Újabb adatok a Duna-konföderációs tervezet nemzetközi sajtóvisszhangjához

The most important document of Kossuth’s emigration has been examined multiple times, but the international media coverage of the plan that was leaked due to the indiscretion of Ignác Helfy has rarely been touched upon. The digitalisation of contemporary newspapers is currently at the point where we can start discussing the media coverage of the plan and examine the various opinions regarding the Danubian Confederation and the arguments for and against it. By reviewing the French, Italian, English, and German newspapers we can see that they discussed the plan that was published in the newspaper Alleanza (The Alliance), but they gave more room to negative opinions and criticism, and they barely even considered Kossuth’s clarifications. It is important to note that Ignác Helfy’s foreword was not published at all, even though he states that it should not be considered an official political document, and the newspapers discussed the plan like it was a complete political program. Due to being more involved the Italian and German language press discussed the plan significantly more, and it can also be seen that apart from the Italians - who had an interest in weakening the Habsburg Empire – every press outlet wrote about the plan either neutrally, or more often in a negative light

Properties of minimally tt-tough graphs

A graph $G$ is minimally $t$-tough if the toughness of $G$ is $t$ and the deletion of any edge from $G$ decreases the toughness. Kriesell conjectured that for every minimally $1$-tough graph the minimum degree $\delta(G)=2$. We show that in every minimally $1$-tough graph $\delta(G)\le\frac{n+2}{3}$. We also prove that every minimally $1$-tough claw-free graph is a cycle. On the other hand, we show that for every $t \in \mathbb{Q}$ any graph can be embedded as an induced subgraph into a minimally $t$-tough graph

Az akut L-kinurenin szulfát kezelés magatartási, szövettani és keringési hatásainak komplex vizsgálata C57Bl/6j egér törzsben

L-Kynurenine (L-KYN) is a central metabolite of tryptophan degradation: known as kynurenine pathway, it is a cascade of enzymatic steps generating biologically active compounds, through which more than 95% of the tryptophan is catabolized. The early phase of the catabolic steps takes place mainly in the liver and the kidneys. However, the metabolization of L-KYN can effectively proceeds in the brain. The blood brain barrier strongly limits the penetrability of the kynurenine metabolites from the periphery to the central nervous system, since most of them can only be transferred by passive diffusion with a very low efficacy. One clear exception is the L-KYN, which can enter the brain with the aid of a large neutral amino acid transporter. Thus, the cerebral kynurenine metabolism is very responsive to the peripheral level of the L-KYN. Preclinical studies have shown that growth in the level of systemic L-KYN is particularly associated with a dose-dependent increase of its direct downstream metabolite kynurenic acid (KYNA) in the central nervous system. Evidence suggests that in the physiologically intact brain the most prominent and rapid change after peripheral L-KYN administration is the peak elevation of KYNA. KYNA is a complex neuromodulator, antioxidant and neuroprotective endogenous molecule. Elevation of brain KYNA content is correlated with attenuation in the concentration of extracellular glutamate, dopamine and acetylcholine in distinct cortical and subcortical brain regions. KYNA influences neurotransmission through multiple actions at the pre- and postsynaptic site. KYNA directly attenuates neurotransmitter release, partly by inhibiting α7 nicotinic acetylcholine (α7nACh) receptor located on presynaptic terminals, and partly by stimulating G-protein-coupled receptor 35 (GPR35) localized on neurons and astrocytes. Thus, even the modest fluctuations in endogenous KYNA can bi-directionally control the extracellular levels of glutamate. KYNA hinders postsynaptic N-methyl-D-aspartate (NMDA) receptor currents by competitive antagonism at allosteric glycine binding site of NMDA receptor. Moreover, in the periphery and in the brain during neuroinflammation, KYNA promotes anti-inflammatory responses due to activation of aryl hydrocarbon receptor and GPR35 receptor expressed by immune-cells, as well as it presumably also modulates neuronal survival through extrasynaptic NMDA receptor blockade. Besides its receptor-mediated actions, KYNA itself is a potent antioxidant. Therefore, elevation of brain KYNA level, either by administration of L-KYN or pharmacological manipulation of the availability of the kynurenine pathway enzymes, has become an attractive strategy to attenuate neuroinflammatory responses and to protect against glutamate induced excitotoxicity associated with ischemic brain injury. Accordingly, we and our collaborators achieved neuroprotection by the administration of L-KYN sulfate (L-KYNs) in experimental models of neurodegenerative diseases and ischemic stroke. Decades after the discovery of the neurotoxic and convulsant properties of glutamate, it has become clear that glutamate hypofunction is also pathogenic and therefore undesirable. Accordingly, in preclinical studies acute or chronic elevation of brain KYNA content, achieved partly by the peripheral administration of L-KYN, has been suggested to trigger alteration in the behavior of rodents: animals expressed hypoactivity or spatial working memory deficit. Moreover, pre- and postnatal chronic L-KYN exposure provoked long-lasting neurochemical and behavioral abnormalities manifested in adulthood. However, the results assessing the behavioral effects of the kynurenerg manipulations emerged from studies that focused mainly on rats, after various-dose of L-KYNs treatment. Implementing similar experiments in mice is of particular importance, because such data is almost absent from the literature. Additionally, the available information concerning the effects of kynurenerg manipulation beyond neuroprotection is quite incomplete, since study on dose-dependent responses to various L-KYNs treatment is not available. On a top of these, L-KYN and KYNA were attributed a direct role in the regulation of the systemic circulation. Namely, L-KYN was identified as an endothelium-derived vasodilator, contributing to peripheral arterial relaxation and regulation of blood pressure during systemic inflammation in rats. Furthermore, intravenous administration of low-dose L-KYN (1 mg/kg) has been shown to increase cerebral blood flow (CBF) in conscious rabbits. Therefore, we hypothesized that acute elevation of systemic L-KYN concentration may exert potential effects on mean arterial blood pressure (MABP) and on resting CBF in the adult mouse brain..

Hungarian named entity recognition with a maximum entropy approach

In the analysis of natural language text a key step is named entity recognition, finding all complex noun phrases that denote persons, organizations, locations, and other entities designated by a name. In this paper we introduce the hunner open source language-independent named entity recognition system, and present results for Hungarian. When the input to hunner is already morphologically analyzed, we apply the system together with the hunpos morphological disambiguator, but hunner is also capable of working on raw (morphologically unanalyzed) text