46 research outputs found
A koronavĂrus-járvány miatti többlethalálozás becslĂ©se Magyarországon
Jelen kutatás során a 60 Ă©ves vagy annál idĹ‘sebb nĂ©pessĂ©g körĂ©ben elĹ‘rejelezzĂĽk a 2020. Ă©vi halálozást havonta, nemek szerint. A Lee–Carter-fĂ©le Ă©s a CBD modell közötti választást a 2019-re szĂłlĂł elĹ‘rejelzĂ©s alapján teszteljĂĽk, vagyis megnĂ©zzĂĽk, hogy a kettĹ‘ közĂĽl melyik lehet alkalmasabb havi projekciĂł elkĂ©szĂtĂ©sĂ©re. EredmĂ©nykĂ©nt látni fogjuk, hogy amennyiben a 2020. Ă©vi tĂ©nyleges halálozási adatokat egy modell szerinti elĹ‘rejelzĂ©ssel vetjĂĽk össze, eltĂ©rĹ‘ Ă©rtĂ©ket kapunk, mint ha az elĹ‘zĹ‘ Ă©vek átlagához viszonyĂtanánk azt. A sztochasztikus mortalitási modellek alkalmazása mellett szĂłl, hogy az elĹ‘zĹ‘ Ă©vekhez törtĂ©nĹ‘ hasonlĂtás nem veszi figyelembe a halandĂłság Ă©vrĹ‘l Ă©vre törtĂ©nĹ‘ javulását, mĂg a halandĂłsági modellek igen. A számĂtások elvĂ©gzĂ©se során három adatforrásra támaszkodunk: a Központi Statisztikai Hivatal (KSH), az elektronikus anyakönyvi rendszer (EAK) Ă©s egy kormányzati portál adatait használjuk fel
Sztochasztikus népesség-előrejelzés magyar adatokon
Jelen kutatás elsĹ‘ felĂ©nek cĂ©lja annak bemutatása, hogy a nemzetközi szakirodalomban elterjedt sztochasztikus mortalitási modellek alkalmasak-e a halálozási arányszám elĹ‘rejelzĂ©sĂ©re Magyarországon Ă©s a kapott eredmĂ©nyek felhasználhatĂłak-e a magyar nĂ©pessĂ©gszám modell alapĂş, valĂłszĂnűsĂ©gi elĹ‘reszámĂtásához. Lee Ă©s Carter 1992-ben megalkotott modellje nagy hatást gyakorolt a sztochasztikus mortalitási modellek fejlĹ‘dĂ©sĂ©re. Lee Ă©s Carter modelljĂ©bĹ‘l kiindulva jött lĂ©tre az általánosĂtott kor–periĂłdus–kohorsz modellkeret (angolul ’generalized age–period–cohort stochastic mortality models’, röviden GAPC). Jelen tanulmány ennek a modellcsaládnak a tagjait ismerteti, illetve alkalmazza magyar adatokon. A cĂ©l a legjobban illeszkedĹ‘ modell megtalálása. (...
A speciális közfoglalkoztatási pilotprogram megvalĂłsĂtása Ă©s hatásmechanizmusa a magyar szociálpolitika eszközrendszerĂ©ben
A gazdasági, társadalmi fejlĹ‘dĂ©s alapja, a szociális biztonság megteremtĂ©sĂ©nek egyaránt feltĂ©tele a teljes foglalkoztatottságra valĂł törekvĂ©s Ă©s a munkavállalás minĹ‘sĂ©gi javĂtása. Ennek sikere a munkavállalási korĂş nĂ©pessĂ©g aktiválásának mĂ©rtĂ©kĂ©n mĂşlik. A hazai aktĂv foglalkoztatáspolitikai eszközök között dominálĂł közfoglalkoztatás egyik speciális, kĂsĂ©rleti programja komplex nĂ©zĹ‘pontbĂłl közelĂt az egĂ©szsĂ©gĂĽgyi Ă©s szociális hátrányaik miatt nehezen foglalkoztathatĂł szemĂ©lyek fejlesztĂ©sĂ©hez, de nem lĂ©p ki az összessĂ©gĂ©ben sikertelen eszközrendszer keretei közĂĽl. Kutatásunkban interjĂşkbĂłl Ă©s dokumentumelemzĂ©sbĹ‘l származĂł informáciĂłkra támaszkodva arra jutottunk, hogy a kĂ©t egymás utáni Ă©vben megvalĂłsult közfoglalkoztatási pilotprogram szemlĂ©letĂ©ben elĹ‘remutatĂł, de tervezĂ©se Ă©s kivitelezĂ©se beleilleszkedik a hazai aktiválási politika ellentmondásos eszköztárába, Ă©s egyben rávilágĂtott a szociális ellátĂłrendszer számos rendszerhibájára is
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
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
Ordering in spatial evolutionary games for pairwise collective strategy updates
Evolutionary games are studied with players located on a square
lattice. During the evolution the randomly chosen neighboring players try to
maximize their collective income by adopting a random strategy pair with a
probability dependent on the difference of their summed payoffs between the
final and initial state assuming quenched strategies in their neighborhood. In
the case of the anti-coordination game this system behaves alike an
anti-ferromagnetic kinetic Ising model. Within a wide region of social dilemmas
this dynamical rule supports the formation of similar spatial arrangement of
the cooperators and defectors ensuring the optimum total payoff if the
temptation to choose defection exceeds a threshold value dependent on the
sucker's payoff. The comparison of the results with those achieved for pairwise
imitation and myopic strategy updates has indicated the relevant advantage of
pairwise collective strategy update in the maintenance of cooperation.Comment: 9 pages, 6 figures; accepted for publication in Physical Review