A stresszválasz hipotalamikus szabályozása = Hypothalamic regulation of the stress response

Vizsgálatainkban funkcionális neuroanatómiai és molekuláris biológiai technikák kombinációjával vizsgáltuk különböző stresszorok hatását a hipotalamusz paraventrikuláris magjának (PVN) a neuroendokrin és a vegetativ szabályozásban szerepet játszó neuroncsoportjaira. Elektronmikroszkópos technikákkal kimutattuk, hogy a neuroendokrin stresszválasz elindításáért felelős kortikotropin-releasing hormont (CRH) termelő idegsejteken GABAerg axonok végződnek és ezek száma, elhelyezkedési mintázata változik krónikus stresszben. A CRH neuronok szomszédságában hisztaminerg axonokat is feltérképeztünk, de ezek nem képeznek szinaptikus kapcsolatot a stresszel kapcsolatos hipotalamikus neuronokkal. A hisztamin hiány hisztidin dekarboxylase génkiütött egerek (HDC-KO) esetében nem okoz eltérést sem a stressz-, sem az anyagcsere szabályozásában szereplő hipotalamikus neuropeptidek expressziójában, mégis az állatokon olyan metabolikus fenotípus alakul ki, melynek jellemzői az elhízás, a glükóz intolerancia és a hiperleptinémia. Leírtuk, hogy a GABAerg gátló tónus felfüggesztése, valamint fizikális-, metabolikus- és immunstresszorok eltérő módon aktiválják a paraventrikuláris mag funkcionálisan különböző neuroncsoportjait és a CRH valamint az arginin vazopresszin (AVP) gének időben és térben eltérő indukcióját eredményezik a PVN-ben. Organotipikus hipotalamusz szelet tenyészeteken igazoltuk, hogy a szteroidok CRH expressziót gátló hatása közvetlenül a parvocelluláris neuronokon érvényesül | The effect of different stress challenges on the functionally distinct cell population in the hypothalamic paraventricular nucleus (PVN) has been studied by combination of anatomical and molecular biological methods. GABAergic terminals have been revealed on the corticotropin-releasing hormone (CRH) synthesizing neurons. The number and spatial distribution of these terminals has been changed after chronic stress. Histaminergic boutons have been identified in close apposition to CRH neurons without any synaptic contact. Lack of histamine in histidine decarboxylase knockout (HDC-KO) mice results in a metabolic phenotype with visceral obesity, glucose intolerance and hiperleptinemia without any detectable changes in the expression of neuropeptides involved in stress or metabolic regulation. We have revealed that suspension of inhibitory GABAergic tone, as well as physical, immune and metabolic challenges differentially recruit functionally distinct domains of the PVN and result in spatially and temporally different upregulation pattern of CRH and AVP genes. Using organotypic hypothalamic slice cultures we have provided evidence for the direct inhibitory effect of corticosteroid hormones on the CRH gene expression in the parvocellular neurons

Az anti-apoptosis mechanizmus vizsgálata agyi ischaemia/hypoxia modellekben = Studies on anti-apoptosis mechanisms in models of brain ischaemia/hypoxia

A hypoxia indukálta sejt nekrózis/apoptózis kivédése vagy mérséklése igéretes kutatási terület az alkalmas terápiás eljárások bevezetésére. In vitro és in vivo modellekben vizsgáltuk a (-)-deprenyl, az antiapoptotikus gént tartalmazó adenovírus vektorok és az ösztrogén hatását a hypoxia/ischemia indukálta változásokon. Neuronális PC12 sejtkultúrában és hippocampus organotipikus tenyészetében a deprenyl csökkenti a nekrózis és apoptózis mértékét, javítja a neuronális regenerációt. Indukálja az antiapoptotikus Bcl-2 és SOD-1 fehérjéket és a GAP-43 plaszticitás proteint. Védi a sejteket az oxidatív károsodástól és fenntartja a mitokondriális membránpotenciált. Vizsgálataink szerint a deprenyl neuroprotektív hatását mitokondriális hatásokon keresztül fejti ki. Az antiapoptotikus Bcl-2 vagy Bcl-XL gént tartalmazó adenovírus vektorok PC12 kultúrában védik a mitokondriális funkciót, csökkentik az apoptotikus sejtek arányát és növelik a GAP-43 expressziót. Az antiapoptotikus génbevitel a cytoprotektív hatás mellett fokozza a javító gének (synapsin-1, nestin, c-fos) expresszióját is. Az ösztrogén neuroprotektív hatása jól ismert, de a repair folyamatokra gyakorolt hatása nem. Nagy-dózisú ösztrogén adás hatását vizsgáltuk gerbilen átmeneti agyi ischemiaban. Adataink azt mutatják, hogy az ösztrogén nem csak neuroprotektív, hanem növeli a GAP-43 és a nestin plaszticitás gének expresszióját, ami kifejezésre jut az állatok jobb viselkedés vizsgálati eredményeiben. | Hypoxia induced cell necrosis and/or apoptosis can be moderated or prevented by antiapoptotic therapies. In in vitro and in vivo models, the impact of (-)-deprenyl, antiapoptotic gen transfer and oestrogen were tested on hypoxia/ischemia induced changes. In neuronal PC12 cell culture and orgatypic hippocampal slice culture, deprenyl reduces necrosis and apoptosis and induces neuronal repair via induction of antiapoptotic Bcl-2, SOD-1 proteins and GAP-43 plasticity protein. Deprenyl protects cells from oxidative damage and helps to mantain mitochondrial membrane potencial. Our new findings support the assumption that the neuroprotective effect of deprenyl is related to the mitochondrial processes. In PC12 culture, the antiapoptotic Bcl-2 and Bcl-XL genes transferred to adenovirus vector protect the mitochondrial fuction, reduce the number of apoptotic cells and augment the expression of GAP-43 protein. The antiapoptotic gene delivery is not only cytoprotective moreover augments the expression of repair genes synapsin-1, nestin, c-fos after hypoxic insults. Neuroprotective effect of oestrogen is well documented however its effect on repair mechanisms is still not elucidated. We investigated the effect of the high-dose oestrogen therapy on cerebral plasticity after transient forebrain ischemia in gerbils. Our novel finding is that oestrogen is not just neuroprotective but increases the expression of plasticity genes GAP-43 and nestin which results better performance of gerbils in behaviour tests

Preparation of Gold Nanocomposites with Tunable Charge and Hydrophobicity via the Application of Polymer/Surfactant Complexation

During the synthesis of gold nanoparticle (NP) assemblies, the interfacial charge and hydrophobicity of the primary particles play a distinguished role. In the present article, we demonstrate that the association of poly­(ethyleneimine) (PEI) capped gold NPs with sodium alkyl sulfates provide a powerful route for the manipulation of these interfacial properties. Dynamic light-scattering, electrophoretic mobility, UV–vis–near-infrared spectroscopy, nanoparticle tracking analysis, and transmission electron microscopy measurements were used to characterize the PEI/surfactant/gold nanoassemblies. The results indicate the formation of gold NPs surrounded by a PEI/surfactant shell with composition-dependent charge and hydrophobicity. The mean size and the aggregation of the nanoassemblies can be fine tuned by the amount of surfactant bound to the primary gold NPs as well as by the application of controlled mixing methods. The specific features of the prepared nanocomposites may be further exploited in next-generation applications

Isolation of Mycoplasma anserisalpingitidis from swan goose (Anser cygnoides) in China

Abstract Background: Mycoplasma anserisalpingitidis causes significant economic losses in the domestic goose (Anser anser) industry in Europe. As 95% of the global goose production is in China where the primary species is the swan goose (Anser cygnoides), it is crucial to know whether the agent is present in this region of the world. Results: Purulent cloaca and purulent or necrotic phallus inflammation were observed in affected animals which represented 1–2% of a swan goose breeding flock (75,000 animals) near Guanghzou, China, in September 2019. From twelve sampled animals the cloaca swabs of five birds (three male, two female) were demonstrated to be M. anserisalpingitidis positive by PCR and the agent was successfully isolated from the samples of three female geese. Based on whole genome sequence analysis, the examined isolate showed high genetic similarity (84.67%) with the European isolates. The antibiotic susceptibility profiles of two swan goose isolates, determined by microbroth dilution method against 12 antibiotics and an antibiotic combination were also similar to the European domestic goose ones with tylvalosin and tiamulin being the most effective drugs. Conclusions: To the best of our knowledge this is the first description of M. anserisalpingitidis infection in swan goose, thus the study highlights the importance of mycoplasmosis in the goose industry on a global scale. Keywords: Antibiotic, China, Mycoplasma, Swan goose, Phallus inflammation, Venereal disease, Whole genom

Recombination Events Shape the Genomic Evolution of Infectious Bronchitis Virus in Europe

Infectious bronchitis of chicken is a high morbidity and mortality viral disease affecting the poultry industry worldwide; therefore, a better understanding of this pathogen is of utmost importance. The primary aim of this study was to obtain a deeper insight into the genomic diversity of field infectious bronchitis virus (IBV) strains using phylogenetic and recombination analysis. We sequenced the genome of 20 randomly selected strains from seven European countries. After sequencing, we created a genome sequence data set that contained 36 European origin field isolates and 33 vaccine strains. When analyzing these 69 IBV genome sequences, we identified 215 recombination events highlighting that some strains had multiple recombination breaking points. Recombination hot spots were identified mostly in the regions coding for non-structural proteins, and multiple recombination hot spots were identified in the nsp2, nsp3, nsp8, and nsp12 coding regions. Recombination occurred among different IBV genotypes and involved both field and vaccine IBV strains. Ninety percent of field strains and nearly half of vaccine strains showed evidence of recombination. Despite the low number and the scattered geographical and temporal origin of whole-genome sequence data collected from European Gammacoronaviruses, this study underlines the importance of recombination as a major evolutionary mechanism of IBVs