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Kiuru, P.

Publications and source records attributed to Kiuru, P..

2 recordsLinked to original sources

The SI compartment model describes embolism spreading in networks of vessels and bordered pits in angiosperm xylem

Plant xylem consists of a network of interconnected vessels, through which water is transported under negative pressure. Filling of vessels with air, or embolism, disturbs this transport process and, in extreme cases, leads to tree mortality. Despite this significance, embolism propagation dynamics are still poorly understood, primarily because xylem is opaque to direct observation. Furthermore, existing models of embolism spreading build excessively on physiological and anatomical parameters, and many misrepresent the inter-vessel pit membrane as a 2D surface. Here, we first extend these physiological models by implementing the pit membrane as a 3D object. Then, we introduce a susceptible-infected (SI) model, a simple stochastic model for tracking spreading through a population, for embolism propagation. After correctly fitting the spreading probability, our SI model reproduces vulnerability curves produced by both the physiological model and empirical data, highlighting that the SI model can address embolism spreading dynamics in plant species, for which detailed physiological data are not available. Furthermore, relating the SI model to the physiological one allows interpreting embolism spreading as a directed percolation process. Elucidating the exact mapping between directed percolation and embolism spreading will likely yield new fundamental insights into the relationships between xylem network architecture and embolism dynamics.

plant biology↗

Putative rapid-acting antidepressant nitrous oxide ("laughing gas") evokes rebound emergence of slow EEG oscillations during which TrkB signaling is induced

Electroconvulsive therapy (ECT) remains among the most efficient antidepressants but it seldom brings immediate remedy. However, a subanesthetic dose of NMDA-R (N-methyl-D-aspartate receptor) blocker ketamine ameliorates symptoms of depression already within hours. Glutamatergic excitability and regulation of TrkB neurotrophin receptor and GSK3{beta} (glycogen synthase kinase 3{beta}) signaling are considered as molecular-level determinants for ketamines antidepressant effects. Recent clinical observations suggests that nitrous oxide (N2O, \"laughing gas\"), another NMDA-R blocking dissociative anesthestic, also produces rapid antidepressant effects but the underlying mechanisms remain essentially unstudied. In this animal study we show that N2O, with a clinically relevant dosing regimen, evokes an emergence of rebound slow EEG (electroencephalogram) oscillations, a phenomenon considered to predict the efficacy and onset-of-action ECT. Very similar rebound slow oscillations are induced by subanesthetic ketamine and flurothyl (a treatment analogous to ECT). These responses become best evident upon drug withdrawal, i.e. after the peak of acute pharmacological actions, when their most prominent effects on cortical excitability have subsided. Most importantly, TrkB and GSK3{beta} signaling remain unchanged during N2O administration (ongoing NMDA-R blockade) but emerge gradually upon gas withdrawal along with increased slow EEG oscillations. Collectively these findings reveal that rapid-acting antidepressants produce cortical excitability that triggers \"a brain state\" dominated by ongoing slow oscillations, sedation and drowsiness during which TrkB and GSK3{beta} signaling alterations are induced.

pharmacology and toxicology↗