Stellungnahme zu: Mit mehr Marktwirtschaft die Energiewende aktiv gestalten - Verantwortung für den Energie- und Industriestandort Nordrhein-Westfalen übernehmen

Antrag der Fraktion der FDP - Drucksache 16/1267. Öffentliche Anhörung des Ausschusses für Wirtschaft, Energie, Industrie, Mittelstand und Handwerk am 20. Februar 2013. Stellungnahme: Die Energiewende ist eine bedeutende gesellschaftliche und ökonomische Herausforderung. Angestrebt wird die Abkehr von Kernenergie und fossilen Energieträgern. An ihre Stelle sollen erneuerbare Energien treten. Wir begrüßen, dass die FDP-Landtagsfraktion in einem höheren Maße wettbewerbliche anstelle administrativer Steuerungsinstrumente für diese Energiewende einfordert. Wir bemängeln jedoch, dass Forderungen vielfach unkonkret bleiben und nähere Festlegungen erforderlich bleiben. Wir meinen, dies geschieht ohne Not, denn konkrete Lösungsalternativen liegen schon heute auf dem Tisch: Vorschläge für eine umfassende Reform der Förderung erneuerbarer Energien sind ebenso bekannt wie alternative Ausgestaltungsmöglichkeiten für das Strommarktdesign

Association of Caldendrin splice isoforms with secretory vesicles in neurohypophyseal axons and the pituitary

AbstractCaldendrin is a neuronal calcium-binding protein, which is highly enriched in the postsynaptic density fraction and exhibits a prominent somato-dendritic distribution in brain. Two additional splice variants derive from the caldendrin gene, which have unrelated N-termini and were previously only detected in the retina. We now show that these isoforms are present in neurohypophyseal axons and on secretory granules of endocrine cells. In light of the described interaction of the Caldendrin C-terminus with Q-type Cav2.1 calcium channels these data suggest that this interaction takes place in neurohypophyseal axons and pituitary cells indicating functions of the short splice variants in triggering Ca2+ transients to a vesicular target interaction

Neonatal Oxytocin Treatment Ameliorates Autistic-Like Behaviors and Oxytocin Deficiency in Valproic Acid-Induced Rat Model of Autism

Autism spectrum disorder (ASD) is characterized by impaired social communication and repetitive/stereotyped behaviors. The neuropeptide oxytocin (OXT) plays a critical role in regulating social behaviors in the central nervous system, as indicated in both human and animal studies. We hypothesized that central OXT deficit is one of causes of etiology of ASD, which may be responsible for the social impairments. To test our hypothesis, central OXT system was examined in valproic acid (VPA)-induced rat model of autism (VPA rat). Our results showed that adolescent VPA rats exhibited a lower level of OXT mRNA and fewer OXT-ir cells in the hypothalamus than control rats. Additionally, OXT concentration in cerebrospinal fluid (CSF) was reduced. The number of OXT-ir cells in the supraoptic nucleus (SON) of neonatal VPA rats was also lower. Autistic-like behaviors were observed in these animals as well. We found that an acute intranasal administration of exogenous OXT restored the social preference of adolescent VPA rats. Additionally, early postnatal OXT treatment had long-term effects ameliorating the social impairments and repetitive behaviors of VPA rats until adolescence. This was accompanied by an increase in OXT-ir cells. Taken together, we demonstrated there was central OXT deficiency in the VPA-induced rat model of autism, and showed evidence that early postnatal OXT treatment had a long-term therapeutic effect on the autistic-like behaviors in VPA rats

Mice with Shank3 Mutations Associated with ASD and Schizophrenia Display Both Shared and Distinct Defects

Genetic studies have revealed significant overlaps of risk genes among psychiatric disorders. However, it is not clear how different mutations of the same gene contribute to different disorders. We characterized two lines of mutant mice with Shank3 mutations linked to ASD and schizophrenia. We found both shared and distinct synaptic and behavioral phenotypes. Mice with the ASD-linked InsG3680 mutatio n manifest striatal synaptic transmission defects before weaning age and impaired juvenile social interaction, coinciding with the early onset of ASD symptoms. On the other hand, adult mice carrying the schizophrenia-linked R1117X mutation show profound synaptic defects in prefrontal cortex and social dominance behavior. Furthermore, we found differential Shank3 mRNA stability and SHANK1/2 upregulation in these two lines. These data demonstrate that different alleles of the same gene may have distinct phenotypes at molecular, synaptic, and circuit levels in mice, which may inform exploration of these relationships in human patients.National Institute of Mental Health (U.S.) (Grant 5R01MH097104)National Institute of Mental Health (U.S.) (Grant 5DP1-MH100706)National Institutes of Health (U.S.) (Grant R01-NS 07312401

qcserenity/serenity: Release 1.5.3

<h2>Release 1.5.3 (25.10.2023)</h2> <h3>Functionalities</h3> <ul> <li>Added two flavors of restricted open-shell HF and KS for the ground-state (Niklas Niemeyer)</li> <li>Fermi-shifted Huzinaga EO Kernel for subsystem TDDFT (Niklas Niemeyer)</li> <li>Laplace-Transform GW (Johannes Tölle, Niklas Niemeyer)</li> <li>Renamed ReadOrbitalsTask to OrbitalsIOTask (Niklas Göllmann)</li> <li>Added the functionality to write Turbomole files (Niklas Göllmann)</li> <li>Added the functionality to write Molden files for both spherical and cartesian harmonics (Niklas Göllmann)</li> <li>Added three schemes to generate complete basis function products for the Cholesky decomposition framework: Simple, First, Complete (Lars Hellmann)</li> <li>Added the functionality to control density fitting for individual contributions (Coulomb, exchange, long-range exchange, correlation)</li> </ul&gt