Adoption of Technology and Regional Convergence in Europe

This paper examines the pattern of convergence in labour productivity across regions due to their ability to adopt technology. Whether regions exhibit a pattern of convergence depends on the degree to which infrastructure conditions are appropriate for the adoption of technological improvements. The ability of a region to adopt or create technology is reflected in the percentage of its labour force employed in technologically dynamic sectors or, more generally, in the resources devoted to science and technology. A high percentage of labour employed in technologically advanced sectors leads a region to a pattern of convergence. This hypothesis is tested using data for the NUTS-2 regions of the EU-27 during the time period 1995-2006. The results suggest that adoption of technology has a significant and positive effect on regional convergence in Europe. The analysis is also shown to have important implications for the direction of regional policy in Europe. To be more specific, regional policies, in order to enhance regional growth and convergence, should encourage employment in advanced technological sectors

Internal and External Sources of Regional Growth

AbstractThis paper examines the pattern of regional growth due to their ability to adopt technology. Whether regions exhibit a ‘high’ or ‘low’ path of growth depends on the adoption of technological improvements. Technology adoption can be either ‘internal’ or ‘external’ to the region. This approach is tested empirically using data for 247 European regions. The results suggest that adoption of technology has a significant and positive effect in regional growth in Europe

ADOPTION OF TECHNOLOGY AND REGIONAL CONVERGENCE IN EUROPE

Abstract: This paper examines the pattern of convergence in labour productivity across regions due to their ability to adopt technology. Whether regions exhibit a pattern of convergence depends on the degree to which infrastructure conditions are appropriate for the adoption of technological improvements. The ability of a region to adopt or create technology is reflected in the percentage of its labour force employed in technologically dynamic sectors or, more generally, in the resources devoted to science and technology. A high percentage of labour employed in technologically advanced sectors leads a region to a pattern of convergence. This hypothesis is tested using data for the NUTS-2 regions of the EU-27 during the time period 1995-2006. The results suggest that adoption of technology has a significant and positive effect on regional convergence in Europe. The analysis is also shown to have important implications for the direction of regional policy in Europe. To be more specific, regional policies, in order to enhance regional growth and convergence, should encourage employment in advanced technological sectors

Otkrivanje delecije kromosoma 1 pomoću tehnike FISH na otiscima ependimoma ukazuje na regiju izvan kromosoma 22 važnu za recidiv tumora

Ependymomas are glial tumors. They constitute approximately 5%-10% of intracranial tumors. Ependymomas are tumors which can recur. Predictive factors of outcome in ependymomas are not well established. Karyotypic studies are relatively scarce and loss of chromosome 22 has been described to correlate with recurrence. We are unaware of any reports involving chromosome 1 aberrations in the malignant progression of ependymomas. Cytogenetic analysis of 4 ependymomas was performed using double-target fluorescent in situ hybridization (FISH) and focusing on chromosomes 1 and 22. One patient had recurrent tumor. FISH was performed on 500 nuclei/tumors. All four cases showed a loss of chromosome 22q, while only one showed an additional loss of chromosome 1p, and it was the one with tumor relapse. We support the presence of tumor suppressor gene on 1p associated with relapse in ependymomas and suggest that the chromosome 1p status by FISH may identify a high risk group of patients harboring this tumor. Additional studies in this direction are needed, as our results refer to a minimal number of individuals analyzed.Ependimomi su glialni tumori. Oni čine otprilike 5%-10% intrakranijskih tumora. Ependimomi su tumori koji se mogu ponavljati. Čimbenici koji bi ukazivali na ishod ependimoma nisu dobro utvrđeni. Kariotipska ispitivanja su relativno rijetka, a opisano je kako gubitak kromosoma 22 korelira s ponovnom pojavom tumora. Nisu nam poznata izvješća o upletenosti aberacija kromosoma 1 u malignoj progresiji ependimoma. U ovoj studiji je citogenetska analiza 4 ependimoma provedena pomoću dvociljne fluorescentne in situ hibridizacije (FISH) i fokusiranja na kromosomima 1 i 22. U jednog se bolesnika radilo o ponovnoj pojavi tumora. FISH je izvedena na 500 jezgara/tumora. Sva četiri slučaja pokazala su gubitak kromosoma 22q, dok je samo jedan, i to onaj s ponovnim razvojem tumora, pokazao dodatni gubitak kromosoma 1p. Priklanjamo se mišljenju kako je prisutnost gena tumorske supresije na 1p udru žena s recidivom kod ependimoma i ukazujemo na to da bi status kromosoma 1p utvrđen pomoću FISH mogao identificirati visoko rizičnu skupinu bolesnika koji nose ovaj tumor. Potrebne su daljnje studije u ovom smjeru, jer se naši rezultati odnose na mali broj analiziranih osoba

Otkrivanje delecije kromosoma 1 pomoću tehnike FISH na otiscima ependimoma ukazuje na regiju izvan kromosoma 22 važnu za recidiv tumora

Ependymomas are glial tumors. They constitute approximately 5%-10% of intracranial tumors. Ependymomas are tumors which can recur. Predictive factors of outcome in ependymomas are not well established. Karyotypic studies are relatively scarce and loss of chromosome 22 has been described to correlate with recurrence. We are unaware of any reports involving chromosome 1 aberrations in the malignant progression of ependymomas. Cytogenetic analysis of 4 ependymomas was performed using double-target fluorescent in situ hybridization (FISH) and focusing on chromosomes 1 and 22. One patient had recurrent tumor. FISH was performed on 500 nuclei/tumors. All four cases showed a loss of chromosome 22q, while only one showed an additional loss of chromosome 1p, and it was the one with tumor relapse. We support the presence of tumor suppressor gene on 1p associated with relapse in ependymomas and suggest that the chromosome 1p status by FISH may identify a high risk group of patients harboring this tumor. Additional studies in this direction are needed, as our results refer to a minimal number of individuals analyzed.Ependimomi su glialni tumori. Oni čine otprilike 5%-10% intrakranijskih tumora. Ependimomi su tumori koji se mogu ponavljati. Čimbenici koji bi ukazivali na ishod ependimoma nisu dobro utvrđeni. Kariotipska ispitivanja su relativno rijetka, a opisano je kako gubitak kromosoma 22 korelira s ponovnom pojavom tumora. Nisu nam poznata izvješća o upletenosti aberacija kromosoma 1 u malignoj progresiji ependimoma. U ovoj studiji je citogenetska analiza 4 ependimoma provedena pomoću dvociljne fluorescentne in situ hibridizacije (FISH) i fokusiranja na kromosomima 1 i 22. U jednog se bolesnika radilo o ponovnoj pojavi tumora. FISH je izvedena na 500 jezgara/tumora. Sva četiri slučaja pokazala su gubitak kromosoma 22q, dok je samo jedan, i to onaj s ponovnim razvojem tumora, pokazao dodatni gubitak kromosoma 1p. Priklanjamo se mišljenju kako je prisutnost gena tumorske supresije na 1p udru žena s recidivom kod ependimoma i ukazujemo na to da bi status kromosoma 1p utvrđen pomoću FISH mogao identificirati visoko rizičnu skupinu bolesnika koji nose ovaj tumor. Potrebne su daljnje studije u ovom smjeru, jer se naši rezultati odnose na mali broj analiziranih osoba

Deciphering osteoarthritis genetics across 826,690 individuals from 9 populations

Osteoarthritis affects over 300 million people worldwide. Here, we conduct a genome-wide association study meta-analysis across 826,690 individuals (177,517 with osteoarthritis) and identify 100 independently associated risk variants across 11 osteoarthritis phenotypes, 52 of which have not been associated with the disease before. We report thumb and spine osteoarthritis risk variants and identify differences in genetic effects between weight-bearing and non-weight-bearing joints. We identify sex-specific and early age-at-onset osteoarthritis risk loci. We integrate functional genomics data from primary patient tissues (including articular cartilage, subchondral bone, and osteophytic cartilage) and identify high-confidence effector genes. We provide evidence for genetic correlation with phenotypes related to pain, the main disease symptom, and identify likely causal genes linked to neuronal processes. Our results provide insights into key molecular players in disease processes and highlight attractive drug targets to accelerate translation

The human DEK oncogene regulates DNA damage response signaling and repair

The human DEK gene is frequently overexpressed and sometimes amplified in human cancer. Consistent with oncogenic functions, Dek knockout mice are partially resistant to chemically induced papilloma formation. Additionally, DEK knockdown in vitro sensitizes cancer cells to DNA damaging agents and induces cell death via p53-dependent and -independent mechanisms. Here we report that DEK is important for DNA double-strand break repair. DEK depletion in human cancer cell lines and xenografts was sufficient to induce a DNA damage response as assessed by detection of γH2AX and FANCD2. Phosphorylation of H2AX was accompanied by contrasting activation and suppression, respectively, of the ATM and DNA-PK pathways. Similar DNA damage responses were observed in primary Dek knockout mouse embryonic fibroblasts (MEFs), along with increased levels of DNA damage and exaggerated induction of senescence in response to genotoxic stress. Importantly, Dek knockout MEFs exhibited distinct defects in non-homologous end joining (NHEJ) when compared to their wild-type counterparts. Taken together, the data demonstrate new molecular links between DEK and DNA damage response signaling pathways, and suggest that DEK contributes to DNA repair