AAV Vector-Mediated Overexpression of CB1 Cannabinoid Receptor in Pyramidal Neurons of the Hippocampus Protects against Seizure-Induced Excitoxicity

The CB1 cannabinoid receptor is the most abundant G-protein coupled receptor in the brain and a key regulator of neuronal excitability. There is strong evidence that CB1 receptor on glutamatergic hippocampal neurons is beneficial to alleviate epileptiform seizures in mouse and man. Therefore, we hypothesized that experimentally increased CB1 gene dosage in principal neurons would have therapeutic effects in kainic acid (KA)-induced hippocampal pathogenesis. Here, we show that virus-mediated conditional overexpression of CB1 receptor in pyramidal and mossy cells of the hippocampus is neuroprotective and moderates convulsions in the acute KA seizure model in mice. We introduce a recombinant adeno-associated virus (AAV) genome with a short stop element flanked by loxP sites, for highly efficient attenuation of transgene expression on the transcriptional level. The presence of Cre-recombinase is strictly necessary for expression of reporter proteins or CB1 receptor in vitro and in vivo. Transgenic CB1 receptor immunoreactivity is targeted to glutamatergic neurons after stereotaxic delivery of AAV to the dorsal hippocampus of the driver mice NEX-cre. Increased CB1 receptor protein levels in hippocampal lysates of AAV-treated Cre-mice is paralleled by enhanced cannabinoid-induced G-protein activation. KA-induced seizure severity and mortality is reduced in CB1 receptor overexpressors compared with AAV-treated control animals. Neuronal damage in the hippocampal CA3 field is specifically absent from AAV-treated Cre-transgenics, but evident throughout cortical areas of both treatment groups. Our data provide further evidence for a role of increased CB1 signaling in pyramidal hippocampal neurons as a safeguard against the adverse effects of excessive excitatory network activity

Némethy, Judit Kesserű: “Szabadságom lett a börtönöm”: Az argentínai magyar emigráció története 1948-1968

Némethy, Judit Kesserű: “Szabadságom lett a börtönöm”: Az argentínai magyar emigráció története 1948-1968 (“My Freedom Became My Prison”: The History of the Hungarian Emigrés in Argentina, 1948-1968). Budapest: A Magyar Nyelv és Kultúra Nemzetközi Társasága, 2003. ISBN 963212 152X, 430 pp. Reviewed by Andrew Ludanyi, Ohio Northern University

Dani, Erzsébet. <i>Identitásgyarmatosítás Erdélyben: Identitásdrámák és interkulturális stratégiák a Trianon utáni székelymagyar irodalomban</i> ('Identity Colonization in Transylvania: The Presence of Identity Narratives and Intercultural Strategies in the Literature of the Székely Magyars After Trianon'). Csíkszereda: Pro-Print Publishers, 2016. 287 pp.

Dani, Erzsébet. Identitásgyarmatosítás Erdélyben: Identitásdrámák és interkulturális stratégiák a Trianon utáni székelymagyar irodalomban ('Identity Colonization in Transylvania: The Presence of Identity Narratives and Intercultural Strategies in the Literature of the Székely Magyars After Trianon'). Csíkszereda: Pro-Print Publishers, 2016. 287 pp

Extreme radiation tolerance of Deinococcus deserti : Characterization of the central regulator IrrE

Les bactéries du genre Deinococcus sont extrêmement tolérantes à de fortes doses de radiations. Des études antérieures ont montré que IrrE est nécessaire à la radiotolérance et à l'induction des gènes de réparation de l'ADN après exposition des cellules à l'irradiation. Pendant des années il est resté inconnu comment IrrE active l'expression de ces gènes. L'objectif de ma thèse était la caractérisation de la voie de signalisation dépendent de IrrE chez Deinococcus deserti. Pour cela, des approches biochimiques et génétiques ont été utilisées. Les premiers résultats ont fortement suggéré que IrrE agit indirectement sur l'activation de l'expression des gènes. En utilisant des expériences in vitro et in vivo, nous avons montré que IrrE de Deinococcus deserti interagit avec DdrO, un régulateur potentiel qui est codé par un gène radio-induit et qui est, comme IrrE, conservé chez les Deinococcus. De plus, IrrE clive DdrO in vitro mais aussi in vivo lorsque les deux protéines sont co-exprimées chez Escherichia coli. Ce clivage est abolit en présence d'un agent chélateur de métaux, l'EDTA. Chez D. deserti, le clivage de DdrO dépendent de IrrE a été observé mais seulement après exposition à l'irradiation. En parallèle, nous avons montré que la répression du promoteur d'un gène radio-inductible est dépendante de DdrO. Nos résultats montrent donc que IrrE est une métalloprotéase et nous proposons que le répresseur DdrO soit désactivé après clivage par IrrE conduisant à l'induction de différents gènes indispensables pour la réparation de l'ADN et la survie des cellules après exposition de Deinococcus à l'irradiation.Deinococcus bacteria are famous for their extreme tolerance to high doses of radiation. Earlier studies have shown that IrrE protein is required for radiation tolerance and for induction of DNA repair genes after exposure of cells to radiation. However, for years it has remained unknown how IrrE activates gene expression. The aim of my thesis was to characterize the IrrE-dependent regulation pathway in Deinococcus deserti. For this, biochemical and genetic approaches were used. The first results strongly suggested that IrrE activates gene expression in an indirect manner. Then, using other in vivo and in vitro experiments, IrrE from Deinococcus deserti was found to interact with DdrO, a predicted regulator encoded by a radiation-induced gene that is, like irrE, highly conserved in Deinococcus. Moreover, IrrE was found to cleave DdrO in vitro and also in vivo when the proteins were co-expressed in Escherichia coli. This cleavage was not observed in the presence of the metal chelator EDTA. In D. deserti, IrrE-dependent cleavage of DdrO was observed only after exposure to radiation. Furthermore, DdrO-dependent repression of the promoter of a radiation-induced gene was shown. Our results demonstrate that IrrE is a metalloprotease and we propose that IrrE-mediated cleavage inactivates repressor protein DdrO, leading to transcriptional induction of various genes required for DNA repair and cell survival after exposure of Deinococcus to radiation

The Bolyai University and minority elite recruitment: 1944–1959

The Bolyai University was the Hungarian half of the current Babeş-Bolyai University in Cluj/Kolozsvár, Transylvania. It was an independent Hungarian University until its merger with the Babeş University in 1959. This merged institution is one of the most important centers of higher education in present-day Romania. However, it has a past that can be traced back to the 16th century within the context of the independent Translvania of John Sigismund and Stephen Báthory. It later evolved into a Habsburg institution, then a Hungarian and a Romanian University. Finally, during World War II it operated as two separate institutions with Hungarian and Romanian faculties respectively. The two were merged by the Gheorghiu-Dej communist government in 1959. Ever since, Hungarian minority intellectuals have called for the restoration of the independent Boylai University. The current paper focuses on the independent Bolyai University between 1944 and 1959. It reflects on its role as the premier institution for the recruitment and training of the Hungarian minority’s cultural and educational elite. The paper links the fate of this institution to the communist transformation of Romania and its consequences for the Hungarians of Transylvania

The Impact of 1956 on the Hungarians of Transylvania

“The Impact of 1956 on the Hungarians of Transylvania”, provides a 50-year retrospective analysis of the political consequences of the Hungarian Revolution of 1956 on the Hungarians in neighboring Romania. It focuses on the inter-ethnic knock-on effects in the Romanian Workers Party, the “Hungarian/Mures-Hungarian Autonomous Region”of Transylvania, and the cultural institutions of the Hungarian minority. It links these developments to present-day Romanian-Hungarian relations, both on the interstate and the intrastate levels