Patterns of Academic Scientific Collaboration at a Distance: Evidence from Southern European Countries

The main objective of this chapter is to examine the trends of academic scientific collaboration (SC) at a distance among public universities located in peripheral countries: Spain, Italy, Greece, and Portugal. The data to capture scientific collaboration consists of a set of co-authored articles published between 2001 and 2010 by universities located in the mentioned Southern countries, indexed by the Science Citation Index expanded (SCI Expanded) of the Information Sciences Institute (ISI) Web of Science (WoS) database. We link this data to institution-level information provided by the EUMIDA dataset. In addition, we retrieved regional data on economic variables from Eurostat. The methodology relies on a descriptive analysis of the evolution of co-publications at different notions of proximity. Our results show a trend toward collaboration over longer distances, although we find heterogeneity by countries and disciplines. Building on our results, we provide some policy implications

The production of university technological knowledge in European regions: evidence from patent data

This paper explores the European regional distribution of the production of new technological knowledge generated by universities, as measured by patent counts. The empirical basis for this study is a unique panel data set of 4,580 European university patents from 1998 to 2004. Our main findings were a strong regional and sectoral concentration of patents, and no average relation between university technological specialization and industrial specialization. Furthermore, our results suggest that variations in regional R&D funding do affect patenting activities in regions, with elasticities showing constant returns to scale, but no evidence was found regarding the industrial potential of the region encouraging the production of new university technological knowledge

HCT116 cells deficient in p21Waf1 are hypersensitive to tyrosine kinase inhibitors and adriamycin through a mechanism unrelated to p21 and dependent on p53

El pdf del artículo es la versión de autor.-- et al.p21Waf1 (p21) was described as a cyclin-dependent kinase inhibitor, but other p21 activities have subsequently been described, including its ability to inhibit apoptosis in some models. Comparative work on the human colon cancer isogenic cell lines HCT116 and HCT116p21-/- led to the proposal that p21 protects colon cancer cells against apoptosis by genotoxic drugs. We asked whether p21 also protected from cell death induced by non-genotoxic drugs, such as tyrosine kinase inhibitors. We found that p21-deficient cells were dramatically more sensitive towards imatinib and gefitinib than parental cells. Interestingly, HCT116p21-/- also showed higher basal activity of protein kinases as c-Abl, c-Src, and Akt. We generated HCT116p21-/- sublines with inducible p21 expression and found that p21 did not rescue the hypersensitivity to imatinib. Moreover, down-regulation of p21 by enforced c-Myc expression or by p21 siRNA did not sensitize parental HCT116 cells. We found that, in HCT116p21-/- cells, p53 showed higher stability, higher transcriptional activity and phosphorylation in serines associated with p53 activity. Furthermore, silencing of p53 with siRNA and inactivation of p53 with a dominant negative mutant rescued the hypersensitive response to kinases inhibitors, 5-fluorouracil and adriamycin in HCT116p21-/- cells. Consistently, HCT116p53-/- cells are more resistant to imatinib than parental cells, suggesting that imatinib activity is partly dependent on p53 in colon cancer cells. We conclude that high p53 activity, rather than p21 deficiency, is the mechanism responsible for hypersensitivity to drugs of HCT116p21-/- cells. Therefore the role of p21 on apoptosis of HCT116 colon cancer cells should be re-evaluated. © 2008 Elsevier B.V. All rights reserved.N.F. is funded by a predoctoral fellowship from the Spanish Ministry of Education and Science (MEC) and from the University of Cantabria. Work at the laboratory of J.L. is funded by MEC grants SAF2005-00461 and Spanish Ministry of Health and Consume (MSC) grant ISCIII-RETIC-RD06/0020. M.D.D. is funded by MSC grant FIS04-1083, and J.M.P. is funded by grants from Fundación de Investigación Médica Mutua Madrileña and MEC grant SAF2006-00371.Peer Reviewe

Unleashing creativity and cooperation: a qualitative case study on designing digital breakouts for social education degrees

This article examines the implementation of a cooperative training workshop for Spanish undergraduate social educators. The workshop aimed to explore the integration of escape rooms and breakouts in teaching, specifically addressing cyberbullying as a curricular topic. A total of 40 students participated in designing and qualitatively evaluating the training workshop. The findings highlight the workshop’s effectiveness in enhancing social education students’ training, preparing them for future professional careers, and enhancing their learning, teamwork, and proficiency in utilising ICT programs and resources. The study underscores the significance of incorporating these innovative approaches to improve student motivation, interest, and overall skill development

Long-term priming of hypothalamic microglia is associated with energy balance disturbances under diet-induced obesity

Exposure of microglia to an inflammatory environment may lead to their priming and exacerbated response to future inflammatory stimuli. Here we aimed to explore hypothalamic microglia priming and its consequences on energy balance regulation. A model of intracerebroventricular administration of neuraminidase (NA, which is present in various pathogens such as influenza virus) was used to induce acute neuroinflammation. Evidences of primed microglia were observed 3 months after NA injection, namely (1) a heightened response of microglia located in the hypothalamic arcuate nucleus after an in vivo inflammatory challenge (high fat diet [HFD] feeding for 10 days), and (2) an enhanced response of microglia isolated from NA-treated mice and challenged in vitro to LPS. On the other hand, the consequences of a previous NA-induced neuroinflammation were further evaluated in an alternative inflammatory and hypercaloric scenario, such as the obesity generated by continued HDF feeding. Compared with sham-injected mice, NA-treated mice showed increased food intake and, surprisingly, reduced body weight. Besides, NA-treated mice had enhanced microgliosis (evidenced by increased number and reactive morphology of microglia) and a reduced population of POMC neurons in the basal hypothalamus. Thus, a single acute neuroinflammatory event may elicit a sustained state of priming in microglial cells, and in particular those located in the hypothalamus, with consequences in hypothalamic cytoarchitecture and its regulatory function upon nutritional challenges.Ministerio de Economía, Industria yCompetitividad, Gobierno de España, Grant/Award Number: SAF2017-83645; Ministeriode Educación y Formación Profesional; Funding for open access charge: Universidadde Málaga/CBU

Anxiety and mild microglial activation in the amygdala two weeks after NA-induced neuroinflammation

A single injection of neuraminidase (NA) within the cerebral ventricles (ICV) triggers an acute neuroinflammation. Neurological complications or behavioral alterations have been associated to neuroinflammation. While some of these symptoms decline with time along with inflammation, the possibility of long-term sequelae should be considered. Thus, we aimed to explore if NA-induced neuroinflammation provokes behavioral or neurological disturbances at medium (2 weeks) and long (10 weeks) term. Rats were ICV injected with NA or saline. First, neurological alterations of the sensorimotor reflexes were not found, suggesting that NA does not cause disturbances in major brain functions. While the open field test revealed normal locomotor capacity in the animals injected with NA, however the evaluation of specific behaviors (rearing and rearing with support) pointed out an increased anxiety state 2 weeks after NA administration, but not at long term (10 weeks). A histological study of brain areas related to emotions (amygdala) and stress response (hypothalamic PVN) revealed no significant differences in the number of microglia or astrocytes. Nevertheless, the morphological analysis of microglial cells demonstrated that, in the amygdala of NA injected rats, microglia presented a morphology consistent with a slightly activated state. Such morphological change, which was evident 2 weeks after NA injection, was virtually reverted 10 weeks post-ICV. These results point out that NA injected ICV may cause anxiety in the medium term (while not affecting other functions like sensorimotor functions or the locomotor capacity), a behavioral alteration that is transient and that concurs with a mild inflammation, evidenced by the overexpression of certain genes and, more notably, by the morphological bias of microglial cells located in the amygdala towards an activated profile.Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech

MYC in chronic myeloid leukemia: Induction of aberrant DNA synthesis and association with poor response to imatinib

El pdf es la versión post-print.-- et al.Untreated chronic myeloid leukemia (CML) progresses from chronic phase to blastic crisis (BC). Increased genomic instability, deregulated proliferation, and loss of differentiation appear associated to BC, but the molecular alterations underlying the progression of CML are poorly characterized. MYC oncogene is frequently deregulated in human cancer, often associated with tumor progression. Genomic instability and induction of aberrant DNA replication are described as effects of MYC. In this report, we studied MYC activities in CML cell lines with conditional MYC expression with and without exposure to imatinib, the front-line drug in CML therapy. In cells with conditional MYC expression, MYC did not rescue the proliferation arrest mediated by imatinib but provoked aberrant DNA synthesis and accumulation of cells with 4C content. We studied MYC mRNA expression in 66 CML patients at different phases of the disease, and we found that MYC expression was higher in CML patients at diagnosis than control bone marrows or in patients responding to imatinib. Further, high MYC levels at diagnosis correlated with a poor response to imatinib. MYC expression did not directly correlate with BCR-ABL levels in patients treated with imatinib. Overall our study suggests that, as in other tumor models, MYC-induced aberrant DNA synthesis in CML cells is consistent with MYC overexpression in untreated CML patients and nonresponding patients and supports a role for MYC in CML progression, possibly through promotion of genomic instability. ©2011 AACR.This work was supported by a grant from the Ministerio de Ciencia e Innovacion of Spain (SAF08-01581) and by the RTICC (Red Temática de Investigación Cooperativa en Cancer, RD06/0020/0017) to J. León and a grant from Instituto de Salud Carlos III (FIS08/0829) to M.D. Delgado.Peer Reviewe

Mapping quantitative trait loci controlling fatty acid composition in olive

22 Páginas; 3 Tablas; 2 FigurasFatty acids are the main components of the olive oil and their composition has a critical influence on the oil quality. However, oil quality evaluation has not been frequently included in the selection of new bred cultivars. This can be due to the difficulties in analyzing oil quality in large set of genotypes and also to the long juvenile period of olive seedlings. Therefore, the identification of molecular markers associated to olive oil quality traits could facilitate their selection in breeding programs of this species. In the present work, the identification of the first QTLs for fatty acids on olive oil is reported. They have been located in a linkage map of a ‘Picual’ × ‘Arbequina’ progeny of the olive breeding program of Córdoba. Correlations among fatty acids are in agreement with previous reports of breeding progenies. QTLs found for oleic and linoleic acids explained 41.1 and 69.7% of the total variability, respectively, and were co-localized in the same linkage groups. In the same region, QTLs for monounsaturated, polyunsaturated and oleic/linoleic ratio were also identified. In other linkage groups, three QTLs for linolenic and one for palmitoleic acid were also located explaining 15.0–28.0% of the total variability. These results could be useful to increase the efficiency of breeding programs aimed at selecting new cultivars with high oleic acid content, and, therefore, with enhanced nutritional properties and oxidative stability of the olive oil.This work was partly supported by OLEAGEN Project funded by the Fundación Genoma España, Junta de Andalucía through Instituto de Investigación y Formación Agraria y Pesquera (IFAPA) and Corporación Tecnológica de Andalucía (CTA).Peer reviewe

Myc Inhibits p27-Induced Erythroid Differentiation of Leukemia Cells by Repressing Erythroid Master Genes without Reversing p27-Mediated Cell Cycle Arrest

Inhibition of differentiation has been proposed as an important mechanism for Myc-induced tumorigenesis, but the mechanisms involved are unclear. We have established a genetically defined differentiation model in human leukemia K562 cells by conditional expression of the cyclin-dependent kinase (Cdk) inhibitor p27 (inducible by Zn2+) and Myc (activatable by 4-hydroxy-tamoxifen). Induction of p27 resulted in erythroid differentiation, accompanied by Cdk inhibition and G1 arrest. Interestingly, activation of Myc inhibited p27-mediated erythroid differentiation without affecting p27-mediated proliferation arrest. Microarray-based gene expression indicated that, in the presence of p27, Myc blocked the upregulation of several erythroid-cell-specific genes, including NFE2, JUNB, and GATA1 (transcription factors with a pivotal role in erythropoiesis). Moreover, Myc also blocked the upregulation of Mad1, a transcriptional antagonist of Myc that is able to induce erythroid differentiation. Cotransfection experiments demonstrated that Myc-mediated inhibition of differentiation is partly dependent on the repression of Mad1 and GATA1. In conclusion, this model demonstrates that Myc-mediated inhibition of differentiation depends on the regulation of a specific gene program, whereas it is independent of p27-mediated cell cycle arrest. Our results support the hypothesis that differentiation inhibition is an important Myc tumorigenic mechanism that is independent of cell proliferation. Copyright © 2008, American Society for Microbiology. All Rights Reserved.This study was supported by grants CICYT SAF05-00461 from the Spanish Ministerio de Educación y Ciencia (MEC), ISCIII-RETIC RD06/0020 from the Spanish Ministerio de Sanidad y Consumo, API-17-05 from the Fundación Marques de Valdecilla (to J.L), and FIS04/1083 (to M.D.D). J.C.A., G.B., and N.F. were supported by fellowships from the MEC, and V.T. was supported by a Lady Tata Memorial Trust award.Peer Reviewe