45 research outputs found

    Informations- und Kommunikationswirtschaft Nordrhein-Westfalen

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    Die Informations- und Kommunikationswirtschaft (IuK-Wirtschaft) gilt vielen Beobachtern als die Wachstumsbranche der Zukunft schlechthin. Die vorliegende, von der Hans-Böckler- Stiftung geförderte Studie, zeigt deutlich, daß dieser nordrhein-westfälische Sektor mittlerweile eine wichtige Größe innerhalb der regionalen Wirtschaftsstruktur darstellt. Den weiteren Boom der Branche könnten allenfalls Personalengpässe im Informatikbereich stoppen. Allerdings, so zeigt die Branchenanalyse des Wirtschaftssektors in Nordrhein- Westfalen, dürfen von ihm keine beschäftigungspolitischen Wunder erwartet werden. Regional konzentriert ist dieser Sektor kaum geeignet, strukturschwachen Regionen schnell auf die Beine zu helfen.According the oppinion of many observers the information und communication sector can be reagarded as one of the most important and promising branche of the future. This study supported by the Hans-Böckler Stiftung, clearly points out the importance of the sector within the regional economy of North-Rhine Westphalia. It seems that only personnel bottlenecks in the field of informatic specialists could stop the further boom of the sector. On the other hand the regionaly concentrated information and communication sector can not be regarded as a promising source of growth for all northrhine-westphalian subregions

    Neue Impulse in der regionalen Industriepolitik

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    Seit der Wirtschafts- und Finanzkrise 2007/8 ist Industrie wieder auf der politischen Agenda. Die programmatischen Initiativen werden nur sehr allmählich mit konkreten Instrumenten unterfüttert. Gewerkschaftliche Initiativen auf der regionalen Ebene zeigen, wie breit das industriepolitische Handlungsfeld angelegt ist, und können Beispiele auch für andere Regionen liefern. Das Spektrum regionaler industriepolitischer Initiativen reicht von den täglichen Auseinandersetzungen um konkrete Projekte über Strategien zur Standortentwicklung, innovationspolitische Strategien bis hin zur Zukunftsgestaltung (Energiewende, Industrie 4.0, Elektromobilität). Erfolgreiche Industriepolitik ist langfristig und in vernetzten Strukturen anzulegen

    High Tech, Low Tech, Construction Tech? Innovationsstrategien der Wertschöpfungskette Bau im europäischen Vergleich

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    Das gängige Bild als Low-Tech-Branche wird der tatsächlichen Innovationsstärke der Bauwirtschaft nicht gerecht. Die technische Innovationskraft der Wertschöpfungskette ist, gemessen an den Patenten, deutlich erkennbar. Die deutsche Bauwirtschaft nimmt hier europaweit die Spitzenposition ein. Eine weitere zentrale Stärke der deutschen Bauwirtschaft im europäischen Vergleich liegt in dem überdurchschnittlichen Anteil industrieller Zulieferer innerhalb der Wertschöpfungskette. Auch bei der Förderung energieeffizienten Bauens nimmt Deutschland eine Spitzenstellung ein. Die Weiterbildungsaktivitäten liegen allerdings unter dem europäischen Durchschnitt. Trotz der Tendenz zu einem europäischen Binnenmarkt mit einheitlichen Standards folgt die Bauwirtschaft noch immer spezifischen nationalen Innovationspfaden und weist unterschiedliche Regulierungen auf, was der Internationalisierung weiterhin enge Grenzen setzt. Europäische Benchmarks dienen als Anregungen zur weiteren Entwicklung des Innovationssystems in Deutschland, können allerdings nicht einfach übertragen werden

    HSP90 is essential for Jak-STAT signaling in classical Hodgkin lymphoma cells

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    In classical Hodgkin lymphoma (cHL) chemotherapeutic regimens are associated with stagnant rates of secondary malignancies requiring the development of new therapeutic strategies. We and others have shown that permanently activated Signal Transducer and Activator of Transcription (STAT) molecules are essential for cHL cells. Recently an overexpression of heat-shock protein 90 (HSP90) in cHL cells has been shown and inhibition of HSP90 seems to affect cHL cell survival. Here we analysed the effects of HSP90 inhibition by geldanamycin derivative 17-AAG or RNA interference (RNAi) on aberrant Jak-STAT signaling in cHL cells. Treatment of cHL cell lines with 17-AAG led to reduced cell proliferation and a complete inhibition of STAT1, -3, -5 and -6 tyrosine phosphorylation probably as a result of reduced protein expression of Janus kinases (Jaks). RNAi-mediated inhibition of HSP90 showed similar effects on Jak-STAT signaling in L428 cHL cells. These results suggest a central role of HSP90 in permanently activated Jak-STAT signaling in cHL cells. Therapeutics targeting HSP90 may be a promising strategy in cHL and other cancer entities associated with deregulated Jak-STAT pathway activation

    Early decrements in bone density after completion of neoadjuvant chemotherapy in pediatric bone sarcoma patients

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    <p>Abstract</p> <p>Background</p> <p>Bone mineral density (BMD) accrual during childhood and adolescence is important for attaining peak bone mass. BMD decrements have been reported in survivors of childhood bone sarcomas. However, little is known about the onset and development of bone loss during cancer treatment. The objective of this cross-sectional study was to evaluate BMD in newly diagnosed Ewing's and osteosarcoma patients by means of dual-energy x-ray absorptiometry (DXA) after completion of neoadjuvant chemotherapy.</p> <p>Methods</p> <p>DXA measurements of the lumbar spine (L2-4), both femora and calcanei were performed perioperatively in 46 children and adolescents (mean age: 14.3 years, range: 8.6-21.5 years). Mean <it>Z</it>-scores, areal BMD (g/cm<sup>2</sup>), calculated volumetric BMD (g/cm<sup>3</sup>) and bone mineral content (BMC, g) were determined.</p> <p>Results</p> <p>Lumbar spine mean Z-score was -0.14 (95% CI: -0.46 to 0.18), areal BMD was 1.016 g/cm<sup>2 </sup>(95% CI: 0.950 to 1.082) and volumetric BMD was 0.330 g/cm<sup>3 </sup>(95% CI: 0.314 to 0.347) which is comparable to healthy peers. For patients with a lower extremity tumor (n = 36), the difference between the affected and non-affected femoral neck was 12.1% (95% CI: -16.3 to -7.9) in areal BMD. The reduction of BMD was more pronounced in the calcaneus with a difference between the affected and contralateral side of 21.7% (95% CI: -29.3 to -14.0) for areal BMD. Furthermore, significant correlations for femoral and calcaneal DXA measurements were found with Spearman-rho coefficients ranging from ρ = 0.55 to ρ = 0.80.</p> <p>Conclusions</p> <p>The tumor disease located in the lower extremity in combination with offloading recommendations induced diminished BMD values, indicating local osteopenia conditions. However, the results revealed no significant decrements of lumbar spine BMD in pediatric sarcoma patients after completion of neoadjuvant chemotherapy. Nevertheless, it has to be taken into account that bone tumor patients may experience BMD decrements or secondary osteoporosis in later life. Furthermore, the peripheral assessment of BMD in the calcaneus via DXA is a feasible approach to quantify bone loss in the lower extremity in bone sarcoma patients and may serve as an alternative procedure, when the established assessment of femoral BMD is not practicable due to endoprosthetic replacements.</p

    On the problem of supersonic gas flow in two-dimensional channel with the oscillating upper wall

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    In the present paper we solve the problem of supersonic gas flow in two-dimensional channel with the moving upper wall making oscillations according to the harmonic law. In order to get a numerical solution for gas dynamics equations we have implemented a difference scheme with space and time approximation of the first order and one with space approximation of the second order. Depending on a type of harmonic law and initial gas inflow conditions, the peculiarities of angle-shock wave propagation in moving curvilinear domains have been investigated. It has been determined that the increase of oscillation amplitude causes the increase of shock wave intensity. It has been shown that under particular oscillation amplitude the moving wall has practically no effect on the flow within the domain

    Genome-wide association analysis of genetic generalized epilepsies implicates susceptibility loci at 1q43, 2p16.1, 2q22.3 and 17q21.32

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    Genetic generalized epilepsies (GGEs) have a lifetime prevalence of 0.3% and account for 20-30% of all epilepsies. Despite their high heritability of 80%, the genetic factors predisposing to GGEs remain elusive. To identify susceptibility variants shared across common GGE syndromes, we carried out a two-stage genome-wide association study (GWAS) including 3020 patients with GGEs and 3954 controls of European ancestry. To dissect out syndrome-related variants, we also explored two distinct GGE subgroups comprising 1434 patients with genetic absence epilepsies (GAEs) and 1134 patients with juvenile myoclonic epilepsy (JME). Joint Stage-1 and 2 analyses revealed genome-wide significant associations for GGEs at 2p16.1 (rs13026414, Pmeta = 2.5 × 10−9, OR[T] = 0.81) and 17q21.32 (rs72823592, Pmeta = 9.3 × 10−9, OR[A] = 0.77). The search for syndrome-related susceptibility alleles identified significant associations for GAEs at 2q22.3 (rs10496964, Pmeta = 9.1 × 10−9, OR[T] = 0.68) and at 1q43 for JME (rs12059546, Pmeta = 4.1 × 10−8, OR[G] = 1.42). Suggestive evidence for an association with GGEs was found in the region 2q24.3 (rs11890028, Pmeta = 4.0 × 10−6) nearby the SCN1A gene, which is currently the gene with the largest number of known epilepsy-related mutations. The associated regions harbor high-ranking candidate genes: CHRM3 at 1q43, VRK2 at 2p16.1, ZEB2 at 2q22.3, SCN1A at 2q24.3 and PNPO at 17q21.32. Further replication efforts are necessary to elucidate whether these positional candidate genes contribute to the heritability of the common GGE syndrome

    Identification of Y-Box Binding Protein 1 As a Core Regulator of MEK/ERK Pathway-Dependent Gene Signatures in Colorectal Cancer Cells

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    Transcriptional signatures are an indispensible source of correlative information on disease-related molecular alterations on a genome-wide level. Numerous candidate genes involved in disease and in factors of predictive, as well as of prognostic, value have been deduced from such molecular portraits, e.g. in cancer. However, mechanistic insights into the regulatory principles governing global transcriptional changes are lagging behind extensive compilations of deregulated genes. To identify regulators of transcriptome alterations, we used an integrated approach combining transcriptional profiling of colorectal cancer cell lines treated with inhibitors targeting the receptor tyrosine kinase (RTK)/RAS/mitogen-activated protein kinase pathway, computational prediction of regulatory elements in promoters of co-regulated genes, chromatin-based and functional cellular assays. We identified commonly co-regulated, proliferation-associated target genes that respond to the MAPK pathway. We recognized E2F and NFY transcription factor binding sites as prevalent motifs in those pathway-responsive genes and confirmed the predicted regulatory role of Y-box binding protein 1 (YBX1) by reporter gene, gel shift, and chromatin immunoprecipitation assays. We also validated the MAPK-dependent gene signature in colorectal cancers and provided evidence for the association of YBX1 with poor prognosis in colorectal cancer patients. This suggests that MEK/ERK-dependent, YBX1-regulated target genes are involved in executing malignant properties

    16p11.2 600 kb Duplications confer risk for typical and atypical Rolandic epilepsy

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    Rolandic epilepsy (RE) is the most common idiopathic focal childhood epilepsy. Its molecular basis is largely unknown and a complex genetic etiology is assumed in the majority of affected individuals. The present study tested whether six large recurrent copy number variants at 1q21, 15q11.2, 15q13.3, 16p11.2, 16p13.11 and 22q11.2 previously associated with neurodevelopmental disorders also increase risk of RE. Our association analyses revealed a significant excess of the 600 kb genomic duplication at the 16p11.2 locus (chr16: 29.5-30.1 Mb) in 393 unrelated patients with typical (n = 339) and atypical (ARE; n = 54) RE compared with the prevalence in 65 046 European population controls (5/393 cases versus 32/65 046 controls; Fisher's exact test P = 2.83 × 10−6, odds ratio = 26.2, 95% confidence interval: 7.9-68.2). In contrast, the 16p11.2 duplication was not detected in 1738 European epilepsy patients with either temporal lobe epilepsy (n = 330) and genetic generalized epilepsies (n = 1408), suggesting a selective enrichment of the 16p11.2 duplication in idiopathic focal childhood epilepsies (Fisher's exact test P = 2.1 × 10−4). In a subsequent screen among children carrying the 16p11.2 600 kb rearrangement we identified three patients with RE-spectrum epilepsies in 117 duplication carriers (2.6%) but none in 202 carriers of the reciprocal deletion. Our results suggest that the 16p11.2 duplication represents a significant genetic risk factor for typical and atypical R
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