Some philosophers hold that it would be impossible for us to do something actively if the physical world were causally closed, i.e., if in the physical world all events were caused by other physical events if they are caused at all. The reason for this view is that these philosophers adhere to what I call the traditional picture of action. Recently, Martine Nida-Rümelin tried to defend this picture by phenomenological considerations. According to the traditional picture a behavior can only count as something an agent does actively if it is ultimately caused by the agent in an agent-causal way. In this paper I adduce three arguments against agent causation: (1) We do not really understand what agent causation is. (2) If agent causation were real, we would be confronted with the strange fact that human agents can only cause certain tiny events in the brain. (3) There is no empirical evidence that agent causation is real. In the last part of my paper I present an alternative account of the difference between what agents do actively and what is done to them., Někteří filosofové se domnívají, že by bylo pro nás nemožné něco aktivně činit, kdyby byl fyzický svět kauzálně uzavřen, tj. Kdyby byly všechny události způsobeny jinými fyzickými událostmi, kdyby byly ve fyzickém světě způsobeny vůbec. Důvodem tohoto názoru je, že tito filozofové dodržují to, čemu říkám tradiční obraz jednání. Nedávno se Martine Nida-Rümelin pokusila tento obraz obhájit fenomenologickými úvahami. Podle tradičního obrazu se chování může počítat pouze jako něco, co agent dělá aktivně, pokud je nakonec způsobeno agentem v kauzálním způsobu. V tomto příspěvku uvádím tři argumenty proti příčinám agenta: (1) Opravdu nechápeme, co je to příčina agenta. (2) Pokud byla příčinná souvislost agenta skutečná, byli bychom konfrontováni s podivnou skutečností, že lidští agenti mohou v mozku způsobit jen určité drobné události. (3) Neexistují žádné empirické důkazy, že příčinná souvislost agentů je skutečná. V poslední části mé práce uvádím alternativní popis rozdílu mezi tím, co agenti aktivně dělají a co se s nimi děje., and Ansgar Beckermann
I review some aspects of recent studies of active galactic nuclei (AGN) and their environments. My approach is from the hypothesis that a single AGN phenomenon includes the plethora of object classes whose acronyms pervade the literature. Particular attention is given to the mechanisms of interaction between the cetral engine and its environment, both with regard to the ways in which the observed radiation is produced on a range of spatial scales and to the ways in which the activity is related to outside influences.
Results of radar observatlons of tho Orionid and Eta Aquarid meteor showers carried out In Budrio (Italy) wlthin the IHW program are compared with the simultaneous data from Ondřejov
(Czechoslovakia). The activlty of these showers Is studied in the relation to the motion of large particles ejected from the comet. The activity was found to be independent on tho approach of the parent comet.
Parallel glucose measurements in blood and other different tissues give us knowledge about dynamics of glycemia changes, which depend on vascularization, distribution space and local utilization by tissues. Such information is important for the understanding of glucose homeostasis and regulation. The aim of our study was to determine the time-lag between blood, brain, and adipose tissue during rapid glucose changes in a male hHTG rat (n=15). The CGMS sensor Guardian RT (Minimed/Medtronic, USA) was inserted into the brain and into the abdominal subcutaneous tissue. Fixed insulin and variable rate of glucose infusion was used to maintain euglycemia during sensor calibration period. At 0 min, 0.5 g/kg of bolus of glucose was administered, and at 50 min, 5 IU/kg of bolus of insulin was administered. Further glucose and insulin infusion was stopped at this time. The experiment was finished at 130 min and animals were euthanized. The time-shift between glycemia changes in blood, brain, and subcutaneous tissue was calculated by identification of the ideal correlation function. Moreover, the time to achieve 90 % of the maximum glucose excursion after intervention (T90) was measured to compare our data with the literature. The time-lag blood vs. brain and blood vs. subcutaneous tissue was 10 (10; 15) min and 15 (15; 25) min, respectively. The difference was statistically significant (P=0.01). T90 after glucose bolus in brain and subcutaneous tissue was 10 min (8.75; 15) and 15 min (13.75; 21.25), respectively. T90 after insulin bolus in brain and subcutaneous tissue was 10 min (10; 15) and 20 min (20; 27.5), respectively. To the contrary, with literature, our results showed earlier glucose level changes in brain in comparison with subcutaneous tissue after glucose and insulin boluses. Our results suggest that glucose dynamics is different within monitored tissues under rapid changing glucose level and we can expect similar behavior in humans. Improved knowledge about glucose distribution and dynamics is important for avoiding hypoglycemia., M. Žourek, P. Kyselová, D. Čechurová, Z. Rušavý., and Seznam literatury
Telmisartan is an angiotensin receptor blocker (ARB) and a selective peroxisome proliferator activated receptor gamma (PPARG) modulator. Recently, we tested metabolic effects of telmisartan (5 mg/kg body weight) in spontaneously hypertensive rats (SHR) fed a diet containing 60 % fructose, a widely used model of the metabolic syndrome. Surprisingly, we observed acute toxic effects of telmisartan. Rats lost body weight rapidly and died within 2 to 3 weeks due to bleeding into the upper gastrointestinal tract. SHR fed a high fructose diet and treated with telmisartan exhibited rapid decrease in blood pressure when compared to the SHR fed a high fructose diet and treated with valsartan. Concentrations of both unconjugated telmisartan and telmisartan glucuronide in the liver of SHR rats fed a high fructose diet were approximately 4 fold higher when compared to Brown Norway (BN) rats fed the same diet. Plasma concentrations of unconjugated telmisartan in the SHR were about 5 fold higher when compared to BN rats while plasma levels of telmisartan glucuronide were similar between the strains. Testing of other rat strains, diets, and the ARB valsartan showed that toxic effects of telmisartan in combination with high fructose diet are specific for the SHR. These results are consistent with the possibility that in some circumstances, SHR are predisposed to telmisartan toxicity possibly because of a genetically determined disturbance in telmisartan metabolism.