Reid and Condillac on Sensation and Perception: A Thought Experiment on Sensory Deprivation

In order to illustrate the difference between sensation and perception, Reid imagines a blind man that by ‘some strange distemper’ has lost all his notions of external objects, but has retained the power of sensation and reasoning. Reid argues that since sensations do not resemble external objects, the blind man could not possibly infer from them any notion of primary qualities. Condillac proposed a similar thought experiment in the Treatise on Sensations. I argue that Condillac can reach a conclusion opposite to that of Reid only by assuming that some particular collections of sensations do indeed resemble the qualities of external objects. Reid had considered a similar case in a manuscript, but he again notices that such complex collections sensations do not resemble the qualities of external objects

X-rays from Radio-Galaxies: BeppoSAX Observations

We briefly review BeppoSAX observations of X-ray bright radio-galaxies. Their X-ray spectra are quite varied, and perhaps surprisingly, any similarity between radio-loud AGN and Seyfert galaxies is the exception rather than the rule. When detected, reprocessing features (iron line and reflection) are generally weak, suggesting two possible scenarios: either: (1) non-thermal (jet?) radiation dilutes the X-ray emission from the disk in radio-loud objects, or (2) the solid angle subtended by the X-ray reprocessing material is smaller in radio-loud than in radio-quiet AGN due to different characteristics of the accretion disk itself.Comment: 6 pages, to appear in `Life Cycles of Radio Galaxies', ed. J. Biretta et al., New Astronomy Review

A network-based rating system and its resistance to bribery

We study a rating system in which a set of individuals (e.g., the customers of a restaurant) evaluate a given service (e.g, the restaurant), with their aggregated opinion determining the probability of all individuals to use the service and thus its generated revenue. We explicitly model the influence relation by a social network, with individuals being influenced by the evaluation of their trusted peers. On top of that we allow a malicious service provider (e.g., the restaurant owner) to bribe some individuals, i.e., to invest a part of his or her expected income to modify their opinion, therefore influencing his or her final gain. We analyse the effect of bribing strategies under various constraints, and we show under what conditions the system is bribery-proof, i.e., no bribing strategy yields a strictly positive expected gain to the service provider

Logistic regression analysis of populations of electrophysiological models to assess proarrythmic risk.

Population-based computational approaches have been developed in recent years and helped to gain insight into arrhythmia mechanisms, and intra- and inter-patient variability (e.g., in drug responses). Here, we illustrate the use of multivariable logistic regression to analyze the factors that enhance or reduce the susceptibility to cellular arrhythmogenic events. As an example, we generate 1000 model variants by randomly modifying ionic conductances and maximal rates of ion transports in our atrial myocyte model and simulate an arrhythmia-provoking protocol that enhances early afterdepolarization (EAD) proclivity. We then treat EAD occurrence as a categorical, yes or no variable, and perform logistic regression to relate perturbations in model parameters to the presence/absence of EADs. We find that EAD formation is sensitive to the conductance of the voltage-gated Na+, the acetylcholine-sensitive and ultra-rapid K+ channels, and the Na+/Ca2+ exchange current, which matches our mechanistic understanding of the process and preliminary sensitivity analysis. The described technique: •allows investigating the factors underlying dichotomous outcomes, and is therefore a useful tool improve our understanding of arrhythmic risk;•is valid for analyzing both deterministic and stochastic models, and various phenomena (e.g., delayed afterdepolarizations and Ca2+ sparks);•is computationally more efficient than one-at-a-time parameter sensitivity analysis

CaMKII-dependent regulation of cardiac Na(+) homeostasis.

Na(+) homeostasis is a key regulator of cardiac excitation and contraction. The cardiac voltage-gated Na(+) channel, NaV1.5, critically controls cell excitability, and altered channel gating has been implicated in both inherited and acquired arrhythmias. Ca(2) (+)/calmodulin-dependent protein kinase II (CaMKII), a serine/threonine kinase important in cardiac physiology and disease, phosphorylates NaV1.5 at multiple sites within the first intracellular linker loop to regulate channel gating. Although CaMKII sites on the channel have been identified (S516, T594, S571), the relative role of each of these phospho-sites in channel gating properties remains unclear, whereby both loss-of-function (reduced availability) and gain-of-function (late Na(+) current, INa L) effects have been reported. Our review highlights investigating the complex multi-site phospho-regulation of NaV1.5 gating is crucial to understanding the genesis of acquired arrhythmias in heart failure (HF) and CaMKII activated conditions. In addition, the increased Na(+) influx accompanying INa L may also indirectly contribute to arrhythmia by promoting Ca(2) (+) overload. While the precise mechanisms of Na(+) loading during HF remain unclear, and quantitative analyses of the contribution of INa L are lacking, disrupted Na(+) homeostasis is a consistent feature of HF. Computational and experimental observations suggest that both increased diastolic Na(+) influx and action potential prolongation due to systolic INa L contribute to disruption of Ca(2) (+) handling in failing hearts. Furthermore, simulations reveal a synergistic interaction between perturbed Na(+) fluxes and CaMKII, and confirm recent experimental findings of an arrhythmogenic feedback loop, whereby CaMKII activation is at once a cause and a consequence of Na(+) loading