A tulajdonnév köznevesülésének jelentésváltozási folyamatai

Semantic changes in the process of appellativisation of proper nouns This paper deals with the semantic processes that take place during the transition of a proper noun to an appellative (i.e. during appellativisation). Tanja Anstatt has developed an effective model by means of which the semantic changes in the process of appellativation can be precisely described. She gives a typology of the appellativised proper nouns on the basis of Volkmar Lehmann’s description of word formation processes, using Polish examples. This model is based on the tropes “metaphor”, “metonymy” and “synecdoche” as results of the (part-) processes of modification, recategorization, profilation, transprofilation and synthetic combination. In general, during the transition process of a proper noun to an appellative more than just one of the above part-processes operate. The author applies Anstatt’s system to Hungarian examples. The author also discusses some misinterpreted examples of appellativised proper nouns that can easily be “unmasked” with the help of the adopted typology. The improved typology presented in the paper, however, does not make a claim to be complete or final; it should rather be taken as a proposal which, with the five part-processes, gives a tool to describe each type of appellativised proper noun. Further investigation of a larger word stock, and especially of words taken from the spoken language, can make the above typology more complete and thus more valid

Managementprozess externer Unternehmenskommunikation über das Medium Corporate Blog

Corporate Blogs sind für die externe Unternehmenskommunikation ein wichtiges, aber zu Teilen noch recht unerforschtes Medium. Der Forschungsstand weist in diesem Feld einen eher grundlagenbildenden Charakter auf. Die Frage wie der Managementprozess externer Unternehmenskommunikation von den Akteuren gestaltet wird und welche Strukturen sowie Regeln diesen Prozess begleiten, sind bisher unbeantwortet geblieben. Diese Forschungslücke soll mittels problemzentrierter Interviews mit den beteiligten Unternehmensakteuren und einer anschließenden Inhaltsanalyse geschlossen werden

Econometric Analysis of Gender Differences in the German Labor Market

Die Dissertation umfasst drei empirische Studien zu Ausmaß, Ursache und Folgen von Geschlechterunterschieden im deutschen Arbeitsmarkt. Diese basieren auf Daten des Instituts für Arbeitsmarkt- und Berufsforschung (IAB) der Bundesanstalt für Arbeit. Ein Kapitel der Dissertation befasst sich mit der Ursache von beruflicher Segregation in deutschen Betrieben. Dazu werden Segregationsindizes für jeden Betrieb errechnet. Diese beschreiben die ungleiche Verteilung von Frauen und Männern auf Berufsgruppen innerhalb der Belegschaft. Anhand verschiedener Paneldatenmodelle werden Organisationsmerkmale identifiziert, welche den Grad an beruflicher Segregation beeinflussen. Insbesondere wird auf den Effekt der Implementierung von Gleichstellungsmaßnahmen eingegangen. Ein weiteres Kapitel der Arbeit untersucht, inwieweit die Wahrnehmung einer potentiellen Elternschaft den Karriereverlauf von Arbeitnehmern beeinflussen kann. Auf Basis von Multivariaten Hazardmodellen sowie Fixed-Effects Modellen wird die Wahrscheinlichkeit einer Elternschaft für kinderlose Männer und Frauen ermittelt, welche simultan in die Berechnung der Wahrscheinlichkeit von Karriereübergängen eingeht. Die Ergebnisse legen nahe, dass ein wahrgenommenes „Schwangerschaftsrisiko“ die berufliche Mobilität von Frauen einschränkt, während für Männer ein beruflicher Aufstieg wahrscheinlicher wird, wenn eine Vaterschaft angenommen wird. Der dritte Teil der Dissertation beschäftigt sich mit geschlechtsspezifischen Lohnunterschieden und dem regionalen Arbeitslosigkeitsniveau. Ein Zusammenhang wird ausgehend von der Theorie der Lohnkurve und der empirischen Beobachtung geschlechtsspezifischer Lohnelastizitäten postuliert und untersucht. Anhand von Dekompositionsverfahren werden Kennzahlen zum Gender Wage Gap auf Kreis- sowie auf Betriebsebene berechnet und auf die Arbeitslosenquote regressiert. Dabei werden zudem regionale Spillovereffekte berücksichtigt

Analyzing nicotinamide adenine dinucleotide phosphate oxidase activation in aging and vascular amyloid pathology

In aging individuals, both protective as well as regulatory immune functions are declining, resulting in an increased susceptibility to infections as well as to autoimmunity. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2-deficiency in immune cell subsets has been shown to be associated with aging. Using intravital marker-free NAD(P)H-fluorescence lifetime imaging, we have previously identified microglia/myeloid cells and astrocytes as main cellular sources of NADPH oxidase (NOX) activity in the CNS during neuroinflammation, due to an overactivation of NOX. The overactivated NOX enzymes catalyze the massive production of the highly reactive O−2, which initiates in a chain reaction the overproduction of diverse reactive oxygen species (ROS). Age-dependent oxidative distress levels in the brain and their cellular sources are not known. Furthermore, it is unclear whether in age- dependent diseases oxidative distress is initiated by overproduction of ROS or by a decrease in antioxidant capacity, subsequently leading to neurodegeneration in the CNS. Here, we compare the activation level of NOX enzymes in the cerebral cortex of young and aged mice as well as in a model of vascular amyloid pathology. Despite the fact that a striking change in the morphology of microglia can be detected between young and aged individuals, we find comparable low-level NOX activation both in young and old mice. In contrast, aged mice with the human APPE693Q mutation, a model for cerebral amyloid angiopathy (CAA), displayed increased focal NOX overactivation in the brain cortex, especially in tissue areas around the vessels. Despite activated morphology in microglia, NOX overactivation was detected only in a small fraction of these cells, in contrast to other pathologies with overt inflammation as experimental autoimmune encephalomyelitis (EAE) or glioblastoma. Similar to these pathologies, the astrocytes majorly contribute to the NOX overactivation in the brain cortex during CAA. Together, these findings emphasize the role of other cellular sources of activated NOX than phagocytes not only during EAE but also in models of amyloid pathology. Moreover, they may strengthen the hypothesis that microglia/monocytes show a diminished potential for clearance of amyloid beta protein

Ferritin H deficiency deteriorates cellular iron handling and worsens Salmonella typhimurium infection by triggering hyperinflammation

Iron is an essential nutrient for mammals as well as for pathogens. Inflammation-driven changes in systemic and cellular iron homeostasis are central for host-mediated antimicrobial strategies. Here, we studied the role of the iron storage protein ferritin H (FTH) for the control of infections with the intracellular pathogen Salmonella enterica serovar Typhimurium by macrophages. Mice lacking FTH in the myeloid lineage (LysM-Cre+/+Fthfl/fl mice) displayed impaired iron storage capacities in the tissue leukocyte compartment, increased levels of labile iron in macrophages, and an accelerated macrophage-mediated iron turnover. While under steady-state conditions, LysM-Cre+/+Fth+/+ and LysM-Cre+/+Fthfl/fl animals showed comparable susceptibility to Salmonella infection, i.v. iron supplementation drastically shortened survival of LysM-Cre+/+Fthfl/fl mice. Mechanistically, these animals displayed increased bacterial burden, which contributed to uncontrolled triggering of NF-κB and inflammasome signaling and development of cytokine storm and death. Importantly, pharmacologic inhibition of the inflammasome and IL-1β pathways reduced cytokine levels and mortality and partly restored infection control in iron-treated ferritin-deficient mice. These findings uncover incompletely characterized roles of ferritin and cellular iron turnover in myeloid cells in controlling bacterial spread and for modulating NF-κB and inflammasome-mediated cytokine activation, which may be of vital importance in iron-overloaded individuals suffering from severe infections and sepsis

A comprehensive microarray-based DNA methylation study of 367 hematological neoplasms

Background: Alterations in the DNA methylation pattern are a hallmark of leukemias and lymphomas. However, most epigenetic studies in hematologic neoplasms (HNs) have focused either on the analysis of few candidate genes or many genes and few HN entities, and comprehensive studies are required. Methodology/Principal Findings: Here, we report for the first time a microarray-based DNA methylation study of 767 genes in 367 HNs diagnosed with 16 of the most representative B-cell (n = 203), T-cell (n = 30), and myeloid (n = 134) neoplasias, as well as 37 samples from different cell types of the hematopoietic system. Using appropriate controls of B-, T-, or myeloid cellular origin, we identified a total of 220 genes hypermethylated in at least one HN entity. In general, promoter hypermethylation was more frequent in lymphoid malignancies than in myeloid malignancies, being germinal center mature B-cell lymphomas as well as B and T precursor lymphoid neoplasias those entities with highest frequency of gene-associated DNA hypermethylation. We also observed a significant correlation between the number of hypermethylated and hypomethylated genes in several mature B-cell neoplasias, but not in precursor B- and T-cell leukemias. Most of the genes becoming hypermethylated contained promoters with high CpG content, and a significant fraction of them are targets of the polycomb repressor complex. Interestingly, T-cell prolymphocytic leukemias show low levels of DNA hypermethylation and a comparatively large number of hypomethylated genes, many of them showing an increased gene expression. Conclusions/Significance: We have characterized the DNA methylation profile of a wide range of different HNs entities. As well as identifying genes showing aberrant DNA methylation in certain HN subtypes, we also detected six genes—DBC1, DIO3, FZD9, HS3ST2, MOS, and MYOD1—that were significantly hypermethylated in B-cell, T-cell, and myeloid malignancies. These might therefore play an important role in the development of different HNs

Down-regulation of the myo-inositol oxygenase gene family has no effect on cell wall composition in Arabidopsis

The enzyme myo-inositol oxygenase (MIOX; E.C. 1.13.99.1) catalyzes the ring-opening four-electron oxidation of myo-inositol into glucuronic acid, which is subsequently activated to UDP-glucuronic acid (UDP-GlcA) and serves as a precursor for plant cell wall polysaccharides. Starting from single T-DNA insertion lines in different MIOX-genes a quadruple knockdown (miox1/2/4/5-mutant) was obtained by crossing, which exhibits greater than 90% down-regulation of all four functional MIOX genes. Miox1/2/4/5-mutant shows no visible phenotype and produces viable pollen. The alternative pathway to UDP-glucuronic acid via UDP-glucose is upregulated in the miox1/2/4/5-mutant as a compensatory mechanism. Miox1/2/4/5-mutant is impaired in the utilization of myo-inositol for seedling growth. The incorporation of myo-inositol derived sugars into cell walls is strongly (>90%) inhibited. Instead, myo-inositol and metabolites produced from myo-inositol such as galactinol accumulate in the miox1/2/4/5-mutant. The increase in galactinol and raffinose family oligosaccharides does not enhance stress tolerance. The ascorbic acid levels are the same in mutant and wild type plants

Filamin A Phosphorylation at Serine 2152 by the Serine/Threonine Kinase Ndr2 Controls TCR-Induced LFA-1 Activation in T Cells

The integrin LFA-1 (CD11a/CD18) plays a critical role in the interaction of T cells with antigen presenting cells (APCs) to promote lymphocyte differentiation and proliferation. This integrin can be present either in a closed or in an open active conformation and its activation upon T-cell receptor (TCR) stimulation is a critical step to allow interaction with APCs. In this study we demonstrate that the serine/threonine kinase Ndr2 is critically involved in the initiation of TCR-mediated LFA-1 activation (open conformation) in T cells. Ndr2 itself becomes activated upon TCR stimulation and phosphorylates the intracellular integrin binding partner Filamin A (FLNa) at serine 2152. This phosphorylation promotes the dissociation of FLNa from LFA-1, allowing for a subsequent association of Talin and Kindlin-3 which both stabilize the open conformation of LFA-1. Our data suggest that Ndr2 activation is a crucial step to initiate TCR-mediated LFA-1 activation in T cells