<?xml version="1.0" encoding="UTF-8"?>
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<title>Volumen 09</title>
<link href="http://sedici.unlp.edu.ar:80/handle/10915/127640" rel="alternate"/>
<subtitle/>
<id>http://sedici.unlp.edu.ar:80/handle/10915/127640</id>
<updated>2026-06-09T12:58:41Z</updated>
<dc:date>2026-06-09T12:58:41Z</dc:date>
<entry>
<title>Physiological Mini Reviews | Volumen 9 | Número 7</title>
<link href="http://sedici.unlp.edu.ar:80/handle/10915/127655" rel="alternate"/>
<author>
<name>Sociedad Chilena de Ciencias Fisiológicas</name>
</author>
<id>http://sedici.unlp.edu.ar:80/handle/10915/127655</id>
<updated>2022-02-17T18:02:59Z</updated>
<published>2016-10-01T00:00:00Z</published>
<summary type="text">Edicion de revista
Physiological Mini Reviews; vol. 9, no. 7
Resúmenes presentados en la XXXI Reunión Anual de la Sociedad Chilena de Ciencias Fisiológicas, realizada en la Región de los Ríos, Chile, entre el 6 y el 9 de septiembre de 2016.
</summary>
<dc:date>2016-10-01T00:00:00Z</dc:date>
<dc:description>Resúmenes presentados en la XXXI Reunión Anual de la Sociedad Chilena de Ciencias Fisiológicas, realizada en la Región de los Ríos, Chile, entre el 6 y el 9 de septiembre de 2016.</dc:description>
</entry>
<entry>
<title>Program and abstracts from The Strategic Workshop Rhythms of Life: Perspectives for Physiological Sciences in the 21St Century</title>
<link href="http://sedici.unlp.edu.ar:80/handle/10915/127653" rel="alternate"/>
<author>
<name>Sociedad Brasileira de Fisiologia</name>
</author>
<id>http://sedici.unlp.edu.ar:80/handle/10915/127653</id>
<updated>2021-11-04T04:03:48Z</updated>
<published>2016-08-01T00:00:00Z</published>
<summary type="text">Articulo
Strategic Workshop Rhythms of Life: Perspectives for Physiological Sciences in the 21St Century (25 de agosto de 2016); Physiological Mini Reviews; vol. 9, no. 4
It is the intention of the Editorial Committee of PMR to add to our publications, special issues with the abstracts of the Congresses of the physiological societies of the Latin American countries who agree to collaborate with our journal, with the main goal of increasing the scientific and academic interaction among our countries.
</summary>
<dc:date>2016-08-01T00:00:00Z</dc:date>
<dc:description>It is the intention of the Editorial Committee of PMR to add to our publications, special issues with the abstracts of the Congresses of the physiological societies of the Latin American countries who agree to collaborate with our journal, with the main goal of increasing the scientific and academic interaction among our countries.</dc:description>
</entry>
<entry>
<title>New concepts in the neurophysiology of sleep and wakefulness</title>
<link href="http://sedici.unlp.edu.ar:80/handle/10915/127652" rel="alternate"/>
<author>
<name>Garay, Arturo</name>
</author>
<author>
<name>Cardinali, Daniel P.</name>
</author>
<id>http://sedici.unlp.edu.ar:80/handle/10915/127652</id>
<updated>2021-11-04T04:03:52Z</updated>
<published>2016-06-01T00:00:00Z</published>
<summary type="text">Revision
Physiological Mini Reviews; vol. 9, no. 3
The neural substrates of sleep and wakefulness form a highly distributed and, to some extent, redundant network, with hypocretin, monoaminergic and cholinergic systems largely promoting wakefulness and GABAergic systems in the preoptic area, hypothalamus and brainstem promoting sleep. The hypocretin/orexin system plays a special role in the promotion of wakefulness and suppression of REM sleep by providing excitatory input to the monoaminergic and cholinergic systems. Sleep is not a unitary state but involves a cyclic alternation between NREM and REM sleep; the pons is critical for generating the multiple components (ie, EEG synchronization, eye movements and muscle atonia) that characterize REM sleep. Recent findings have implicated the participation of hypothalamus, through MCH/GABA that provide a critical input to pontine generator of REM sleep. The timing of sleep and wakefulness is regulated by an interaction between the circadian pacemaker located in the hypothalamic SCN and a sleep homeostatic system whose anatomic location is yet to be definitively identified. Among various neurochemicals, extracellular AD and nNOS/NK1 accumulate in the BF as wakefulness is extended and inhibits cortically projecting cholinergic neurons, thereby influencing cortical activity. In the future, it seems reasonable to expect a spreading of these insights from basic to clinical grounds for a better understanding of the causes and mechanisms of sleep disorders and the generation of novel therapeutics in sleep medicine.
</summary>
<dc:date>2016-06-01T00:00:00Z</dc:date>
<dc:description>The neural substrates of sleep and wakefulness form a highly distributed and, to some extent, redundant network, with hypocretin, monoaminergic and cholinergic systems largely promoting wakefulness and GABAergic systems in the preoptic area, hypothalamus and brainstem promoting sleep. The hypocretin/orexin system plays a special role in the promotion of wakefulness and suppression of REM sleep by providing excitatory input to the monoaminergic and cholinergic systems. Sleep is not a unitary state but involves a cyclic alternation between NREM and REM sleep; the pons is critical for generating the multiple components (ie, EEG synchronization, eye movements and muscle atonia) that characterize REM sleep. Recent findings have implicated the participation of hypothalamus, through MCH/GABA that provide a critical input to pontine generator of REM sleep. The timing of sleep and wakefulness is regulated by an interaction between the circadian pacemaker located in the hypothalamic SCN and a sleep homeostatic system whose anatomic location is yet to be definitively identified. Among various neurochemicals, extracellular AD and nNOS/NK1 accumulate in the BF as wakefulness is extended and inhibits cortically projecting cholinergic neurons, thereby influencing cortical activity. In the future, it seems reasonable to expect a spreading of these insights from basic to clinical grounds for a better understanding of the causes and mechanisms of sleep disorders and the generation of novel therapeutics in sleep medicine.</dc:description>
</entry>
<entry>
<title>The tango between pka and camkii signaling in cardiac pacemaker cells</title>
<link href="http://sedici.unlp.edu.ar:80/handle/10915/127651" rel="alternate"/>
<author>
<name>Yaniv, Yael</name>
</author>
<id>http://sedici.unlp.edu.ar:80/handle/10915/127651</id>
<updated>2021-11-04T04:03:55Z</updated>
<published>2016-12-01T00:00:00Z</published>
<summary type="text">Revision
Physiological Mini Reviews; vol. 9, no. 8
The sinoatrial node is the primary pacemaker that controls the heart rate under normal conditions. Although the heart rate was originally measured thousands of years ago, the mechanisms that control the spontaneous beating of the sinoatrial node (SAN) are still under debate. In the last century, SAN function was mostly investigated by electrophysiological tools. Therefore, not surprisingly, the major mechanisms that control SAN function were thought to be related only to membranal ionic modulations. Recent biophysical, biochemical and imaging techniques have shed new light on the role of intrinsic pacemaker mechanisms on SAN function. Specifically, the role of post-translational modification signaling on SAN function has been explored using numerical and experimental tools. We describe here the major breakthroughs related to these signaling mechanisms in SAN cells. We conclude that the recent findings are only the tip of the iceberg in the fascinating world of downstream post-translational modification signaling, and we point out future research directions that may increase our knowledge of pacemaker function.
</summary>
<dc:date>2016-12-01T00:00:00Z</dc:date>
<dc:description>The sinoatrial node is the primary pacemaker that controls the heart rate under normal conditions. Although the heart rate was originally measured thousands of years ago, the mechanisms that control the spontaneous beating of the sinoatrial node (SAN) are still under debate. In the last century, SAN function was mostly investigated by electrophysiological tools. Therefore, not surprisingly, the major mechanisms that control SAN function were thought to be related only to membranal ionic modulations. Recent biophysical, biochemical and imaging techniques have shed new light on the role of intrinsic pacemaker mechanisms on SAN function. Specifically, the role of post-translational modification signaling on SAN function has been explored using numerical and experimental tools. We describe here the major breakthroughs related to these signaling mechanisms in SAN cells. We conclude that the recent findings are only the tip of the iceberg in the fascinating world of downstream post-translational modification signaling, and we point out future research directions that may increase our knowledge of pacemaker function.</dc:description>
</entry>
<entry>
<title>The cell as a gel: materials for a conceptual discussion</title>
<link href="http://sedici.unlp.edu.ar:80/handle/10915/127650" rel="alternate"/>
<author>
<name>Bagatolli, Luis A.</name>
</author>
<author>
<name>Stock, Roberto P.</name>
</author>
<id>http://sedici.unlp.edu.ar:80/handle/10915/127650</id>
<updated>2021-11-04T04:03:57Z</updated>
<published>2016-08-01T00:00:00Z</published>
<summary type="text">Revision
Physiological Mini Reviews; vol. 9, no. 5
Recent results from our laboratory support the view that the intracellular milieu cannot be treated as a homogeneous dilute system and, more importantly, reveal for the first time a dynamical coupling between intracellular water and an active metabolic process involving fluctuations in ATP concentration. These results are difficult to understand in light of the premises that currently underpin the description of the function of cellular systems, e.g. van’t Hoff’s ideal solution theory, diffusion and mass action kinetics. Particularly, they emphasize the need to incorporate features of the cell interior that have been largely overlooked in the dominant model of the cell, such as crowding and limited availability of free water. This article discusses this problem by reconsidering an alternate view, called the association-induction hypothesis, which emphasizes the relevance of emergent properties of the cell cytosol during cellular function. This hypothesis provides a very reasonable theoretical framework to explain recently reported observations about the dynamical coupling of mechanochemical (i.e. viscoelastic) properties of the cell cytoplasm and cellular chemical transformations (metabolism).; Los resultados experimentales obtenidos recientemente en nuestro laboratorio apoyan la idea que el medio intracelular no puede ser tratado como un sistema homogéneo (o solución diluida), revelando además por primera vez un acoplamiento dinámico entre el comportamiento colectivo del agua intracelular y un proceso metabólico activo que muestra fluctuaciones en la concentración de ATP. Estos nuevos resultados -que son difíciles de interpretar en base a los supuestos más generalmente utilizados para interpretar las bases fisicoquímicas de la fisiología de los sistemas celulares (p.ej. teoría de las soluciones ideales de van't Hoff, difusión, y cinética de acción de masas)- subrayan la necesidad urgente de incorporar características importantes del interior celular, tales como el hacinamiento molecular y la escasa disponibilidad de agua libre. Este artículo analiza críticamente este problema considerando una hipótesis alternativa, llamada hipótesis de asociación-inducción, la cual hace hincapié en la importancia de las propiedades emergentes del citosol durante la función celular. Esta hipótesis proporciona un marco teórico razonable para explicar nuestras observaciones, particularmente el acoplamiento dinámico entre las propiedades mecanoquímicas (o viscoelásticas) del citoplasma celular y las transformaciones químicas (metabolismo) en el interior celular.
</summary>
<dc:date>2016-08-01T00:00:00Z</dc:date>
<dc:description>Recent results from our laboratory support the view that the intracellular milieu cannot be treated as a homogeneous dilute system and, more importantly, reveal for the first time a dynamical coupling between intracellular water and an active metabolic process involving fluctuations in ATP concentration. These results are difficult to understand in light of the premises that currently underpin the description of the function of cellular systems, e.g. van’t Hoff’s ideal solution theory, diffusion and mass action kinetics. Particularly, they emphasize the need to incorporate features of the cell interior that have been largely overlooked in the dominant model of the cell, such as crowding and limited availability of free water. This article discusses this problem by reconsidering an alternate view, called the association-induction hypothesis, which emphasizes the relevance of emergent properties of the cell cytosol during cellular function. This hypothesis provides a very reasonable theoretical framework to explain recently reported observations about the dynamical coupling of mechanochemical (i.e. viscoelastic) properties of the cell cytoplasm and cellular chemical transformations (metabolism).

Los resultados experimentales obtenidos recientemente en nuestro laboratorio apoyan la idea que el medio intracelular no puede ser tratado como un sistema homogéneo (o solución diluida), revelando además por primera vez un acoplamiento dinámico entre el comportamiento colectivo del agua intracelular y un proceso metabólico activo que muestra fluctuaciones en la concentración de ATP. Estos nuevos resultados -que son difíciles de interpretar en base a los supuestos más generalmente utilizados para interpretar las bases fisicoquímicas de la fisiología de los sistemas celulares (p.ej. teoría de las soluciones ideales de van't Hoff, difusión, y cinética de acción de masas)- subrayan la necesidad urgente de incorporar características importantes del interior celular, tales como el hacinamiento molecular y la escasa disponibilidad de agua libre. Este artículo analiza críticamente este problema considerando una hipótesis alternativa, llamada hipótesis de asociación-inducción, la cual hace hincapié en la importancia de las propiedades emergentes del citosol durante la función celular. Esta hipótesis proporciona un marco teórico razonable para explicar nuestras observaciones, particularmente el acoplamiento dinámico entre las propiedades mecanoquímicas (o viscoelásticas) del citoplasma celular y las transformaciones químicas (metabolismo) en el interior celular.</dc:description>
</entry>
<entry>
<title>A general theory to explain heart rate and cardiac contractility changes with advancing age</title>
<link href="http://sedici.unlp.edu.ar:80/handle/10915/127649" rel="alternate"/>
<author>
<name>Tsutsui, Kenta</name>
</author>
<author>
<name>Monfredi, Oliver J.</name>
</author>
<author>
<name>Lakatta, Edward G.</name>
</author>
<id>http://sedici.unlp.edu.ar:80/handle/10915/127649</id>
<updated>2021-11-04T04:04:00Z</updated>
<published>2016-04-01T00:00:00Z</published>
<summary type="text">Revision
Physiological Mini Reviews; vol. 9, no. 2
Sinus node dysfunction and chronic heart failure have been, and will continue to be , major health issue issues in humans for the foreseeable future future. The heartbeat originateoriginates from spontaneously firing sinoatrial nodal (SAN) pacemaker cells. A coupledcoupled-clock system underlies the robust and flexible automaticity in these cells cells. The basal action potential (AP) firing rate of SAN cells is largely determined by the degree of phosphorylation o of critical proteins in th the coupledcoupled-clock system. Autonomic neuronal signaling from the brain effects changes in AP firing rate via modulatmodulation of cAMP and cAMP cAMP-mediated PKAPKA-dependent phosphorylationphosphorylation. Age -associated alterationalterations in intrinsic SAN cell behavior and associated changes in brainbrain-heart communication play cent ral role roles in the development of SAN cell pacemaker failure. This minimini-review provides integrated insights into the molecular mechanisms underlying the effects of aging on deterioration in beating rate and contractility of the heart in animal models and in apparently healthy humans.
</summary>
<dc:date>2016-04-01T00:00:00Z</dc:date>
<dc:description>Sinus node dysfunction and chronic heart failure have been, and will continue to be , major health issue issues in humans for the foreseeable future future. The heartbeat originateoriginates from spontaneously firing sinoatrial nodal (SAN) pacemaker cells. A coupledcoupled-clock system underlies the robust and flexible automaticity in these cells cells. The basal action potential (AP) firing rate of SAN cells is largely determined by the degree of phosphorylation o of critical proteins in th the coupledcoupled-clock system. Autonomic neuronal signaling from the brain effects changes in AP firing rate via modulatmodulation of cAMP and cAMP cAMP-mediated PKAPKA-dependent phosphorylationphosphorylation. Age -associated alterationalterations in intrinsic SAN cell behavior and associated changes in brainbrain-heart communication play cent ral role roles in the development of SAN cell pacemaker failure. This minimini-review provides integrated insights into the molecular mechanisms underlying the effects of aging on deterioration in beating rate and contractility of the heart in animal models and in apparently healthy humans.</dc:description>
</entry>
<entry>
<title>Hepatocyte aquaporins in bile physiology and disease</title>
<link href="http://sedici.unlp.edu.ar:80/handle/10915/127642" rel="alternate"/>
<author>
<name>Marinelli, Raúl A.</name>
</author>
<author>
<name>Marrone, Julieta</name>
</author>
<author>
<name>Soria, Leandro R.</name>
</author>
<id>http://sedici.unlp.edu.ar:80/handle/10915/127642</id>
<updated>2021-11-03T12:09:32Z</updated>
<published>2016-02-01T00:00:00Z</published>
<summary type="text">Revision
Physiological Mini Reviews; vol. 9, no. 1
Bile formation by hepatocytes is an osmotic secretory process resulting from the canalicular secretion of water in response to osmotic gradients created by the active transport of solutes, primarily bile salts, and other organic anions. Thus bile secretion would be ultimately dependent on the canalicular expression of bile salt and organic anion transporters as well as the osmotic water permeability of the canalicular plasma membrane domain, mainly determined by aquaporin-8 (AQP8) water channels. Compelling experimental evidence suggests that canalicular AQP8 facilitates the osmotically-coupled transport of solute and water during the formation of bile. Downregulation of AQP8-mediated hepatocyte canalicular water permeability is found in rat models of hepatocellular cholestasis suggesting that defective hepatocyte AQP8 expression is involved in the molecular mechanisms of bile secretory failure. The study of AQP function in liver has provided new insights into normal bile physiology and disease mechanisms, and may yield novel therapies to improve certain cholestatic conditions.
</summary>
<dc:date>2016-02-01T00:00:00Z</dc:date>
<dc:description>Bile formation by hepatocytes is an osmotic secretory process resulting from the canalicular secretion of water in response to osmotic gradients created by the active transport of solutes, primarily bile salts, and other organic anions. Thus bile secretion would be ultimately dependent on the canalicular expression of bile salt and organic anion transporters as well as the osmotic water permeability of the canalicular plasma membrane domain, mainly determined by aquaporin-8 (AQP8) water channels. Compelling experimental evidence suggests that canalicular AQP8 facilitates the osmotically-coupled transport of solute and water during the formation of bile. Downregulation of AQP8-mediated hepatocyte canalicular water permeability is found in rat models of hepatocellular cholestasis suggesting that defective hepatocyte AQP8 expression is involved in the molecular mechanisms of bile secretory failure. The study of AQP function in liver has provided new insights into normal bile physiology and disease mechanisms, and may yield novel therapies to improve certain cholestatic conditions.</dc:description>
</entry>
<entry>
<title>The health of physiology: a perspective</title>
<link href="http://sedici.unlp.edu.ar:80/handle/10915/127641" rel="alternate"/>
<author>
<name>O’Halloran, Ken D.</name>
</author>
<id>http://sedici.unlp.edu.ar:80/handle/10915/127641</id>
<updated>2021-11-03T12:09:24Z</updated>
<published>2016-10-01T00:00:00Z</published>
<summary type="text">Revision
Physiological Mini Reviews; vol. 9, no. 6
What does a health check for Physiology in the 21st century reveal? Has it run its course as a research discipline? Will it soon be confined to the lecture halls and libraries of contemporary institutions? Or on the contrary, does it have a bright future, a central role to play in the pursuit of fundamental knowledge for the benefit of human health? Physiology's current predicament is a paradox of sorts: increasingly invisible, and to some in rapid irreversible decline, yet it appears never as popular in terms of Society membership, and global celebrations of the discipline, which demonstrably go from strength to strength. As with any conundrum, there are elegant solutions, and a growing interest within the community to seek them out. Against the backdrop of significant failings of the modern reductionist approach, Physiology, with its holistic approach to integrative function of complex organisms, has never seemed so relevant and important. Yet there are worrying signs. Morale in many camps is low. Brand Physiology appears in poor shape to those pulling the purse strings; past its heyday, dated, maybe even dead! Many others at the centre and fringes of the discipline are optimistic for Physiology's future, but it is increasingly clear that physiologists must take action, not so as to merely protect Physiology per se, but critically, so as to ensure it is enabled to contribute to the delivery of ambitious expectations set by the wider community, notably funders spending public monies. Physiology is essential to the realisation of plans for better health outcomes. It is pivotal to progress, once one accepts that progress is a slow incremental affair. It is timely that many conversations have commenced with a view to charting a course for Physiology through troubled waters. I hope to add constructively to the debate with observations and discussion serving to nudge Physiology ever closer to centre stage, where she belongs, in the theatre of the life sciences.
</summary>
<dc:date>2016-10-01T00:00:00Z</dc:date>
<dc:description>What does a health check for Physiology in the 21st century reveal? Has it run its course as a research discipline? Will it soon be confined to the lecture halls and libraries of contemporary institutions? Or on the contrary, does it have a bright future, a central role to play in the pursuit of fundamental knowledge for the benefit of human health? Physiology's current predicament is a paradox of sorts: increasingly invisible, and to some in rapid irreversible decline, yet it appears never as popular in terms of Society membership, and global celebrations of the discipline, which demonstrably go from strength to strength. As with any conundrum, there are elegant solutions, and a growing interest within the community to seek them out. Against the backdrop of significant failings of the modern reductionist approach, Physiology, with its holistic approach to integrative function of complex organisms, has never seemed so relevant and important. Yet there are worrying signs. Morale in many camps is low. Brand Physiology appears in poor shape to those pulling the purse strings; past its heyday, dated, maybe even dead! Many others at the centre and fringes of the discipline are optimistic for Physiology's future, but it is increasingly clear that physiologists must take action, not so as to merely protect Physiology per se, but critically, so as to ensure it is enabled to contribute to the delivery of ambitious expectations set by the wider community, notably funders spending public monies. Physiology is essential to the realisation of plans for better health outcomes. It is pivotal to progress, once one accepts that progress is a slow incremental affair. It is timely that many conversations have commenced with a view to charting a course for Physiology through troubled waters. I hope to add constructively to the debate with observations and discussion serving to nudge Physiology ever closer to centre stage, where she belongs, in the theatre of the life sciences.</dc:description>
</entry>
</feed>
