitric oxide synthase, heat shock protein 70, all p < 0.01 vs lipopolysaccharides). 2) SHR rats showed histological, structural, and functional changes with increasing systolic blood pressure (154 ± 8 mmHg vs. 122 ± 7 mmHg in Wistar Kyoto rats, p < 0.01); Inflammatory-oxidative markers also increased, and nitric oxide and heat shock protein 70 decreased. Conversely, indole-3-carbinol reduced oxidative-inflammatory markers and systolic blood pressure (133 ± 8 mmHg, p < 0.01 vs. SHR). 3) indole-3-carbinol reduced reperfusion arrhythmias from 8/10 in SHR to 0/10 (p = 0.0007 by Fisher's exact test). Conclusions: Indole-3-carbinol reduces the inflammatory-oxidative-proarrhythmic process of hypertension. The nitric oxide and heat shock protein 70 are relevant mechanisms of indole-3-carbinol protective actions. Further studies with this pleiotropic phytochemical as a promising cardioprotective are guaranteed.Fil: Prado, Natalia Jorgelina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Ramirez, Daniela Andrea. Laboratorio de Cromatografía Para Agroalimentos; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Biología Agrícola de Mendoza. Universidad Nacional de Cuyo. Facultad de Ciencias Agrarias. Instituto de Biología Agrícola de Mendoza; ArgentinaFil: Mazzei, Luciana Jorgelina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Parra, Micaela. Universidad Nacional de Cuyo; ArgentinaFil: Casarotto, Mariana. Universidad Nacional de Cuyo; ArgentinaFil: Calvo, Juan Pablo. Universidad Nacional de Cuyo; ArgentinaFil: Cuello Carrión, Fernando Darío. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Ponce Zumino, Amira Zulma. Universidad Nacional de Cuyo; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Diez, Emiliano Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Camargo, Alejandra Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Biología Agrícola de Mendoza. Universidad Nacional de Cuyo. Facultad de Ciencias Agrarias. Instituto de Biología Agrícola de Mendoza; ArgentinaFil: Manucha, Walter Ariel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad del Aconcagua. Facultad de Ciencias Médicas; Argentin

Antiarrhythmic mechanisms of Malbec wine and resveratrol in isolated rat heart

Oxidative stress during myocardial reperfusion contributes to ventricular arrhythmias onset. We aim to evaluate the antiarrhythmic effect of Malbec wine and resveratrol and compare them with the synthetic antioxidant tiron. Since alcohol use is controversial, we also assessed dealcoholized wine.Isolated hearts from male Sprague Dawley rats were perfused with Krebs-Henseleit solution added with: Malbec wine (5 ml/L), resveratrol (10 μM,) compared to controls with alcohol (0.5 ml/L); dealcoholized wine (5 ml/L), tiron (10 mM) were compared with controls without alcohol. Epicardial action potentials were analyzed during basal state, regional ischemia and reperfusion (10 minutes each period). The incidence of arrhythmias was determined. Te antioxidant effect was assessed in left ventricle homogenates and expressed as a percentage of inhibition of the ABTS?+ radical.Malbec wine and resveratrol reduced reperfusion arrhythmias in 56% and 50%, respectively, compared to 100% incidence in the control group with alcohol. Dealcoholized wine reduced arrhythmias to 50% compared to non-alcoholic control (90.5%), but tiron did not protect (69%). Te free radicals inhibitory effect increased with all the compounds (resveratrol 54.2%, tiron 43.2%, Malbec wine 42.9%, dealcoholized wine 40.2%) with respect to the control groups (with alcohol 23.5%, without alcohol 21.2%). Resveratrol shortened action potential duration and prevented ischemic depolarization. Malbec prevented ischemic-induced action potential shortening. We conclude that Malbec wine and resveratrol are antiarrhythmic beyond their antioxidant properties. Alcohol content or was not essential. Protection from ischemic action potential changes could be relevant to the antiarrhythmic effect of both resveratrol and wine.Fil: Prado, Natalia Jorgelina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Perdicaro DJ. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Parra, M. Universidad Nacional de Cuyo Facultad de Ciencias Médicas; ArgentinaFil: Carrión AM. Universidad Nacional de Cuyo Facultad de Ciencias Médicas; ArgentinaFil: Miatello RM. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Renna NF. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Ponce Zumino AZ. Universidad Nacional de Cuyo Facultad de Ciencias Médicas; ArgentinaFil: Vazquez Prieto M. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Diez ER. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentin

Reperfusion arrhythmias increase after superior cervical ganglionectomy due to conduction disorders and changes in repolarization

Pharmacological concentrations of melatonin reduce reperfusion arrhythmias, but less is known about the antiarrhythmic protection of the physiological circadian rhythm of melatonin. Bilateral surgical removal of the superior cervical ganglia irreversibly suppresses melatonin rhythmicity. This study aimed to analyze the cardiac electrophysiological effects of the loss of melatonin circadian oscillation and the role played by myocardial melatonin membrane receptors, SERCA2A, TNFα, nitrotyrosine, TGFβ, KATP channels, and connexin 43. Three weeks after bilateral removal of the superior cervical ganglia or sham surgery, the hearts were isolated and submitted to ten minutes of regional ischemia followed by ten minutes of reperfusion. Arrhythmias, mainly ventricular tachycardia, increased during reperfusion in the ganglionectomy group. These hearts also suffered an epicardial electrical activation delay that increased during ischemia, action potential alternants, triggered activity, and dispersion of action potential duration. Hearts from ganglionectomized rats showed a reduction of the cardioprotective MT2 receptors, the MT1 receptors, and SERCA2A. Markers of nitroxidative stress (nitrotyrosine), inflammation (TNFα), and fibrosis (TGFβ and vimentin) did not change between groups. Connexin 43 lateralization and the pore-forming subunit (Kir6.1) of KATP channels increased in the experimental group. We conclude that the loss of the circadian rhythm of melatonin predisposes the heart to suffer cardiac arrhythmias, mainly ventricular tachycardia, due to conduction disorders and changes in repolarization.Fil: Prado, Natalia Jorgelina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo; ArgentinaFil: Muñoz, Estela Maris. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; ArgentinaFil: Farías Altamirano, Luz Estefanía. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; ArgentinaFil: Aguiar, Francisco. Universidad Nacional de Cuyo; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; ArgentinaFil: Ponce Zumino, Amira Zulma. Universidad Nacional de Cuyo; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Ruiz Sánchez, Francisco Javier. Universidad Nacional de Cuyo; ArgentinaFil: Miatello, Roberto Miguel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo; ArgentinaFil: Pueyo, Esther. Universidad de Zaragoza; España. Centro de Investigación Biomédica en Red en el área temática de Bioingeniería, Biomateriales y Nanomedicina; EspañaFil: Diez, Emiliano Raúl. Universidad Nacional de Cuyo; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentin