261 research outputs found

    Socratic Ignorance

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    In Plato’s Apology, Socrates famously claimed to know nothing. This Socratic claim to ignorance pervades all of Plato’s early dialogues, and it raises many puzzling questions. By working through these puzzles, we can come to understand the figure of Socrates much better, and we can also gain some insight into the nature and purpose of philosophy

    It is No Longer I that Do it...

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    Augustine on the Mind\u27s Search for Itself

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    Z dziecięcych rozważań nad szczęściem

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    Szczęście jest czymś, co każdy musi znaleźć sam dla siebie. Powstaje zatem pytanie: Jak? Najlepiej przekonujemy się o tym, co tak naprawdę myślimy, w momencie, gdy skonfrontujemy nasze wyobrażenia i poglądy z innymi, kiedy to uzewnętrzniamy je i poznajemy, co inni uważają na dany temat. Nawet jeśli chodzi o tak trudną ustalenia „pełnię szczęścia”. Gareth Matthews omówił opowieść dotyczącą „szczęścia” z dziećmi z różnych krajów (USA, Japonii, Chin). Rozmowy te pokazały, że dzieci również mają różne koncepcje „szczęścia”, że każde na swój sposób je odczuwa i że w każdym przypadku co innego przybliża je do odczuwania „pełni szczęścia”. Właśnie przez tego rodzaju rozmowy, dyskusje filozoficzne, wzmacnia się wyobraźnię moralną dzieci. Ta jest niezbędna do rozwoju moralnego dzieci, by stały się gotowe do podejmowania decyzji moralnych, a co za tym idzie do podejmowania odpowiedzialności. Również innym istotnym elementem jest refleksja moralna, tj. refleksja nad zasadami moralnymi czy nad motywacją towarzyszącą postępowaniu. Tej refleksji dzieci mogą doświadczyć właśnie podczas dyskusji filozoficznych. Dzięki temu poznają, jak postępuje człowiek moralny. Tego rodzaju filozoficzne rozważania mogą przynieść korzyść nie tylko dzieciom, ale również nauczycielom czy rodzicom

    学齢期の子どもたちのためのプラントン

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    訳 : 寺田, 俊

    Opportunity to assimilate and pressure to discriminate can generate cultural divergence in the laboratory

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    Formal models of cultural evolution have illustrated circumstances under which behavioral traits that have no inherent advantage over others can undergo positive selection pressure. One situation in which this may occur is when the behavior functions as a social marker, and there is pressure to identify oneself as a member of a particular group. Our aim in the current study was to determine whether participants organized into subpopulations could effectively exploit variation in a completely novel behavior to advertise themselves as belonging to a particular subpopulation, such that discrimination between in-group and out-group members was possible and subpopulations exhibited increasing distinctiveness. Eighty participants took part, organized into four subpopulations, each comprised of five four-member generations. They each completed a tower-building task, used in previous experimental studies of cultural evolution. An incentive payment structure was imposed with the aim of motivating participants to advertise themselves as belonging to a particular subpopulation, and to distinguish in-group members from members of other subpopulations. The first generation were exposed to photographs of randomly-assigned "seed" towers, and later generations were exposed to photographs of the towers built by the members of the previous generation of their own subpopulation. Participants were able to discriminate towers built by in-group members of the same generation, from towers built by out-group members. Over generations, tower designs evolved such that they were increasingly identifiable as belonging to a particular subpopulation. Arbitrary traits, which had no prior advantage, became associated with group membership, providing empirical support for theoretical models

    Sudden cardiac death and inherited channelopathy: the basic electrophysiology of the myocyte and myocardium in ion channel disease

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    Mutations involving cardiac ion channels result in abnormal action potential formation or propagation, leading to cardiac arrhythmias. Despite the large impact on society of sudden cardiac death resulting from such arrhythmias, understanding of the underlying cellular mechanism is poor and clinical risk stratification and treatment consequently limited. Basic research using molecular techniques, as well as animal models, has proved extremely useful in improving our knowledge of inherited arrhythmogenic syndromes. This offers the practitioner tools to accurately diagnose rare disorders and provides novel markers for risk assessment and a basis for new strategies of treatment

    Abnormal Ca2+ homeostasis, atrial arrhythmogenesis, and sinus node dysfunction in murine hearts modeling RyR2 modification

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    Ryanodine receptor type 2 (RyR2) mutations are implicated in catecholaminergic polymorphic ventricular tachycardia (CPVT) thought to result from altered myocyte Ca(2+) homeostasis reflecting inappropriate “leakiness” of RyR2-Ca(2+) release channels arising from increases in their basal activity, alterations in their phosphorylation, or defective interactions with other molecules or ions. The latter include calstabin, calsequestrin-2, Mg(2+), and extraluminal or intraluminal Ca(2+). Recent clinical studies additionally associate RyR2 abnormalities with atrial arrhythmias including atrial tachycardia (AT), fibrillation (AF), and standstill, and sinus node dysfunction (SND). Some RyR2 mutations associated with CPVT in mouse models also show such arrhythmias that similarly correlate with altered Ca(2+) homeostasis. Some examples show evidence for increased Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) phosphorylation of RyR2. A homozygotic RyR2-P2328S variant demonstrates potential arrhythmic substrate resulting from reduced conduction velocity (CV) in addition to delayed afterdepolarizations (DADs) and ectopic action potential (AP) firing. Finally, one model with an increased RyR2 activity in the sino-atrial node (SAN) shows decreased automaticity in the presence of Ca(2+)-dependent decreases in I(Ca, L) and diastolic sarcoplasmic reticular (SR) Ca(2+) depletion

    Real-time extraction of the Madden-Julian oscillation using empirical mode decomposition and statistical forecasting with a VARMA model

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    A simple guide to the new technique of empirical mode decomposition (EMD) in a meteorological-climate forecasting context is presented. A single application of EMD to a time series essentially acts as a local high-pass filter. Hence, successive applications can be used to produce a bandpass filter that is highly efficient at extracting a broadband signal such as the Madden-Julian Oscillation (MJO). The basic EMD method is adapted to minimize end effects, such that it is suitable for use in real time. The EMD process is then used to efficiently extract the MJO signal from gridded time series of outgoing longwave radiation (OLR) data. A range of statistical models from the general class of vector autoregressive moving average (VARMA) models was then tested for their suitability in forecasting the MJO signal, as isolated by the EMD. A VARMA (5, 1) model was selected and its parameters determined by a maximum likelihood method using 17 yr of OLR data from 1980 to 1996. Forecasts were then made on the remaining independent data from 1998 to 2004. These were made in real time, as only data up to the date the forecast was made were used. The median skill of forecasts was accurate (defined as an anomaly correlation above 0.6) at lead times up to 25 days
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