Dra. Laura Vivas
My postgraduate work with Dr. Emma Chiaraviglio at the Ferreyra Institute (1984-1989) concerned the neural control of thirst and salt appetite. This work provided electrophysiological evidence that the brain has osmo-sodium sensors outside the hypothalamus in cells of the Organum Vasculosum of the Lamina Terminalis (telencephalon). This nucleus is one of the specialized neural structures called circumventricular organs and it initiates the appropriate behavioral responses to losses of body water and sodium. Thanks to this novel finding I got an international recognition, a two-year post-doctoral fellowship (1990 and 1991) from the Howard Florey Institute of Medicine and Experimental Physiology, University of Melbourne, Australia. There I worked with one of the most prestigious groups in this area of study, led by Dr. Michael McKinley, doing several collaborative works on the central control of water and salt intake and excretion, discriminating mechanisms and central regulatory areas. Since I returned to Argentina (1992) I lead the Hydroelectrolyte Homeostasis Laboratory of the Ferreyra Institute and joined CONICET as an Assistant researcher, being promoted to the position of Independent Researcher in 2005 and Principal Researcher in 2013. I currently hold that position at CONICET and I am also Principal Professor, at the School of Biology, University of Cordoba.
Dr. Víctor Ramírez Amaya
Dr. Víctor Ramírez Amaya obtained he’s Bachelor in Psychology in the School ofPsychology from the National Autonomous University of México (UNAM) and obtained he’s PhD in biomedical science in the Institute of Celular Physiology from the same University in 1999. He then worked in a post-doctoral fellowship under the sponsorship of the Human Frontiers Science Program (HFSP) in the Arizona research division of neural systems memory and aging from the University of Arizona, in Tucson Arizona USA, under the supervision of Dr. Carol Barnes. In 2005 he became a principal researcher in the Institute of Neurobiology from UNAM, and from 2013 to 2016 he became professor and researcher in the Autonomus University of Queretaro (UAQ). He is currently an independent researcher from the “Consejo Nacional de Investigaciones Científicas y Técnicas” (CONICET), and is part of the “Balance Hidrosalino e Hipertensión” laboratory from the “Instituto Ferreyra in Córdoba, Argentina. He had focus he’s studies in systems neuroscience and the neurobiology of cognition, and currently is interested in the integral characterization of wellbeing, which is seen as a group of abilities dependent on the optimal function of the brain reward system, that impact in the rest of the organism. Particularly interesting is to explain the role of structural plasticity of the brain reward system, as is hippocampal neurogenesis, in the ability of the organism to adapt to stress and the interaction of this kind of plasticity with the function of the immune system and metabolism, as well as to functionally characterize the brain reward system circuits involve in the development of resilience and other wellbeing skills.
Dra. Andrea Godino
Dr. Andrea Godino graduated as a Biologist at the National University of Cordoba, Argentina and obtained her Ph.D. in Biological Sciences at the same University in 2009. She continued her studies during a postdoc period in the lab of Alcohol, Ontogeny and Learning, where she studied the effect of prenatal ethanol exposure in the sodium and water balance of the offspring.
She is currently a Researcher of the National Council for Scientific and Technical Research (CONICET) in the category of Research associate/Faculty and is a professor of faculty of Psychology at the National University of Cordoba. Her group studies the mechanisms and neurochemical systems involved in the appearance of sodium appetite and the perinatal programming effects of high sodium consumption during the pregnancy.
Dra. Ximena Elizabeth Caeiro
Dr. Ximena Caeiro obtained her degree in Biology at the National University of Córdoba (Argentina) and her PhD in Biology at the Faculty of Exact Physical and Natural Sciences of the same University in 2008. She developed her postdoctoral studies in the Neurophysiology Laboratory of INIMEC- CONICET concerning the participation of sex chromosome complement in sexually dimorphic bradycardic baroreflex responses.
She is currently an Assistant Researcher of the National Council of Scientific and Technological Research (CONICET) and assistant professor in Human Physiology of the Institute of Biomedical Sciences of Córdoba (IUCBC) University. The main focus of study is to understand cardiovascular sexual dimorphism, analyzing the neurochemical systems and central circuits involved in sex differences in blood pressure regulation as well as their alterations and implications in the evolution of hypertension.
Dra. Melina Mara Musri
Dr. Melina Musri is currently Associate Researcher of the National Council of Scientific and Technical Research (CONICET), Principal Investigator of the Laboratory of Epigenetics and Cell Differentiation at the Ferreyra Research Institute. Dr. Musri developed her Ph.D. thesis at the University of Barcelona (UB), Spain, and continued her postdoctoral studies at the Department of Pneumology, Hospital Clinic of Barcelona (UB) in Spain. Then, with a Sara Borrell contract from Carlos III Institute from Spanish Government, she spent two years in the same laboratory and two years at the Faculty of Biology and Pre-Clinical Medicine, University of Regensburg (UR) to study noncoding RNAs. Dr. Musri returned to Argentina with the program of relocation of Argentinian Scientists in 2014 to establish her own research group.
Her research work could be summarized as the study of mechanisms of gene expression regulation and cell phenotypic changes in physiology and pathology. During the early years, Dr. Musri was involved in the study of obesity and metabolic syndrome-related pathogenic mechanisms. Specifically, she focused on the role of histone modifications during adipogenesis and its link to obesity. During these years the role of histone methylation was assumed as an irreversible mark and its function was mostly unknown. Dr. Musri contributed to the field reporting that in committed preadipocyte, dimethylation of lysine 4 of Histone 3 (2mK4H3) in promoter regions of key adipogenic genes both signals and is a key event for those genes to be expressed later during differentiation (Musri et al. 2006). She also reported the importance of histone methylation during adipogenesis and the role of the histone demethylase KDM1a in both adipogenesis and obesity (Musri et al. 2010; Hanzu and Musri et al. 2013). During her postdoctoral studies she focused in what became her current main research line, the study of molecular mechanisms of cell phenotypic switch during the development of vascular remodeling (VR). VR plays a critical role in cardio-pulmonary disorders such as pulmonary hypertension (PH) and chronic obstructive pulmonary disease (COPD). It is currently known that VR is caused by excessive proliferation of cells bearing a dedifferentiated or transdifferentiated phenotype. However, due to the profound phenotypic switch that vascular cells undergo during VR, the underlying cellular and molecular mechanisms driving the structural changes of blood vessels is not fully understood yet. Dysregulation of angiogenic factors seems to be one of the triggering factors (Garcia-Lucio et al. 2016). The current hypothesis postulates that cell populations from different origins: 1) SMC subjected to phenotypic switch (Coll-Bonfill et al. 2016, Musri et al. 2018, and revised in Coll-Bonfill et al. 2016), 2) trans-differentiation of both endothelial cells (EC) and endothelial progenitor cells (EPC) through an endothelial to mesenchymal transition (EnMT) process (Diez and Musri et al. 2010), 3) proliferation of myofibroblast and 4) recruitment of circulating mesenchymal cells, contribute to the narrowing of pulmonary vessels. This is based in the study of different cell lineages in vitro or with conventional immunohistochemical analysis using a limited number of markers, many of which are lost during the development of the disease limiting the capacity of identifying the true origin of the neointimal cells. The current projects of her laboratory aim to fill this gap by rigorously analyze the identity and true ratio of the SMC and EC contributing to the development of vascular remodeling associated to pulmonary vascular remodeling in vivo and the underlying molecular mechanisms involved in this process. In addition the main interest of the laboratory is to understand the molecular mechanisms driving the phenotypic switch of smooth muscle cells, with special interests in epigenetic processes. To this end they use in vitro models of smooth muscle cell differentiation and in vivo models of vascular remodeling such as hypoxia-induced pulmonary hypertension and vascular remodeling induced by carotid artery ligation.