Lohnpolitische Koordinierung in der EU: Wie Gewerkschaften agieren

In den letzten Monaten hat sich die Diskussion über mehr wirtschaftspolitische Koordinierung in der EU und insbesondere in der Europäischen Wirtschafts- und Währungsunion intensiviert. Dabei wurde unter anderem die unterschiedliche Entwicklung der preislichen Wettbewerbsfähigkeit thematisiert. In diesem Zusammenhang sind die seit einigen Jahren von den europäischen Branchengewerkschaftsverbänden forcierten Bemühungen zur Koordinierung der Lohnverhandlungen von besonderem Interesse, da die daraus resultierenden Lohnpolitiken womöglich Folgen für den weiteren Bedarf an wirtschaftspolitischer Abstimmung in der Europäischen Wirtschafts- und Währungsunion haben könnten. Am Beispiel des 1997 gegründeten Lohnverhandlungsnetzwerks der IG Metall in Nordrhein-Westfalen und der Metallgewerkschaften Belgiens sowie der Niederlande wird in diesem Beitrag die tatsächliche Effektivität der grenzüberschreitenden lohnpolitischen Koordinierung untersucht, sowohl hinsichtlich der Zielsetzungen der Gewerkschaften als auch der Wirtschaftspolitik der EU. Es zeigt sich, dass das gewerkschaftliche Ziel einer produktivitätsorientierten Lohnentwicklung seit der Einrichtung des Netzwerks tendenziell erreicht werden konnte. Für eine Orientierung an der jüngst in der „Europa 2020“- Strategie bekräftigten Lohnleitlinie der EU-Wirtschaftspolitik konnte hingegen keine Evidenz gefunden werden.

Sub-Doppler spectroscopy of Rb atoms in a sub-micron vapor cell in the presence of a magnetic field

We report the first use of an extremely thin vapor cell (thickness ~ 400 nm) to study the magnetic-field dependence of laser-induced-fluorescence excitation spectra of alkali atoms. This thin cell allows for sub-Doppler resolution without the complexity of atomic beam or laser cooling techniques. This technique is used to study the laser-induced-fluorescence excitation spectra of Rb in a 50 G magnetic field. At this field strength the electronic angular momentum J and nuclear angular momentum I are only partially decoupled. As a result of the mixing of wavefunctions of different hyperfine states, we observe a nonlinear Zeeman effect for each sublevel, a substantial modification of the transition probabilities between different magnetic sublevels, and the appearance of transitions that are strictly forbidden in the absence of the magnetic field. For the case of right- and left- handed circularly polarized laser excitation, the fluorescence spectra differs qualitatively. Well pronounced magnetic field induced circular dichroism is observed. These observations are explained with a standard approach that describes the partial decoupling of I and J states

CXCR6 marks a novel subset of T-bet(lo)Eomes(hi) natural killer cells residing in human liver

This work was funded by a Wellcome Trust Investigator Award to MKM funding KS and LP, MRC Career Development Award to CD, MRC Clinical Research Training Fellowship to DP, Wellcome Trust Henry Dale Fellowship to VM

Gastrointestinal Hyperplasia with Altered Expression of DNA Polymerase β

Background: Altered expression of DNA polymerase β (Pol β) has been documented in a large percentage of human tumors. However, tumor prevalence or predisposition resulting from Pol β over-expression has not yet been evaluated in a mouse model. Methodology/Principal Findings: We have recently developed a novel transgenic mouse model that over-expresses Pol β. These mice present with an elevated incidence of spontaneous histologic lesions, including cataracts, hyperplasia of Brunner's gland and mucosal hyperplasia in the duodenum. In addition, osteogenic tumors in mice tails, such as osteoma and osteosarcoma were detected. This is the first report of elevated tumor incidence in a mouse model of Pol β over-expression. These findings prompted an evaluation of human gastrointestinal tumors with regard to Pol β expression. We observed elevated expression of Pol β in stomach adenomas and thyroid follicular carcinomas, but reduced Pol β expression in esophageal adenocarcinomas and squamous carcinomas. Conclusions/Significance: These data support the hypothesis that balanced and proficient base excision repair protein expression and base excision repair capacity is required for genome stability and protection from hyperplasia and tumor formation

Balancing repair and tolerance of DNA damage caused by alkylating agents

Alkylating agents constitute a major class of frontline chemotherapeutic drugs that inflict cytotoxic DNA damage as their main mode of action, in addition to collateral mutagenic damage. Numerous cellular pathways, including direct DNA damage reversal, base excision repair (BER) and mismatch repair (MMR), respond to alkylation damage to defend against alkylation-induced cell death or mutation. However, maintaining a proper balance of activity both within and between these pathways is crucial for a favourable response of an organism to alkylating agents. Furthermore, the response of an individual to alkylating agents can vary considerably from tissue to tissue and from person to person, pointing to genetic and epigenetic mechanisms that modulate alkylating agent toxicity

The Cycad Genotoxin MAM Modulates Brain Cellular Pathways Involved in Neurodegenerative Disease and Cancer in a DNA Damage-Linked Manner

Methylazoxymethanol (MAM), the genotoxic metabolite of the cycad azoxyglucoside cycasin, induces genetic alterations in bacteria, yeast, plants, insects and mammalian cells, but adult nerve cells are thought to be unaffected. We show that the brains of adult C57BL6 wild-type mice treated with a single systemic dose of MAM acetate display DNA damage (O6-methyldeoxyguanosine lesions, O6-mG) that remains constant up to 7 days post-treatment. By contrast, MAM-treated mice lacking a functional gene encoding the DNA repair enzyme O6-mG DNA methyltransferase (MGMT) showed elevated O6-mG DNA damage starting at 48 hours post-treatment. The DNA damage was linked to changes in the expression of genes in cell-signaling pathways associated with cancer, human neurodegenerative disease, and neurodevelopmental disorders. These data are consistent with the established developmental neurotoxic and carcinogenic properties of MAM in rodents. They also support the hypothesis that early-life exposure to MAM-glucoside (cycasin) has an etiological association with a declining, prototypical neurodegenerative disease seen in Guam, Japan, and New Guinea populations that formerly used the neurotoxic cycad plant for food or medicine, or both. These findings suggest environmental genotoxins, specifically MAM, target common pathways involved in neurodegeneration and cancer, the outcome depending on whether the cell can divide (cancer) or not (neurodegeneration). Exposure to MAM-related environmental genotoxins may have relevance to the etiology of related tauopathies, notably, Alzheimer's disease