Generalisierter Krampfanfall während der Anlage einer axillären Plexusblockade

Die Anaesthesiologie - Eine junge Patientin erleidet während der Anlage einer axillären Plexusblockade einen generalisierten Krampfanfall. Die Mechanismen, im Wesentlichen die vermutlich...     

Evaluation of low-viscosity bulk-fill composites regarding marginal and internal adaptation

This study aimed at evaluating the marginal and internal adaptation of low-viscosity bulk-fill composites to enamel and dentin using a self-etch or an etch-and-rinse adhesive without and with artificial ageing. Hundred and twenty-eight MOD cavities in extracted molars were assigned to eight groups (n = 16), restored with the adhesives OptiBond FL (OFL) or Xeno V+ (X) and two low-viscosity bulk-fill composites SDR or x-tra base, covered with Premise. Tetric EvoCeram Bulk Fill and Premise served as a control. n = 8 per group were subjected to prolonged water storage (180 days) and thermocycling (2500×). Scanning electron microscopy was used to determine marginal gaps (MG) and interfacial adhesive defects (IAD). There were no significant differences between composite types in 44 out of 48 (MG) or 43/48 (IAD) comparisons. More MG were observed with X than with OFL (14 out of 16 comparisons, two significant), while in 16 of 16 comparisons with X more IAD were observed (14 significant). After artificial ageing, MG generally increased (9/16 significant), compared to IAD (one significant). The performance of the investigated composite types concerning the integrity of the tooth-composites interface was comparable. Compared to the 1-step self-etch system, the bond with the 3-step etch-and-rinse adhesive was raised.

     

Epilepsie,Schlaf und plötzlicher unerwarteter Tod

Clinical Epileptology - Der plötzliche unerwartete Tod stellt eine seltene, aber schwerwiegende Komplikation für Epilepsiepatienten dar. Das Risiko hierfür ist u. a. nachts und...     

Autorisierte Übersetzung Zusammenfassung der Praxisleitlinien: Inzidenzraten und Risikofaktoren des plötzlichen unerwarteten Todes bei Epilepsie

Clinical Epileptology - Ziel dieser Praxisleitlinie ist es, die Häufigkeit von plötzlichen unerwarteten Todesfällen bei Epilepsie (SUDEP) in verschiedenen Epilepsiepopulationen zu...     

Environmental and Pharmacological Modulation of Amphetamine-Induced 50-kHz Ultrasonic Vocalizations in Rats

Rats emit high-frequency 50-kHz ultrasonic vocalizations (USV) in appetitive situations like social interactions. Drugs of abuse are probably the most potent non-social elicitors of 50-kHz USV, possibly reflecting their euphorigenic properties. Psychostimulants induce the strongest elevation in 50-kHz USV emission, particularly amphetamine (AMPH), either when applied systemically or locally into the nucleus accumbens (Nacc). Emission of AMPH-induced 50-kHz USV depends on test context, such as the presence of conspecifics, and can be manipulated pharmacologically by targeting major neurotransmitter systems, including dopamine (DA), noradrenaline (NA), and serotonin (5-HT), but also protein kinase C (PKC) signaling. Several D₁ and D₂ receptor antagonists, as well as typical and atypical antipsychotics block the AMPH-induced elevation in 50-kHz USV. Inhibiting D₁ and D₂ receptors in the Nacc abolishes AMPH-induced 50-kHz USV, indicating a key role for this brain area. NA neurotransmission also regulates AMPH-induced 50-kHz USV emission given that α₁ receptor antagonists and α₂ receptor agonists exert attenuating effects. Supporting the involvement of the 5-HT system, AMPH-induced 50-kHz USV are attenuated by 5-HT_2C receptor activation, whereas 5-HT_2C receptor antagonism leads to the opposite effect. Finally, treatment with lithium, tamoxifen, and myricitrin was all found to result in a complete abolishment of the AMPH-induced increase in 50-kHz USV, suggesting the involvement of PKC signaling. Neurotransmitter systems involved in AMPH-induced 50-kHz USV emission only partially overlap with other AMPH-induced behaviors like hyperlocomotion. The validity of AMPH-induced 50-kHz USV as a preclinical model for neuropsychiatric disorders is discussed, particularly with relevance to altered drive and mood seen in bipolar disorder.