Potential implications of labour market opening in Germany and Austria on emigration from Poland

The aim of this study is to present the characteristic of present-day migrants and the potential for possible migration after the opening of the labour markets in Austria and Germany. The econometric analysis shows that differences in unemployment rates between sending and receiving countries were the most important for changes in the emigration from Poland in the period 2002-2009. Mostly due to persistence of these differences the intruduction of the open-door policy by two last EU countries in the spring of 2011 can intensify the further emigration flows from Poland. Data concerning the structure of the present emigration in Germany indicate that emigrants from Poland are mainly persons with vocational and secondary education, working primarily in the sections of services (e.g. health care and social assistance, accommodation and catering). There is also a relatively high percentage of persons employed in agriculture and the construction sector. These sectors will probably continue to be the most frequent workplace for emigrants, where the internal supply of work seems insufficient to meet the needs of this part of the German economy. The current limitations push better educated emigrants from Poland to work mainly as specialists in the sectors of economy preferred by Germany or as self-employed persons. The caps applied by German authorities concerning the number of Polish employees on secondment under the framework of the cross-border provision of services remain underused. Moreover, German data (which do not cover persons holding dual nationality) indicate that for the time being emigration from Poland is, to a large extent, circulatory by nature. Examples of other EU countries which already opened their labour markets indicate that the removal of barriers to access may increase emigration in the first year, but the differences and changes in unemployment rates among countries are a much more important factor for migratory flows, particularly at a later stage. The opening of labour markets in Germany and Austria may contribute to a change in the nature of the present short-term to a more permanent migration from Poland. The first part of the study presents information on the existing work limitations for Poles in Germany and the characteristics of the present emigrants from Poland to Germany and Austria. The second part discusses determinants of emigration in 2002-2009, putting a special emphasis on those countries which already managed to open their labour markets for the ‘new’ EU members. The third part delivers the estimates of possible emigration changes from Poland to Germany and Austria that are going to happen after 1 May 2011.labour migration, open-door policy, Poland, Germany, determinants of migration

Potential implications of labour market opening in Germany and Austria on emigration from Poland

The aim of this study is to present the characteristic of present-day migrants and the potential for possible migration after the opening of the labour markets in Austria and Germany. The econometric analysis shows that differences in unemployment rates between sending and receiving countries were the most important for changes in the emigration from Poland in the period 2002-2009. Mostly due to persistence of these differences the intruduction of the open-door policy by two last EU countries in the spring of 2011 can intensify the further emigration flows from Poland. Data concerning the structure of the present emigration in Germany indicate that emigrants from Poland are mainly persons with vocational and secondary education, working primarily in the sections of services (e.g. health care and social assistance, accommodation and catering). There is also a relatively high percentage of persons employed in agriculture and the construction sector. These sectors will probably continue to be the most frequent workplace for emigrants, where the internal supply of work seems insufficient to meet the needs of this part of the German economy. The current limitations push better educated emigrants from Poland to work mainly as specialists in the sectors of economy preferred by Germany or as self-employed persons. The caps applied by German authorities concerning the number of Polish employees on secondment under the framework of the cross-border provision of services remain underused. Moreover, German data (which do not cover persons holding dual nationality) indicate that for the time being emigration from Poland is, to a large extent, circulatory by nature. Examples of other EU countries which already opened their labour markets indicate that the removal of barriers to access may increase emigration in the first year, but the differences and changes in unemployment rates among countries are a much more important factor for migratory flows, particularly at a later stage. The opening of labour markets in Germany and Austria may contribute to a change in the nature of the present short-term to a more permanent migration from Poland. The first part of the study presents information on the existing work limitations for Poles in Germany and the characteristics of the present emigrants from Poland to Germany and Austria. The second part discusses determinants of emigration in 2002-2009, putting a special emphasis on those countries which already managed to open their labour markets for the ‘new’ EU members. The third part delivers the estimates of possible emigration changes from Poland to Germany and Austria that are going to happen after 1 May 2011

Ultrasound-detected subclinical inflammation was better reflected by the disease activity score (DAS-28) in patients with suspicion of inflammatory arthritis compared to established rheumatoid arthritis

Limited data are available about the ultrasound (US)-detected inflammatory features in patients with suspicion of inflammatory arthritis (S-IA) vs. established rheumatoid arthritis (RA). Our study aimed to assess if the presence of power Doppler (PD) can be predicted by a combination of clinical, laboratory and US parameters. We conducted a real-life, retrospective cohort study comparing clinical, laboratory and US parameters of 108 patients with established RA and 93 patients with S-IA. We propose a PD signal prediction model based on a beta-binomial distribution for PD variable using a mix of outcome measures. Patients with RA in clinical remission had significantly more active inflammation and erosions on US when compared with patients with S-IA with similar disease scores (p = 0.03 and p = 0.01, respectively); however, RA patients with different disease activity score (DAS-28) scores had similar PD scores (p = 0.058). The PD scores did not correlate with erosions (p = 0.38) or DAS-28 scores (p = 0.28) in RA patients, but they correlated with high disease activity in S-IA patients (p = 0.048). Subclinical inflammation is more common in patients with RA in clinical remission or with low disease activity than in patients with S-IA; therefore, US was more useful in assessing for true remission in RA rather than diagnosing IA in patients with low disease activity scores. This is the first study to propose a PD prediction model integrating several outcome measures in the two different groups of patients. Further research into validating this model can minimise the risk of underdiagnosing subclinical inflammation

Yotiao, a Novel Protein of Neuromuscular Junction and Brain That Interacts with Specific Splice Variants of NMDA Receptor Subunit NR1

The molecular machinery underlying neurotransmitter receptor immobilization at postsynaptic sites is poorly understood. The NMDA receptor subunit NR1 can form clusters in heterologous cells via a mechanism dependent on the alternatively spliced C1 exon cassette in its intracellular C-terminal tail, suggesting a functional interaction between NR1 and the cytoskeleton. The yeast two-hybrid screen was used here to identify yotiao, a novel coiled coil protein that interacts with NR1 in a C1 exon-dependent manner. Yotiao mRNA (11 kb) is present modestly in brain and abundantly in skeletal muscle and pancreas. On Western blots, yotiao appears as an approximately 230 kDa band that is present in cerebral cortex, hippocampus, and cerebellum. Biochemical studies reveal that yotiao fractionates with cytoskeleton-associated proteins and with the postsynaptic density. With regard to immunohistochemistry, two anti-yotiao antibodies display a somatodendritic staining pattern similar to each other and to the staining pattern of NR1. Yotiao was colocalized by double-label immunocytochemistry with NR1 in rat brain and could be coimmunoprecipitated with NR1 from heterologous cells. Thus yotiao is an NR1-binding protein potentially involved in cytoskeletal attachment of NMDA receptors. Consistent with a general involvement in postsynaptic structure, yotiao was also found to be specifically concentrated at the neuromuscular junction in skeletal muscle

Multiplicity and transverse momentum fluctuations in inelastic proton-proton interactions at the CERN Super Proton Synchrotron

Measurements of multiplicity and transverse momentum fluctuations of charged particles were performed in inelastic p+p interactions at 20, 31, 40, 80 and 158 GeV/c beam momentum. Results for the scaled variance of the multiplicity distribution and for three strongly intensive measures of multiplicity and transverse momentum fluctuations \$\Delta[P_{T},N]\$, \$\Sigma[P_{T},N]\$ and \$\Phi_{p_T}\$ are presented. For the first time the results on fluctuations are fully corrected for experimental biases. The results on multiplicity and transverse momentum fluctuations significantly deviate from expectations for the independent particle production. They also depend on charges of selected hadrons. The string-resonance Monte Carlo models EPOS and UrQMD do not describe the data. The scaled variance of multiplicity fluctuations is significantly higher in inelastic p+p interactions than in central Pb+Pb collisions measured by NA49 at the same energy per nucleon. This is in qualitative disagreement with the predictions of the Wounded Nucleon Model. Within the statistical framework the enhanced multiplicity fluctuations in inelastic p+p interactions can be interpreted as due to event-by-event fluctuations of the fireball energy and/or volume.Comment: 18 pages, 12 figure

LEDGF1-326 Decreases P23H and Wild Type Rhodopsin Aggregates and P23H Rhodopsin Mediated Cell Damage in Human Retinal Pigment Epithelial Cells

P23H rhodopsin, a mutant rhodopsin, is known to aggregate and cause retinal degeneration. However, its effects on retinal pigment epithelial (RPE) cells are unknown. The purpose of this study was to determine the effect of P23H rhodopsin in RPE cells and further assess whether LEDGF(1-326), a protein devoid of heat shock elements of LEDGF, a cell survival factor, reduces P23H rhodopsin aggregates and any associated cellular damage.ARPE-19 cells were transiently transfected/cotransfected with pLEDGF(1-326) and/or pWT-Rho (wild type)/pP23H-Rho. Rhodopsin mediated cellular damage and rescue by LEDGF(1-326) was assessed using cell viability, cell proliferation, and confocal microscopy assays. Rhodopsin monomers, oligomers, and their reduction in the presence of LEDGF(1-326) were quantified by western blot analysis. P23H rhodopsin mRNA levels in the presence and absence of LEDGF(1-326) was determined by real time quantitative PCR.P23H rhodopsin reduced RPE cell viability and cell proliferation in a dose dependent manner, and disrupted the nuclear material. LEDGF(1-326) did not alter P23H rhodopsin mRNA levels, reduced its oligomers, and significantly increased RPE cell viability as well as proliferation, while reducing nuclear damage. WT rhodopsin formed oligomers, although to a smaller extent than P23H rhodopsin. Further, LEDGF(1-326) decreased WT rhodopsin aggregates.P23H rhodopsin as well as WT rhodopsin form aggregates in RPE cells and LEDGF(1-326) decreases these aggregates. Further, LEDGF(1-326) reduces the RPE cell damage caused by P23H rhodopsin. LEDGF(1-326) might be useful in treating cellular damage associated with protein aggregation diseases such as retinitis pigmentosa

Prenatal Cocaine Exposure Increases Synaptic Localization of a Neuronal RasGEF, GRASP-1 via Hyperphosphorylation of AMPAR Anchoring Protein, GRIP

Prenatal cocaine exposure causes sustained phosphorylation of the synaptic anchoring protein, glutamate receptor interacting protein (GRIP1/2), preventing synaptic targeting of the GluR2/3-containing alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-type glutamate receptors (AMPARs; J. Neurosci. 29: 6308–6319, 2009). Because overexpression of GRIP-associated neuronal rasGEF protein (GRASP-1) specifically reduces the synaptic targeting of AMPARs, we hypothesized that prenatal cocaine exposure enhances GRASP-1 synaptic membrane localization leading to hyper-activation of ras family proteins and heightened actin polymerization. Our results show a markedly increased GRIP1-associated GRASP-1 content with approximately 40% reduction in its rasGEF activity in frontal cortices (FCX) of 21-day-old (P21) prenatal cocaine-exposed rats. This cocaine effect is the result of a persistent protein kinase C (PKC)- and downstream Src tyrosine kinase-mediated GRIP phosphorylation. The hyperactivated PKC also increased membrane-associated GRASP-1 and activated small G-proteins RhoA, cdc42/Rac1 and Rap1 as well as filamentous actin (F-actin) levels without an effect on the phosphorylation state of actin. Since increased F-actin facilitates protein transport, our results suggest that increased GRASP-1 synaptic localization in prenatal cocaine-exposed brains is an adaptive response to restoring the synaptic expression of AMPA-GluR2/3. Our earlier data demonstrated that persistent PKC-mediated GRIP phosphorylation reduces GluR2/3 synaptic targeting in prenatal cocaine-exposed brains, we now show that the increased GRIP-associated GRASP-1 may contribute to the reduction in GluR2/3 synaptic expression and AMPAR signaling defects

Production of Λ-hyperons in inelastic p+p interactions at 158 GeV/c

Inclusive production of Λ -hyperons was measured with the large acceptance NA61/SHINE spectrometer at the CERN SPS in inelastic p+p interactions at beam momentum of 158 GeV/c . Spectra of transverse momentum and transverse mass as well as distributions of rapidity and x F are presented. The mean multiplicity was estimated to be 0.120±0.006(stat.)±0.010(sys.). The results are compared with previous measurements and predictions of the Epos , U r qmd and Fritiof models

An intergenic risk locus containing an enhancer deletion in 2q35 modulates breast cancer risk by deregulating IGFBP5 expression

Breast cancer is the most diagnosed malignancy and the second leading cause of cancer mortality in females. Previous association studies have identified variants on 2q35 associated with the risk of breast cancer. To identify functional susceptibility loci for breast cancer, we interrogated the 2q35 gene desert for chromatin architecture and functional variation correlated with gene expression. We report a novel intergenic breast cancer risk locus containing an enhancer copy number variation (enCNV; deletion) located approximately 400Kb upstream to IGFBP5, which overlaps an intergenic ERα-bound enhancer that loops to the IGFBP5 promoter. The enCNV is correlated with modified ERα binding and monoallelic-repression of IGFBP5 following estrogen treatment. We investigated the association of enCNV genotype with breast cancer in 1,182 cases and 1,362 controls, and replicate our findings in an independent set of 62,533 cases and 60,966 controls from 41 case control studies and 11 GWAS. We report a dose-dependent inverse association of 2q35 enCNV genotype (percopy OR=0.68 95%CI 0.55-0.83, P=0.0002; replication OR=0.77 95%CI 0.73-0.82, P=2.1x10(-19)) and identify 13 additional linked variants (r(2)>0.8) in the 20Kb linkage block containing the enCNV (P=3.2x10(-15) - 5.6x10(-17)). These associations were independent of previously reported 2q35 variants, rs13387042/rs4442975 and rs16857609, and were stronger for ER-positive than ER-negative disease. Together, these results suggest that 2q35 breast cancer risk loci may be mediating their effect through IGFBP5