Ex vivo infection of human embryonic spinal cord neurons prior to transplantation into adult mouse cord

<p>Abstract</p> <p>Background</p> <p>Genetically modified pseudorabies virus (Prv) proved suitable for the delivery of foreign genes to rodent embryonic neurons <it>ex vivo </it>and maintaining foreign gene expression after transplantation into spinal cord in our earlier study. The question arose of whether human embryonic neurons, which are known to be more resistant to Prv, could also be infected with a mutant Prv. Specifically, we investigated whether a mutant Prv with deleted ribonucleotide reductase and early protein 0 genes has the potential to deliver marker genes (gfp and β-gal) into human embryonic spinal cord neurons and whether the infected neurons maintain expression after transplantation into adult mouse cord.</p> <p>Results</p> <p>The results revealed that the mutant Prv effectively infected human embryonic spinal cord neurons <it>ex vivo </it>and the grafted cells exhibited reporter gene expression for several weeks. Grafting of infected human embryonic cells into the spinal cord of immunodeficient (rnu-/rnu-) mice resulted in the infection of some of the host neurons.</p> <p>Discussion</p> <p>These results suggest that Prv is suitable for the delivery of foreign genes into transplantable human cells. This delivery method may offer a new approach to use genetically modified cells for grafting in animal models where spinal cord neuronal loss or axon degeneration occurs.</p

An Observational Study on the Pharmacokinetics of Oseltamivir in Lactating Influenza Patients

Influenza infection may lead to serious complications in the postpartum period, therefore, oseltamivir treatment in these patients and their breastfed infants is of great importance. However, the pharmacokinetics of oseltamivir in postpartum lactating women with acute influenza infection, and the consequent infant exposure to oseltamivir are still unknown, and these data would help in assessing risk and the need for dose adjustment in breastfed infants

Választási ígéretek és kormányzati teljesítés Magyarországon, 1990-2014

A Választási ígéretek és kormányzati teljesítés Magyarországon, 1990-2010 kutatási projekt úttörő jellegű a magyar politikatudományban. Megvalósulásával új tudományos eredményeket várunk arról, hogy milyen a kapcsolat a pártok kampányígéretei és a tényleges kormánypolitika között, és – egy későbbi szakaszban – arról is, hogy a kormányok teljesítménye hogyan hat a szavazói viselkedésre. A kutatás eredményeképpen pontosabb képet remélünk a kormánypolitika kiszámíthatóságáról, a kormányzást végző politikai vezetők autonómiájáról, azaz arról, hogy tevékenységük mennyiben követi a választói akaratot és mennyire van kitéve a szavazópolgárok ellenőrzésének. E kérdések megválaszolása segít abban, hogy többet tudjunk meg a demokrácia, a mindenkori kormánypolitika és a közpolitika minőségéről. A kutatási projekt jelenlegi célja annak megállapítása, hogy a magyarországi pártok (1) mennyiben tesznek világos, számon kérhető ígéreteket, (2) ezeket kormányra kerülve mennyire teljesítik, és (3) milyen tényezők befolyásolják a választási ígéretek egyértelműségét és végrehajtását. A projekt nyílt, arra törekszik, hogy az ígéretekkel kapcsolatos egyéb kutatásokat is ösztönözzön. A fájlok tartalma: - letéti nyilatkozat - kódkönyv - Fidesz, MSZP, SZDSZ 2002-es lekódolt kampányígéreteinek adatbázisai (.sav) - MSZP és SZDSZ összesített adatbázis (.xlsx

Increased Survival and Reinnervation of Cervical Motoneurons by Riluzole after Avulsion of the C7 Ventral Root

Although adult motoneurons do not die if their axons are injured at some distance from the cell body, they are unable to survive injury caused by ventral root avulsion. Some of the injured motoneurons can be rescued if the ventral root is re-inserted into the spinal cord. Brachial plexus injuries that involve the complete or partial avulsion of one or more cervical ventral roots can be treated successfully only if satisfactory numbers of motoneurons remain alive following such an injury at the time of reconstructive surgery. Here we investigated the various strategies that could be used to rescue injured rat cervical motoneurons. The seventh cervical ventral root (C7) was avulsed and various therapeutic approaches were applied to induce motoneuronal survival and regeneration. Avulsion of the root without reimplantation resulted in very low numbers of surviving motoneurons (65 ± 8 SEM), while treatment of the injured motoneurons with riluzole resulted in high numbers of surviving motoneurons (637 ± 26 SEM). When the C7 ventral root was reimplanted or a peripheral nerve implant was used to guide the regenerating axons to a muscle, considerable numbers of motoneurons regenerated their axons (211 ± 15 SEM and 274 ± 28 SEM, respectively). Much greater numbers of axons regenerated when reimplantation was followed by riluzole treatment (573 ± 9 SEM). These results show that injured adult motoneurons can be rescued by riluzole treatment, even if they cannot regenerate their axons. Reinnervation of the peripheral targets can also be further improved with riluzole treatment

Up-regulation of cerebral carbonic anhydrase by anoxic stress in piglets

The resuscitation of asphyxiated babies is associated with changes in cerebral protein synthesis that can influence the neurological outcome. Insufficient gas exchange results in rapid shifts in extracellular and intracellular pH. Carbonic anhydrase (CA) plays an important role in buffering acute changes in pH in the brain. We investigated whether asphyxia/re-ventilation influences the expression of cerebral CA isoforms (CA-II, CA-III and CA-IV) in anaesthetized newborn pigs. The cerebral cortex, hippocampus, cerebellum and retina were sampled, and prepared for either CA immunohistochemistry or CA immunoblotting from piglets subjected to asphyxia (10 min) followed by 2-4 h of re-ventilation, and also from normoxic controls. The CA immunoreactivity (IR) of all the isoforms studied was weak in the controls, apart from staining of a few oligodendrocytes in the subcortical white matter, some astrocytes in the superficial layer of the cerebral cortex, the cerebellar Purkinje cells and the retinal Muller cells that possessed moderate CA-II IR. However, asphyxia induced a marked increase in the CA IR of all isoforms in all the cerebral regions investigated and the retina after 4 h of survival. The pyramidal cells of the frontal cortex and hippocampus displayed the most conspicuous increase in CA IR. Immunoblotting confirmed increased levels of all the CA isoenzymes. We conclude that raised CA levels after asphyxia may contribute to the compensatory mechanisms that protect against the pathological changes in the neonatal CNS