Restoring EU competitiveness

With the advent of the digital revolution in the 1990s, productivity growth in the EU began to slip behind that in the US and other leading trading partners. This trend has undermined the comparative ability of European firms to compete and to provide rewarding jobs and a high standard of living. Low comparative productivity and misallocation of investment, alongside many structural weaknesses, help explain why the global crisis hit Europe so hard, and why EU-wide recovery still presents such a challenge. Since 1990, the inflation-adjusted absolute GDP per capita gap between the EU and US has increased by more than 50%. In absolute terms, the GDP per capita of EU regions has diverged since 1990, not converged. Productivity growth in the EU has trailed the US since the mid-1990s and was hit harder during the crisis than in other regions.Eine chronische Investitionsschwäche in wichtigen Bereichen, ineffiziente und fragmentierte Finanzmärkte sowie institutionelle Hemmnisse sind die Ursache dafür, dass Europa sein Potenzial für ein langfristiges, nachhaltiges Wachstum und für die Verstärkung seiner Wettbewerbsfähigkeit nicht nutzt. Sieben Krisenjahre in Folge haben viel Vertrauen zerstört, einen Rückgang der Gesamtinvestitionen bewirkt und strukturelle Investitionslücken vergrößert. Dieser Bericht untersucht, wie die Wettbewerbsfähigkeit der EU langfristig wiederhergestellt werden kann und welche Aufgaben der öffentliche Sektor dabei übernehmen kann. Im Mittelpunkt des Berichts stehen die Grundvoraussetzungen für einen Erfolg, der langfristiger Investitionen bedarf und für unser Wohlergehen in Zukunft entscheidend ist. Der Bericht enthält Informationen darüber, wie strategische Prioritäten festgelegt werden und warum die Maßnahmen zur Ankurbelung langfristiger, wettbewerbsfördernder Investitionen auf europäischer Ebene verstärkt werden müsse

Tumour-derived CSF2/granulocyte macrophage colony stimulating factor controls myeloid cell accumulation and progression of gliomas

BACKGROUND: Malignant tumours release factors, which attract myeloid cells and induce their polarisation to pro-invasive, immunosuppressive phenotypes. Brain-resident microglia and peripheral macrophages accumulate in the tumour microenvironment of glioblastoma (GBM) and induce immunosuppression fostering tumour progression. Macrophage colony stimulating factors (CSFs) control the recruitment of myeloid cells during peripheral cancer progression, but it is disputable, which CSFs drive their accumulation in gliomas. METHODS: The expression of CSF2 (encoding granulocyte-macrophage colony stimulating factor) was determined in TCGA datasets and five human glioma cell lines. Effects of stable CSF2 knockdown in glioma cells or neutralising CSF2 or receptor CSF2Rα antibodies on glioma invasion were tested in vitro and in vivo. RESULTS: CSF2 knockdown or blockade of its signalling reduced microglia-dependent glioma invasion in microglia-glioma co-cultures. CSF2-deficient human glioma cells encapsulated in cell-impermeable hollow fibres and transplanted to mouse brains, failed to attract microglia, but stimulated astrocyte recruitment. CSF2-depleted gliomas were smaller, attracted less microglia and macrophages, and provided survival benefit in tumour-bearing mice. Apoptotic microglia/macrophages were detected in CSF2-depleted tumours. CONCLUSIONS: CSF2 is overexpressed in a subset of mesenchymal GBMs in association with high immune gene expression. Tumour-derived CSF2 attracts, supports survival and induces pro-tumorigenic polarisation of microglia and macrophages

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Abstract. A 3D culture system was used to investigate the behaviour of mesothelial cells present in the wall of human processus vaginalis peritonei. Small tissue fragments placed on collagen sponges were cultured for 7, 14 and 21 days in medium supplemented with 10% FBS, and analysed for the expression and distribution of cytokeratins (CKAE1-AE3, CK19), p63, Ki-67, vimentin, CD34, and HBME-1. Before culture, flat mesothelial cells displayed immunoreactivity for cytokeratins, vimentin and HBME-1, while p63 and CD34 were negative. Mesenchymal cells within the stroma were vimentin-positive and endothelial cells of small vessels displayed positive staining for CD34. Cytokeratins, p63 and HBME-1 were negative in all stromal cells. In cultured fragments, flat mesothelial cells positive for vimentin, cytokeratins and HBME-1 proliferated, lining the fragment surface and migrating into the sponge. Capillaries showed morphological alterations; however, their immunoreactivity was comparable with the stroma prior to culture. Cells that had migrated into the sponge and displayed characteristics of mesothelial progenitors, predominantly spindleshaped and stellate, showed heterogeneous expression of markers especially in late phases of cultivation. These cells were constantly positive for vimentin, a small fraction was cytokeratin-positive and a few displayed HBME-1 immunoreactivity. CD34 was found in cells forming small cavities into the matrix, resembling newly formed blood vessels. Cells that had migrated into the sponge could be isolated and expanded in coculture with feeder NIH.3T3 fibroblasts. This system is suitable for studying growth and behaviour of mesothelial cells within their natural environment, providing a good method for isolation and expansion of their progenitor cells

Protection of mice against syngeneic C1300 neuroblastoma challenge by immunization with membranes of C1300 neuroblastoma cells.

Male A/J mice 2-3 months old were inoculated sc with membranes from syngeneic C1300 neuroblastoma cells (clone NB6R) in complete Freund's adjuvant. Significant immunoprophylaxis was noted in the sensitized mice upon sc challenge with viable NB6R cells. During the experiment (60 days from viable cell challenge), each control mouse developed a palpable tumor and died within 50 days. Complete protection was obtained with a program of 4 inoculations of NB6R cell membranes. Each mouse given only 1 inoculation of NB6R cell membranes developed a palpable tumor, but afer 60 days only 1 mouse in 7 had died, which indicated a significant degree of protection. With in vitro tests of lymphocyte proliferation, rosette formation, and complement fixation, it was shown that these mice had mounted both cellular and humoral immune response against the tumor cells