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Endocannabinoids (eCBs) anandamide (AEA) and 2-arachidonoylglycerol (2-AG) were shown to be involved in the basis of trauma-induced behavioral changes, particularly contextual conditioned fear, however, their ligand-specific effects and possible interactions are poorly understood. Here we assessed specific eCB effects and interactions on acquisition of contextual conditioned fear employing electric footshocks in a rat model. We selectively increased eCB levels by pharmacological blockade of the degrading enzymes of AEA by URB597 and 2-AG by JZL184 before traumatization either systemically or locally in relevant brain areas, the prelimbic cortex (PrL), ventral hippocampus (vHC) and basolateral amygdala (BLA). Following traumatization, a series of contextual reminders were conducted during which conditioned fear was assessed. While systemic URB597-treatment during traumatization only slightly enhanced the acquisition of contextual conditioned fear, administration of the compound in the PrL and vHC led to the acquisition of stable, lasting conditioned fear, resistant to extinction. These effects of URB597 were blocked by simultaneous administration of JZL184. Similar treatment effects did not occur in the BLA. Treatment effects were not secondary to alterations in locomotor activity or nociception. Our findings suggest that AEA and 2-AG functionally interact in the regulation of acquisition of contextual conditioned fear. AEA signaling in the PrL and vHC is a crucial promoter of fear acquisition while 2-AG potentially modulates this effect. The lack of eCB effects in the BLA suggests functional specificity of eCBs at distinct brain sites.

The role of vasopressin in aggression received much attention in recent years. However, vasopressin has complex roles on social behavior, which are affected by social experience, motivation and hormonal background, suggesting that its effects depend on the condition of subjects. This hypothesis was tested here by studying the impact of vasopressin deficiency on aggressiveness in reproductively naive and reproductively experienced males, as well as in lactating females, with special reference to the patterns and contexts of attack behavior. We also studied effects on impulsiveness, a behavioral feature strongly related to aggression. Vasopressin deficiency did not affect aggressiveness in reproductively experienced males, decreased the share of violent attacks in reproductively inexperienced males without affecting total attack counts, and suppressed maternal aggression in both early and late phases of lactation; violent forms of attack were decreased in the latter but not the former phase. Changes in aggression appeared unrelated to general changes in maternal behaviors. Impulsivity in the delay discounting task was markedly decreased by vasopressin deficiency in lactating females but not males. Taken together, our findings confirm that vasopressin has an impact on aggressiveness, but show that this impact depends on the condition of subjects, and suggest that the effects of vasopressin on maternal aggression develop in conjunction with impulsivity. Interestingly, overall effects on aggression and specific effects on violent attacks dissociated in both males and females, which hints to the possibility that vasopressin has distinct roles in the development of escalated forms of aggression.

Vasopressin (AVP)-deficient Brattleboro rats develop a specific behavioral profile, which-among other things-include altered cognitive performance. This profile is markedly affected by alterations in neuroendocrine state of the animal such as during lactation. Given the links between AVP and cognition we hypothesized that AVP deficiency may lead to changes in impulsivity that is under cognitive control and the changes might be altered by lactation. Comparing virgin and lactating AVP-deficient female Brattleboro rats to their respective controls, we assessed the putative lactation-dependent effects of AVP deficiency on impulsivity in the delay discounting paradigm. Furthermore, to investigate the basis of such effects, we assessed possible interactions of AVP deficiency with GABAergic and serotonergic signaling and stress axis activity, systems playing important roles in impulse control. Our results showed that impulsivity was unaltered by AVP deficiency in virgin rats. In contrast a lactation-induced increase in impulsivity was abolished by AVP deficiency in lactating females. We also found that chlordiazepoxide-induced facilitation of GABAergic and imipramine-induced enhancement of serotonergic activity in virgins led to increased and decreased impulsivity, respectively. In contrast, during lactation these effects were visible only in AVP-deficient rats. These rats also exhibited increased stress axis activity compared to virgin animals, an effect that was abolished by AVP deficiency. Taken together, AVP appears to play a role in the regulation of impulsivity exclusively during lactation: it has an impulsivity increasing effect which is potentially mediated via stress axis-dependent mechanisms and fine-tuning of GABAergic and serotonergic function.

In this article we aim at achieving trusted data collection from heterogeneous distributed sources including legacy systems and human end users. We adopt an agent-like approach where we are able to send agents to host platforms connected to legacy systems. Functionality of agents may vary while we are solving the trust between host platforms, legacy systems and agents. We had not used any existing multi-agent system but we extended an existing production grade service platform called Jini and implemented agents above Jini services. The core of this work is about how we adopted the Jini platform to host agents. We also provide examples about the implementation and integration of the platform in a real world example — a crisis management domain. We present our current achievements and plans concerning the implementation of the proposed platform.

Endocannabinoid (eCB) signaling is a major contributor in the regulation of behavioral responses to traumas [1] and acquisition of traumatic memories [2]. ECBs anandamide (AEA) and 2-arachidonoilglycerol (2-AG) were reported to differentially affect particular aspects of behaviour [3] but their specific role in the regulation of responses to traumatic events is yet to be clarified. Furthermore, AEA and 2-AG signaling were recently shown to interact [4] which can possibly have functional relevance in their behavioral effects as well. Here we aimed to describe the specific contribution of eCBs and their interactions in the regulation of acute responses to a traumatic event and the acquisition of traumatic memories. We employed electric footshocks to traumatize Wistar rats in which eCB signaling was enhanced by the specific pharmacological blockade of the degrading enzyme of AEA by URB597 and 2-AG by JZL184. Treatments were delivered either systemically (URB597: 0.3 mg/kg; JZL184: 16 mg/kg) or locally to brain areas relevant in the regulation of traumatic memory, the ventral hippocampus (vHC), prelimbic cortex (PrL) and basolateral amygdala (BLA) (URB597: 1 ng/0.5 ul; JZL184: 1 ug/0.5 ul). To elucidate whether the effects of enhanced eCB signaling are modulated via cannabinoid receptor type-1 (CB1R), CB1R antagonist AM251 (1 mg/kg) was simultaneously administered with URB597 and JZL184. Systemic administration of JZL148 dampened acute fear responses to footshocks measured by freezing behavior, which was blocked by parallel treatment with URB597 (one-way ANOVA: F(4,46)=13.59; p

Mono-(Co) and bimetallic (Fe-Co) catalysts supported by either 13X zeolite or CaCO 3 were doped with potassium and tested in carbon nanotube (CNT) production using the chemical vapor deposition (CVD) method. In order to increase comparability, the evaluation of the performance of the catalysts a combinatorial arrangement was also used. Catalyst samples were characterized by carbon deposit and carbon yield values. For qualitative characterization, products were investigated by transmission electron microscopy.

Example There exists a space X with a sharp base and a perfect mapping f : X → Y onto a space Y which does not have a sharp base. It is known that a spaces with a sharp base have a point-countable sharp base. This can be sharpened to “point-finite” on the set of isolated points. Theorem If X has a sharp base then X has a point-countable sharp base which is point-finite on the set Z of isolated points. (Hence Z is an F σ set.) A topological proof of the previous theorem is given but the theorem follows from a more general combinatorial statement about certain subsets of κ × κ . This last statement is proved using a set-theoretic argument.

We show that there is a perfectly normal non-metrizable manifold if there is a Luzin subset of the real line, and that there is a countably compact perfectly normal non-metrizable manifold in any model of set-theory obtained by adding Cohen reals to a model of ZFC + ⋄ .

We investigate when countable multiplicity of jigsawed bases and similar collections on sets of various sizes implies metrizability in compact and countably compact spaces.

We prove various reflection theorems in locally nice spaces using Axiom R.

For every uncountable cardinal κ we construct, in ZFC, a space X κ such that (a) the product of X κ with every metrizable space is normal; (b) X κ has an increasing ω 1 -cover by open sets that has no refinement by ⩽κ many closed sets. This answers a question of M.E. Rudin. It also proves a conjecture of K. Morita on a characterization of metrizability in terms normality of products.

We construct, in ZFC, a hereditarily collectionwise normal, hereditarily metaLindelof, hereditarily realcompact Dowker space. This answers a question of R. Hodel (also asked by S. Watson and D. Burke) and another question of M.E. Rudin.

For every regular cardinal κ we construct a hereditarily normal, countably paracompact space X κ which has an increasing open cover W = { W μ : μ ϵ ω 1 } such that W has no refinement by ⩽ κ closed sets. By work of Chiba, Przymusinski and Rudin, the existence of such a space proves a conjecture of Morita that σ-locally compact metrizable spaces are precisely the spaces whose product with every normal, countably paracompact space is normal. The spaces X κ are the first known examples of hereditarily normal ω 1 -Dowker spaces.

A topological property P is called n -additive in n th power (or weakly n -additive) if a topological space X has P as soon as X n = ∪{ Y i : i ϵ n } where all Y i have P. If P is n -additive in n th power for all natural n ⩾ 1, we say that P is weakly finitely additive. The main question we deal with in this paper is whether metrizability is weakly finitely additive. It was proved by Tkachuk (1994) that it is so in the class of regular spaces with Souslin property. Metrizability was also proved by Tkachuk (1994) to be weakly finitely additive in the class of Hausdorff compact spaces. We generalize this last result, showing that metrizability is weakly finitely additive in the class of regular pseudocompact spaces. We also prove that if X n is a regular Lindelof space then it is metrizable if represented as a union of its n metrizable subspaces. We show that there is an example of a Tychonoff nonmetrizable space X such that X n is a union of two metrizable subspaces for all n ⩾ 1. The method of constructing this example can be used to solve several problems stated by Tkachuk (1994).

A ladder system L on the set of limit ordinals is defined by iterated ccc forcing. The natural topological space X L derived from L is a locally compact, locally countable scattered space of height 2 which is ↗-normal, is a Morita P -space (and thus, countably metacompact), but the space is not perfect or normal. Then we discuss a number of reasons why such a space cannot exist in ZFC and in fact, in many models.

Many of earlier and recent results obtained for p -spaces and their relatives can be extended by using a simple and natural concept (relative compactness) which was defined and investigated in an earlier paper of the author. In the present paper extensions of recent metrization theorems concerning p -spaces are dealt with. A recent metrization theorem of J. Nagata is extended to relative compactness. Under the assumption of the continuum hypothesis A.V. Arhangel'skiǐ's problem asking whether a space, each subspace of which is a paracompact p -space, contains a dense metrizable subspace, is solved affirmatively (and for the generality of relative compactness). Some results concerning the behaviour of the first axiom of countability and its generalizations under relative compactness are also included.

We prove that a locally connected, rim-Lindelof, submeta Lindelof, normal, ⩽ω 2 -collectionwise T 2 space is paracompact. Further, if ‘Lindelof’ is replaced by ‘compact’, then ‘⩽ω 2 -collectionwise T 2 ’ can be omitted.

The notions of an S δ set and an R δ set are introduced. A space is S -perfect ( R -perfect) if each closed set is an S δ set ( R δ ) set. Conditions are given which indicate when spaces are S -perfect or R -perfect. Examples are given of spaces which do not have these properties and examples are given of spaces with these properties that are not perfect spaces. The images of S -perfect and R -perfect spaces under various types of mappings are investigated.

It is proven that under V = L, every locally compact, countably paracompact space is collectionwise normal with respect to compact sets. From this it can be shown that under V = L, submetacompact implies paracompact in the class of locally compact, countably paracompact spaces.

In this paper the structure of hereditarily strong Σ-spaces (hsΣ-spaces, for short) is dealt with. The main result asserts that an hsΣ-space is the disjoint union of two σ subspaces one of which is an F σ , the other a G δ subset. Examples are given that in many ways, this decomposition cannot be improved. Then we investigate the question when an hsΣ-space is a σ-space. It is shown that a GO-space (or a first countable compactum) is metrizable iff it is an hsΣ-space, thereby proving a conjecture of J. van Wouwe. σ-spaces are characterized as being identical with perfect hsΣ-spaces. The question whether a Lindelof, first countable hsΣ-space is a σ-space is shown to be independent of set theory. A characterization of hsΣ-spaces with no compact subsets of cardinality >2 ω is given.