The University of Buenos Aires is the largest university in Argentina and the second largest university by enrollment in Latin America. Founded on August 12, 1821 in the city of Buenos Aires, it consists of 13 departments, 6 hospitals, 10 museums and is linked to 4 high schools: Colegio Nacional de Buenos Aires, Escuela Superior de Comercio Carlos Pellegrini, Instituto Libre de Segunda Enseñanza and Escuela de Educación Técnica Profesional en Producción Agropecuaria y Agroalimentaria.Entry to any of the available programmes of study in the university is open to anyone with a secondary school degree; in most cases, students who have successfully completed high school must pass a first year called CBC, which stands for Ciclo Básico Común . Only upon completion of this first year may the student enter the chosen school; until then, they must attend courses in different buildings, and have up to 3 years to finish the 6 or 7 subjects assigned in two groups of 3 or 4. Each subject is of one semester duration . If someone passes all 6 subjects in their respective semester, the CBC will take only one year. Potential students of economics, instead, take a 2-year common cycle, the "CBG" , comprising 12 subjects.The UBA has no central campus. A centralized Ciudad Universitaria was started in the 1960s, but contains only two schools, with the others at different locations in Buenos Aires. Access to the university is free of charge for everyone, including foreigners. However, the postgraduate programs charge tuition fees that can be covered with research scholarships for those students with outstanding academic performance.The university has produced more Nobel Prize laureates than any other Spanish-speaking institution. It is currently the best ranked Argentine university in college and university rankings, present at number 197 of the Top Universities 2008 and at number 151-200 of the 2010 Shanghai Jiao Tong University ranking. According to the 2010 University Ranking by Academic Performance , the university is the best in Argentina and the 247th in the world, and, according to TopUniversities, it is the 46th best university in the world taking into account employer reputation. Wikipedia.
Jorge F.,University of Buenos Aires
Physiological Reviews | Year: 2010
The mechanism of epithelial fluid transport remains unsolved, which is partly due to inherent experimental difficulties. However, a preparation with which our laboratory works, the corneal endothelium, is a simple leaky secretory epithelium in which we have made some experimental and theoretical headway. As we have reported, transendothelial fluid movements can be generated by electrical currents as long as there is tight junction integrity. The direction of the fluid movement can be reversed by current reversal or by changing junctional electrical charges by polylysine. Residual endothelial fluid transport persists even when no anions (hence no salt) are being transported by the tissue and is only eliminated when all local recirculating electrical currents are. Aquaporin (AQP) 1 is the only AQP present in these cells, and its deletion in AQP1 null mice significantly affects cell osmotic permeability (by ∼40%) but fluid transport much less (∼20%), which militates against the presence of sizable water movements across the cell. In contrast, AQP1 null mice cells have reduced regulatory volume decrease (only 60% of control), which suggests a possible involvement of AQP1 in either the function or the expression of volume-sensitive membrane channels/transporters. A mathematical model of corneal endothelium we have developed correctly predicts experimental results only when paracellular electro-osmosis is assumed rather than transcellular local osmosis. Our evidence therefore suggests that the fluid is transported across this layer via the paracellular route by a mechanism that we attribute to electro-osmotic coupling at the junctions. From our findings we have developed a novel paradigm for this preparation that includes 1) paracellular fluid flow; 2) a crucial role for the junctions; 3) hypotonicity of the primary secretion; and 4) an AQP role in regulation rather than as a significant water pathway. These elements are remarkably similar to those proposed by the laboratory of Adrian Hill for fluid transport across other leaky epithelia. Copyright © 2010 the American Physiological Society.
Galigniana M.D.,University of Buenos Aires
Chemistry and Biology | Year: 2012
In this issue of Chemistry & Biology, Grossman et al. report a study on aldosterone-dependent nuclear translocation of the mineralocorticoid receptor (MR). They analyze the dependency of MR retrotransport, DNA-binding, and transcriptional activity on Hsp90 and demonstrate that MR dimerization is a nuclear event. © 2012 Elsevier Ltd All rights reserved.
Rabinovich G.,CONICET |
Rabinovich G.,University of Buenos Aires |
Immunity | Year: 2012
Numerous regulatory programs have been identified that contribute to the restoration of homeostasis at the conclusion of immune responses and to safeguarding against the detrimental effects of chronic inflammation and autoimmune pathology. Malignant cells may usurp these pathways to create immunosuppressive networks that thwart antitumor responses. Herein we review the role of endogenous lectins (C-type lectins, siglecs, and galectins) and specific N- and O-glycans generated by the coordinated action of glycosyltransferases and glycosidases that together promote regulatory signals that control immune cell homeostasis. We also discuss the mechanisms by which glycan-dependent regulatory programs integrate into canonical circuits that amplify or silence immune responses related to autoimmunity and neoplastic disease. © 2012 Elsevier Inc..
Golombek D.A.,CONICET |
Rosenstein R.E.,University of Buenos Aires
Physiological Reviews | Year: 2010
Mammalian circadian rhythms are controlled by endogenous biological oscillators, including a master clock located in the hypothalamic suprachiasmatic nuclei (SCN). Since the period of this oscillation is of ∼24 h, to keep synchrony with the environment, circadian rhythms need to be entrained daily by means of Zeitgeber ("time giver") signals, such as the light-dark cycle. Recent advances in the neurophysiology and molecular biology of circadian rhythmicity allow a better understanding of synchronization. In this review we cover several aspects of the mechanisms for photic entrainment of mammalian circadian rhythms, including retinal sensitivity to light by means of novel photopigments as well as circadian variations in the retina that contribute to the regulation of retinal physiology. Downstream from the retina, we examine retinohypothalamic communication through neurotransmitter (glutamate, aspartate, pituitary adenylate cyclase-activating polypeptide) interaction with SCN receptors and the resulting signal transduction pathways in suprachiasmatic neurons, as well as putative neuron-glia interactions. Finally, we describe and analyze clock gene expression and its importance in entrainment mechanisms, as well as circadian disorders or retinal diseases related to entrainment deficits, including experimental and clinical treatments. Copyright © 2010 the American Physiological Society.
Austin A.T.,University of Buenos Aires
Trends in Ecology and Evolution | Year: 2011
The classic ecological paradigm for deserts, that all processes are controlled by water availability, has limited our imagination for exploring other controls on the cycling of carbon and nutrients in aridland ecosystems. This review of recent studies identifies alternative mechanisms that challenge the idea that all soil processes in aridlands are proximately water-limited, and highlights the significance of photodegradation of aboveground litter and the overriding importance of spatial heterogeneity as a modulator of biotic responses to water availability. Aridlands currently occupy >30% of the terrestrial land surface and are expanding. It is therefore critical to incorporate these previously unappreciated mechanisms in our understanding of aridland biogeochemistry to mitigate the effects of desertification and global change. © 2011 Elsevier Ltd.