Kompetenciamenedzsment az Európai Unió közszolgálatában - kiválasztás = Competency management in EU civil service - selection

Human capital is the key resource of every organisation, which endeavours to achieve the organizational goal. Implementing a competence-based approach has been a major trend in HR management in recent past. These statements apply to today main international player, to the European Union as well. Europe's partly supranational organization has evolved the principles, the schemes for selection, career advancement and compensation and the rights and obligations of its secretariat during the 20th century. This paper will discuss the role of competencies in the EU civil service system in particular, in recruitment. The relevancy of the issue is proven by the fact that improving competency-based approach has been a strategic goal during the 2010 concurs reform. This essay defines competency as "the ability of successful action" grouping them into three: knowledge, skills and attitudes and evaluating them during the two important selection phases: recruitment and concurs

Kompetenciamenedzsment az Európai Unió közszolgálatában - kiválasztás = Competency management in EU civil service - selection

Human capital is the key resource of every organisation, which endeavours to achieve the organizational goal. Implementing a competence-based approach has been a major trend in HR management in recent past. These statements apply to today main international player, to the European Union as well. Europe's partly supranational organization has evolved the principles, the schemes for selection, career advancement and compensation and the rights and obligations of its secretariat during the 20th century. This paper will discuss the role of competencies in the EU civil service system in particular, in recruitment. The relevancy of the issue is proven by the fact that improving competency-based approach has been a strategic goal during the 2010 concurs reform. This essay defines competency as "the ability of successful action" grouping them into three: knowledge, skills and attitudes and evaluating them during the two important selection phases: recruitment and concurs

THE ORIGIN OF HEAVY METAL CONTENT IN SOILS OF AGGTELEK KARST (NE HUNGARY)

The origin of the high heavy metal content in the soils near Lake Vörös on Aggtelek-Karst (NE Hungary) was studied by detailed examination of the elemental composition and distribution in a depth profile of the soil formed on slope sediments of red clay redzina. This work was focused on Cu, Zn and Pb contents because these elements can indicate supposed hydrothermal ore formation processes in this area. For examining the spatial distribution of Cu, Zn and Pb in the studied area we have extended our research further 13 soil samples. In addition, the elemental composition of limestone bedrock of the soils was also investigated. Our results show both natural and anthropogenic influence on heavy metal content in soils. However the results do not undoubtedly confirm the same geochemical origin of the studied elements

Amyloid-β1-42 Disrupts Synaptic Plasticity by Altering Glutamate Recycling at the Synapse.

Alzheimer's disease (AD) is the most prevalent form of neurodegenerative disorders characterized by neuritic plaques containing amyloid-β peptide (Aβ) and neurofibrillary tangles. Evidence has been reported that Aβ(1-42) plays an essential pathogenic role in decreased spine density, impairment of synaptic plasticity, and neuronal loss with disruption of memory-related synapse function, all associated with AD. Experimentally, Aβ(1-42) oligomers perturb hippocampal long-term potentiation (LTP), an electrophysiological correlate of learning and memory. Aβ was also reported to perturb synaptic glutamate (Glu)-recycling by inhibiting excitatory-amino-acid-transporters. Elevated level of extracellular Glu leads to activation of perisynaptic receptors, including NR2B subunit containing NMDARs. These receptors were shown to induce impaired LTP and enhanced long-term depression and proapoptotic pathways, all central features of AD. In the present study, we investigated the role of Glu-recycling on Aβ(1-42)-induced LTP deficit in the CA1. We found that Aβ-induced LTP damage, which was mimicked by the Glu-reuptake inhibitor TBOA, could be rescued by blocking the NR2B subunit of NMDA receptors. Furthermore, decreasing the level of extracellular Glu using a Glu scavenger also restores TBOA or Aβ induces LTP damage. Overall, these results suggest that reducing ambient Glu in the brain can be protective against Aβ-induced synaptic disruption

Abeta(1-42) Enhances Neuronal Excitability in the CA1 via NR2B Subunit-Containing NMDA Receptors

Neuronal hyperexcitability is a phenomenon associated with early Alzheimer's disease. The underlying mechanism is considered to involve excessive activation of glutamate receptors; however, the exact molecular pathway remains to be determined. Extracellular recording from the CA1 of hippocampal slices is a long-standing standard for a range of studies both in basic research and in neuropharmacology. Evoked field potentials (fEPSPs) are regarded as the input, while spiking rate is regarded as the output of the neuronal network; however, the relationship between these two phenomena is not fully clear. We investigated the relationship between spontaneous spiking and evoked fEPSPs using mouse hippocampal slices. Blocking AMPA receptors (AMPARs) with CNQX abolished fEPSPs, but left firing rate unchanged. NMDA receptor (NMDAR) blockade with MK801 decreased neuronal spiking dose dependently without altering fEPSPs. Activating NMDARs by small concentration of NMDA induced a trend of increased firing. These results suggest that fEPSPs are mediated by synaptic activation of AMPARs, while spontaneous firing is regulated by the activation of extrasynaptic NMDARs. Synaptotoxic Abeta(1-42) increased firing activity without modifying evoked fEPSPs. This hyperexcitation was prevented by ifenprodil, an antagonist of the NR2B NMDARs. Overall, these results suggest that Abeta(1-42) induced neuronal overactivity is not dependent on AMPARs but requires NR2B