Energiewende mit einem 'EEG-Soli' gerechter finanzieren: die sozialen Auswirkungen der Energiewende

Die Ökostromumlage (EEG-Umlage) steigt im Jahr 2015 auf ein neues Rekordniveau. Wegen der regressiven Wirkung der EEG-Umlage, die im Kern eine Verbrauchssteuerfinanzierung ist, sind davon Haushalte mit niedrigen und mittleren Einkommen besonders stark betroffen. Wie kann die Energiewende sozial gerechter finanziert werden? Die Energiewendekosten sollten entsprechend der Leistungsfähigkeit der Stromverbraucher über eine Erhöhung des Solidaritätszuschlags auf den Einkommens- und Körperschaftssteuerbetrag finanziert werden. Die progressive Wirkung des Einkommensteuertarifs könnte genutzt und die Gewinne der Kapitalgesellschaften einbezogen werden. Beschäftigte aus dem Niedriglohnsektor würden davon profitieren, weil das Solidaritätszuschlagsgesetz diejenigen von der Steuerpflicht ausnimmt, die kein oder nur ein geringes Einkommen haben

"Solidarische Mindestrente": BGE (Bedingungsloses Grundeinkommen) durch die Hintertür?

Von der zunehmenden Altersarmut in Deutschland sind besonders Personen mit unsteten Erwerbsbiografien, frühere Niedriglohn- und geringfügig Beschäftigte, Hartz-IV-Empfänger und prekäre Selbständige betroffen. Die Absenkung des allgemeinen Rentenniveaus auf 42 Prozent verschärft das Problem. Diesem negativen Trend setzt die Linkspartei ihr Konzept einer »solidarischen Mindestrente« in Höhe von 1.050 Euro entgegen. Anspruch darauf sollen alle in Deutschland lebenden Menschen unabhängig von einer vorherigen Beitragszahlung in der Rentenversicherung haben. Vermögen in Höhe von 20.000 Euro und ein Freibetrag für »Altersvorsorge« in Höhe von 48.750 Euro sollen unberücksichtigt bleiben. Ebenfalls unberücksichtigt bleiben soll eine selbstgenutzte Immobilie mit bis zu 130 Quadratmetern Wohnfläche. Der gewerkschaftliche Ansatz und der Ansatz der Linkspartei unterscheiden sich hinsichtlich der Strategien zur Altersarmutsbekämpfung nunmehr fundamental dadurch, dass die Gewerkschaften im Sinne ihrer Bürgerversicherungs-/ Erwerbstätigenversicherungsansätze prekär Beschäftigte in die gesetzliche Rentenversicherung einbeziehen bzw. sie darin halten wollen, während die Linkspartei nunmehr den Ausstieg aus der gesetzlichen Rentenversicherung mit libertär geprägten Anreizen belohnen und dabei Vermögende begünstigen will

The regulation of cytokine networks in hippocampal CA1 differentiates extinction from those required for the maintenance of contextual fear memory after recall

We investigated the distinctiveness of gene regulatory networks in CA1 associated with the extinction of contextual fear memory (CFM) after recall using Affymetrix GeneChip Rat Genome 230 2.0 Arrays. These data were compared to previously published retrieval and reconsolidation-attributed, and consolidation datasets. A stringent dual normalization and pareto-scaled orthogonal partial least-square discriminant multivariate analysis together with a jack-knifing-based cross-validation approach was used on all datasets to reduce false positives. Consolidation, retrieval and extinction were correlated with distinct patterns of gene expression 2 hours later. Extinction-related gene expression was most distinct from the profile accompanying consolidation. A highly specific feature was the discrete regulation of neuroimmunological gene expression associated with retrieval and extinction. Immunity–associated genes of the tyrosine kinase receptor TGFβ and PDGF, and TNF families’ characterized extinction. Cytokines and proinflammatory interleukins of the IL-1 and IL-6 families were enriched with the no-extinction retrieval condition. We used comparative genomics to predict transcription factor binding sites in proximal promoter regions of the retrieval-regulated genes. Retrieval that does not lead to extinction was associated with NF-κB-mediated gene expression. We confirmed differential NF-κBp65 expression, and activity in all of a representative sample of our candidate genes in the no-extinction condition. The differential regulation of cytokine networks after the acquisition and retrieval of CFM identifies the important contribution that neuroimmune signalling plays in normal hippocampal function. Further, targeting cytokine signalling upon retrieval offers a therapeutic strategy to promote extinction mechanisms in human disorders characterised by dysregulation of associative memory

Neuropeptidomic analysis of the embryonic Japanese quail diencephalon

<p>Abstract</p> <p>Background</p> <p>Endogenous peptides such as neuropeptides are involved in numerous biological processes in the fully developed brain but very little is known about their role in brain development. Japanese quail is a commonly used bird model for studying sexual dimorphic brain development, especially adult male copulatory behavior in relation to manipulations of the embryonic endocrine system. This study uses a label-free liquid chromatography mass spectrometry approach to analyze the influence of age (embryonic days 12 vs 17), sex and embryonic day 3 ethinylestradiol exposure on the expression of multiple endogenous peptides in the developing diencephalon.</p> <p>Results</p> <p>We identified a total of 65 peptides whereof 38 were sufficiently present in all groups for statistical analysis. Age was the most defining variable in the data and sex had the least impact. Most identified peptides were more highly expressed in embryonic day 17. The top candidates for EE₂exposure and sex effects were neuropeptide K (downregulated by EE₂in males and females), gastrin-releasing peptide (more highly expressed in control and EE₂exposed males) and gonadotropin-inhibiting hormone related protein 2 (more highly expressed in control males and displaying interaction effects between age and sex). We also report a new potential secretogranin-2 derived neuropeptide and previously unknown phosphorylations in the C-terminal flanking protachykinin 1 neuropeptide.</p> <p>Conclusions</p> <p>This study is the first larger study on endogenous peptides in the developing brain and implies a previously unknown role for a number of neuropeptides in middle to late avian embryogenesis. It demonstrates the power of label-free liquid chromatography mass spectrometry to analyze the expression of multiple endogenous peptides and the potential to detect new putative peptide candidates in a developmental model.</p

Proteomic Evaluation of Neonatal Exposure to 2,2′,4,4′,5-Pentabromodiphenyl Ether

Exposure to the brominated flame retardant 2,2′,4,4′,5-pentabromodiphenyl ether (PBDE-99) during the brain growth spurt disrupts normal brain development in mice and results in disturbed spontaneous behavior in adulthood. The neurodevelopmental toxicity of PBDE-99 has been reported to affect the cholinergic and catecholaminergic systems. In this study we use a proteomics approach to study the early effect of PBDE-99 in two distinct regions of the neonatal mouse brain, the striatum and the hippocampus. A single oral dose of PBDE-99 (12 mg/kg body weight) or vehicle was administered to male NMRI mice on neonatal day 10, and the striatum and the hippocampus were isolated. Using two-dimensional fluorescence difference gel electrophoresis (2D-DIGE), we found 40 and 56 protein spots with significantly (p < 0.01) altered levels in the striatum and the hippocampus, respectively. We used matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI–ToF–MS) to determine the protein identity of 11 spots from the striatum and 10 from the hippocampus. We found that the levels of proteins involved in neurodegeneration and neuroplasticity (e.g., Gap-43/neuromodulin, stathmin) were typically altered in the striatum, and proteins involved in metabolism and energy production [e.g., α-enolase; γ-enolase; ATP synthase, H(+) transporting, mitochondrial F(1) complex, β subunit (Atp5b); and α-synuclein] were typically altered in the hippocampus. Interestingly, many of the identified proteins have been linked to protein kinase C signaling. In conclusion, we identify responses to early exposure to PBDE-99 that could contribute to persistent neurotoxic effects. This study also shows the usefulness of proteomics to identify potential biomarkers of developmental neurotoxicity of organohalogen compounds

Faced with inequality: chicken do not have a general dosage compensation of sex-linked genes

<p>Abstract</p> <p>Background</p> <p>The contrasting dose of sex chromosomes in males and females potentially introduces a large-scale imbalance in levels of gene expression between sexes, and between sex chromosomes and autosomes. In many organisms, dosage compensation has thus evolved to equalize sex-linked gene expression in males and females. In mammals this is achieved by X chromosome inactivation and in flies and worms by up- or down-regulation of X-linked expression, respectively. While otherwise widespread in systems with heteromorphic sex chromosomes, the case of dosage compensation in birds (males ZZ, females ZW) remains an unsolved enigma.</p> <p>Results</p> <p>Here, we use a microarray approach to show that male chicken embryos generally express higher levels of Z-linked genes than female birds, both in soma and in gonads. The distribution of male-to-female fold-change values for Z chromosome genes is wide and has a mean of 1.4–1.6, which is consistent with absence of dosage compensation and sex-specific feedback regulation of gene expression at individual loci. Intriguingly, without global dosage compensation, the female chicken has significantly lower expression levels of Z-linked compared to autosomal genes, which is not the case in male birds.</p> <p>Conclusion</p> <p>The pronounced sex difference in gene expression is likely to contribute to sexual dimorphism among birds, and potentially has implication to avian sex determination. Importantly, this report, together with a recent study of sex-biased expression in somatic tissue of chicken, demonstrates the first example of an organism with a lack of global dosage compensation, providing an unexpected case of a viable system with large-scale imbalance in gene expression between sexes.</p

Striatal Proteomic Analysis Suggests that First L-Dopa Dose Equates to Chronic Exposure

L-3,4-dihydroxypheylalanine (L-dopa)-induced dyskinesia represent a debilitating complication of therapy for Parkinson's disease (PD) that result from a progressive sensitization through repeated L-dopa exposures. The MPTP macaque model was used to study the proteome in dopamine-depleted striatum with and without subsequent acute and chronic L-dopa treatment using two-dimensional difference in-gel electrophoresis (2D-DIGE) and mass spectrometry. The present data suggest that the dopamine-depleted striatum is so sensitive to de novo L-dopa treatment that the first ever administration alone would be able (i) to induce rapid post-translational modification-based proteomic changes that are specific to this first exposure and (ii), possibly, lead to irreversible protein level changes that would be not further modified by chronic L-dopa treatment. The apparent equivalence between first and chronic L-dopa administration suggests that priming would be the direct consequence of dopamine loss, the first L-dopa administrations only exacerbating the sensitization process but not inducing it

Effects of the Histone Deacetylase Inhibitor Valproic Acid on Human Pericytes In Vitro

Microvascular pericytes are of key importance in neoformation of blood vessels, in stabilization of newly formed vessels as well as maintenance of angiostasis in resting tissues. Furthermore, pericytes are capable of differentiating into pro-fibrotic collagen type I producing fibroblasts. The present study investigates the effects of the histone deacetylase (HDAC) inhibitor valproic acid (VPA) on pericyte proliferation, cell viability, migration and differentiation. The results show that HDAC inhibition through exposure of pericytes to VPA in vitro causes the inhibition of pericyte proliferation and migration with no effect on cell viability. Pericyte exposure to the potent HDAC inhibitor Trichostatin A caused similar effects on pericyte proliferation, migration and cell viability. HDAC inhibition also inhibited pericyte differentiation into collagen type I producing fibroblasts. Given the importance of pericytes in blood vessel biology a qPCR array focusing on the expression of mRNAs coding for proteins that regulate angiogenesis was performed. The results showed that HDAC inhibition promoted transcription of genes involved in vessel stabilization/maturation in human microvascular pericytes. The present in vitro study demonstrates that VPA influences several aspects of microvascular pericyte biology and suggests an alternative mechanism by which HDAC inhibition affects blood vessels. The results raise the possibility that HDAC inhibition inhibits angiogenesis partly through promoting a pericyte phenotype associated with stabilization/maturation of blood vessels

Genomic and Peptidomic Characterization of the Developing Avian Brain

Chicken and Japanese quail are commonly used models in developmental and sex specific neuroendocrine research. There is relatively little known about the mechanisms behind their sex specific brain development, especially regarding the impact of the sex chromosomes (male: ZZ, female ZW) in relation to gonadal hormones. This thesis explores several aspects of these processes. Gene expression analysis with cDNA and Affymetrix arrays on brain tissue from both pre-gonadal embryos and embryos with differentiated gonads indicate a strong sex chromosomal presence in sexual dimorphic somatic tissue development in both chicken and Japanese quail. This sex chromosome pattern seems to remain in adult brain tissue. The data demonstrates that chicken males exhibit a significant level of Z-gene dosage compared to females in both somatic and germ line derived embryonic tissues. Several avian sex determination gene candidates (MHM non-coding RNA, DMRT1, HINTW, and HINTZ) were analyzed by real-time PCR. DMRT1 is dosage compensated in male brain tissue, in contrast to its reported gene dosage in male gonads. Early embryonic ethinylestradiol (EE2) exposure did not affect male or female neural gene expression patterns during later development. A peptidomics analysis on quail embryonic day 12 (ed12) and ed17 diencephalon by LC-MS identified over 60 endogenous peptides and analyzed the expression patterns for 38 of them with regard to age, sex and early EE2 exposure. There was a general upregulation between ed12 and ed17, but no clear sex effects were detected. Multivariate analysis indicates that EE2 exposed individuals differ from control individuals in a gender independent manner, and that Gonadotropin-inhibiting hormone related peptide 2 (GnIH-RP2) is a candidate for EE2 induced peptidomic alterations in male embryonic brain

Genomic and Peptidomic Characterization of the Developing Avian Brain

Chicken and Japanese quail are commonly used models in developmental and sex specific neuroendocrine research. There is relatively little known about the mechanisms behind their sex specific brain development, especially regarding the impact of the sex chromosomes (male: ZZ, female ZW) in relation to gonadal hormones. This thesis explores several aspects of these processes. Gene expression analysis with cDNA and Affymetrix arrays on brain tissue from both pre-gonadal embryos and embryos with differentiated gonads indicate a strong sex chromosomal presence in sexual dimorphic somatic tissue development in both chicken and Japanese quail. This sex chromosome pattern seems to remain in adult brain tissue. The data demonstrates that chicken males exhibit a significant level of Z-gene dosage compared to females in both somatic and germ line derived embryonic tissues. Several avian sex determination gene candidates (MHM non-coding RNA, DMRT1, HINTW, and HINTZ) were analyzed by real-time PCR. DMRT1 is dosage compensated in male brain tissue, in contrast to its reported gene dosage in male gonads. Early embryonic ethinylestradiol (EE2) exposure did not affect male or female neural gene expression patterns during later development. A peptidomics analysis on quail embryonic day 12 (ed12) and ed17 diencephalon by LC-MS identified over 60 endogenous peptides and analyzed the expression patterns for 38 of them with regard to age, sex and early EE2 exposure. There was a general upregulation between ed12 and ed17, but no clear sex effects were detected. Multivariate analysis indicates that EE2 exposed individuals differ from control individuals in a gender independent manner, and that Gonadotropin-inhibiting hormone related peptide 2 (GnIH-RP2) is a candidate for EE2 induced peptidomic alterations in male embryonic brain