Preliminary Calculation of αs\alpha_s from Green Functions with Dynamical Quarks

We present preliminary results on the computation of the QCD running coupling constant in the $\widetilde{MOM}$ scheme and Landau gauge with two flavours of dynamical Wilson quarks. Gluon momenta range up to about 7 GeV ($\beta =$ 5.6, 5.8 and 6.0) with a constant dynamical-quark mass. This range already allows to exhibit some evidence for a sizable $1/\mu^2$ correction to the asymptotic behaviour, as in the quenched approximation, although a fit without power corrections is still possible with a reasonable $\chi^2$. Following the conclusions of our quenched study, we take into account $1/\mu^2$ correction to the asymptotic behaviour. We find $\Lambda_{\rm \bar{MS}}^{N_f=2} = 264(27) {\rm MeV} \times [{a^{-1}(5.6,0.1560)}/{2.19 {\rm GeV}}]$, which leads to $\alpha_s(M_Z) = 0.113(3)(4)$. The latter result has to be taken as a preliminary indication rather than a real prediction in view of the systematic errors still to be controlled. Still, being two sigmas below the experimental result makes it very encouraging.Comment: 14 pages, 3 figs., 2 tabs., revte

Kahler Moduli Inflation Revisited

We perform a detailed numerical analysis of inflationary solutions in Kahler moduli of type IIB flux compactifications. We show that there are inflationary solutions even when all the fields play an important role in the overall shape of the scalar potential. Moreover, there exists a direction of attraction for the inflationary trajectories that correspond to the constant volume direction. This basin of attraction enables the system to have an island of stability in the set of initial conditions. We provide explicit examples of these trajectories, compute the corresponding tilt of the density perturbations power spectrum and show that they provide a robust prediction of n_s approximately 0.96 for 60 e-folds of inflation.Comment: 27 pages, 9 figure

Do ResearchGate Scores create ghost academic reputations?

[EN] The academic social network site ResearchGate (RG) has its own indicator, RG Score, for its members. The high profile nature of the site means that the RG Score may be used for recruitment, promotion and other tasks for which researchers are evaluated. In response, this study investigates whether it is reasonable to employ the RG Score as evidence of scholarly reputation. For this, three different author samples were investigated. An outlier sample includes 104 authors with high values. A Nobel sample comprises 73 Nobel winners from Medicine and Physiology, Chemistry, Physics and Economics (from 1975 to 2015). A longitudinal sample includes weekly data on 4 authors with different RG Scores. The results suggest that high RG Scores are built primarily from activity related to asking and answering questions in the site. In particular, it seems impossible to get a high RG Score solely through publications. Within RG it is possible to distinguish between (passive) academics that interact little in the site and active platform users, who can get high RG Scores through engaging with others inside the site (questions, answers, social networks with influential researchers). Thus, RG Scores should not be mistaken for academic reputation indicators.Alberto Martin-Martin enjoys a four-year doctoral fellowship (FPU2013/05863) granted by the Ministerio de Educacion, Cultura, y Deporte (Spain). Enrique Orduna-Malea holds a postdoctoral fellowship (PAID-10-14), from the Polytechnic University of Valencia (Spain).Orduña Malea, E.; Martín-Martín, A.; Thelwall, M.; Delgado-López-Cózar, E. (2017). Do ResearchGate Scores create ghost academic reputations?. Scientometrics. 112(1):443-460. https://doi.org/10.1007/s11192-017-2396-9S4434601121Bosman, J. & Kramer, B. (2016). Innovations in scholarly communication—data of the global 2015–2016 survey. Available at: http://zenodo.org/record/49583 #. Accessed December 11, 2016.González-Díaz, C., Iglesias-García, M., & Codina, L. (2015). Presencia de las universidades españolas en las redes sociales digitales científicas: Caso de los estudios de comunicación. El profesional de la información, 24(5), 1699–2407.Goodwin, S., Jeng, W., & He, D. (2014). Changing communication on ResearchGate through interface updates. Proceedings of the American Society for Information Science and Technology, 51(1), 1–4.Hicks, D., Wouters, P., Waltman, L., de Rijcke, S., & Rafols, I. (2015). The Leiden Manifesto for research metrics. Nature, 520(7548), 429–431.Hoffmann, C. P., Lutz, C., & Meckel, M. (2015). A relational altmetric? Network centrality on ResearchGate as an indicator of scientific impact. Journal of the Association for Information Science and Technology, 67(4), 765–775.Jiménez-Contreras, E., de Moya Anegón, F., & Delgado López-Cózar, E. (2003). The evolution of research activity in Spain: The impact of the National Commission for the Evaluation of Research Activity (CNEAI). Research Policy, 32(1), 123–142.Jordan, K. (2014a). Academics’ awareness, perceptions and uses of social networking sites: Analysis of a social networking sites survey dataset (December 3, 2014). Available at: http://dx.doi.org/10.2139/ssrn.2507318 . Accessed December 11, 2016.Jordan, K. (2014b). Academics and their online networks: Exploring the role of academic social networking sites. First Monday, 19(11). Available at: http://dx.doi.org/10.5210/fm.v19i11.4937 . Accessed December 11, 2016.Jordan, K. (2015). Exploring the ResearchGate score as an academic metric: reflections and implications for practice. Quantifying and Analysing Scholarly Communication on the Web (ASCW’15), 30 June 2015, Oxford. Available at: http://ascw.know-center.tugraz.at/wp-content/uploads/2015/06/ASCW15_jordan_response_kraker-lex.pdf . Accessed December 11, 2016.Kadriu, A. (2013). Discovering value in academic social networks: A case study in ResearchGate. Proceedings of the ITI 2013—35th Int. Conf. on Information Technology Interfaces Information Technology Interfaces, pp. 57–62.Kraker, P. & Lex, E. (2015). A critical look at the ResearchGate score as a measure of scientific reputation. Proceedings of the Quantifying and Analysing Scholarly Communication on the Web workshop (ASCW’15), Web Science conference 2015. Available at: http://ascw.know-center.tugraz.at/wp-content/uploads/2016/02/ASCW15_kraker-lex-a-critical-look-at-the-researchgate-score_v1-1.pdf . Accessed December 11, 2016.Li, L., He, D., Jeng, W., Goodwin, S. & Zhang, C. (2015). Answer quality characteristics and prediction on an academic Q&A Site: A case study on ResearchGate. Proceedings of the 24th International Conference on World Wide Web Companion, pp. 1453–1458.Martín-Martín, A., Orduna-Malea, E., Ayllón, J. M. & Delgado López-Cózar, E. (2016). The counting house: measuring those who count. Presence of Bibliometrics, Scientometrics, Informetrics, Webometrics and Altmetrics in the Google Scholar Citations, ResearcherID, ResearchGate, Mendeley & Twitter. Available at: https://arxiv.org/abs/1602.02412 . Accessed December 11, 2016.Martín-Martín, A., Orduna-Malea, E. & Delgado López-Cózar, E. (2016). The role of ego in academic profile services: Comparing Google Scholar, ResearchGate, Mendeley, and ResearcherID. Researchgate, Mendeley, and Researcherid. The LSE Impact of Social Sciences blog. Available at: http://blogs.lse.ac.uk/impactofsocialsciences/2016/03/04/academic-profile-services-many-mirrors-and-faces-for-a-single-ego . Accessed December 11, 2016.Matthews, D. (2016). Do academic social networks share academics’ interests?. Times Higher Education. Available at: https://www.timeshighereducation.com/features/do-academic-social-networks-share-academics-interests . Accessed December 11, 2016.Memon, A. R. (2016). ResearchGate is no longer reliable: leniency towards ghost journals may decrease its impact on the scientific community. Journal of the Pakistan Medical Association, 66(12), 1643–1647.Mikki, S., Zygmuntowska, M., Gjesdal, Ø. L. & Al Ruwehy, H. A. (2015). Digital presence of norwegian scholars on academic network sites-where and who are they?. Plos One 10(11). Available at: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0142709 . Accessed December 11, 2016.Nicholas, D., Clark, D., & Herman, E. (2016). ResearchGate: Reputation uncovered. Learned Publishing, 29(3), 173–182.Orduna-Malea, E., Martín-Martín, A., & Delgado López-Cózar, E. (2016). The next bibliometrics: ALMetrics (Author Level Metrics) and the multiple faces of author impact. El profesional de la información, 25(3), 485–496.Ortega, Jose L. (2015). Relationship between altmetric and bibliometric indicators across academic social sites: The case of CSIC’s members. Journal of informetrics, 9(1), 39–49.Ortega, Jose L. (2016). Social network sites for scientists. Cambridge: Chandos.Ovadia, S. (2014). ResearchGate and Academia. edu: Academic social networks. Behavioral & Social Sciences Librarian, 33(3), 165–169.Thelwall, M., & Kousha, K. (2015). ResearchGate: Disseminating, communicating, and measuring Scholarship? Journal of the Association for Information Science and Technology, 66(5), 876–889.Thelwall, M. & Kousha, K. (2017). ResearchGate articles: Age, discipline, audience size and impact. Journal of the Association for Information Science and Technology, 68(2), 468–479.Van Noorden, R. (2014). Online collaboration: Scientists and the social network. Nature, 512(7513), 126–129.Wilsdon, J., Allen, L., Belfiore, E., Campbell, P., Curry, S., Hill, S. et al. (2015). The Metric Tide: Independent Review of the Role of Metrics in Research Assessment and Management. HEFCE. Available at: http://doi.org/10.13140/RG.2.1.4929.1363 . Accessed December 11, 2016

A multi-stage genome-wide association study of bladder cancer identifies multiple susceptibility loci.

We conducted a multi-stage, genome-wide association study of bladder cancer with a primary scan of 591,637 SNPs in 3,532 affected individuals (cases) and 5,120 controls of European descent from five studies followed by a replication strategy, which included 8,382 cases and 48,275 controls from 16 studies. In a combined analysis, we identified three new regions associated with bladder cancer on chromosomes 22q13.1, 19q12 and 2q37.1: rs1014971, (P = 8 × 10⁻¹²) maps to a non-genic region of chromosome 22q13.1, rs8102137 (P = 2 × 10⁻¹¹) on 19q12 maps to CCNE1 and rs11892031 (P = 1 × 10⁻⁷) maps to the UGT1A cluster on 2q37.1. We confirmed four previously identified genome-wide associations on chromosomes 3q28, 4p16.3, 8q24.21 and 8q24.3, validated previous candidate associations for the GSTM1 deletion (P = 4 × 10⁻¹¹) and a tag SNP for NAT2 acetylation status (P = 4 × 10⁻¹¹), and found interactions with smoking in both regions. Our findings on common variants associated with bladder cancer risk should provide new insights into the mechanisms of carcinogenesis

Functional Characterization of the Plasmodium falciparum Chloroquine-Resistance Transporter (PfCRT) in Transformed Dictyostelium discoideum Vesicles

Chloroquine (CQ)-resistant Plasmodium falciparum malaria has been a global health catastrophe, yet much about the CQ resistance (CQR) mechanism remains unclear. Hallmarks of the CQR phenotype include reduced accumulation of protonated CQ as a weak base in the digestive vacuole of the erythrocyte-stage parasite, and chemosensitization of CQ-resistant (but not CQ-sensitive) P. falciparum by agents such as verapamil. Mutations in the P. falciparum CQR transporter (PfCRT) confer CQR; particularly important among these mutations is the charge-loss substitution K→T at position 76. Dictyostelium discoideum transformed with mutant PfCRT expresses key features of CQR including reduced drug accumulation and verapamil chemosensitization.We describe the isolation and characterization of PfCRT-transformed, hematin-free vesicles from D. discoideum cells. These vesicles permit assessments of drug accumulation, pH, and membrane potential that are difficult or impossible with hematin-containing digestive vacuoles from P. falciparum-infected erythrocytes. Mutant PfCRT-transformed D. discoideum vesicles show features of the CQR phenotype, and manipulations of vesicle membrane potential by agents including ionophores produce large changes of CQ accumulation that are dissociated from vesicular pH. PfCRT in its native or mutant form blunts the ability of valinomycin to reduce CQ accumulation in transformed vesicles and decreases the ability of K(+) to reverse membrane potential hyperpolarization caused by valinomycin treatment.Isolated vesicles from mutant-PfCRT-transformed D. discoideum exhibit features of the CQR phenotype, consistent with evidence that the drug resistance mechanism operates at the P. falciparum digestive vacuole membrane in malaria. Membrane potential apart from pH has a major effect on the PfCRT-mediated CQR phenotype of D. discoideum vesicles. These results support a model of PfCRT as an electrochemical potential-driven transporter in the drug/metabolite superfamily that (appropriately mutated) acts as a saturable simple carrier for the facilitated diffusion of protonated CQ

Plasma and Muscle Myostatin in Relation to Type 2 Diabetes

OBJECTIVE: Myostatin is a secreted growth factor expressed in skeletal muscle tissue, which negatively regulates skeletal muscle mass. Recent animal studies suggest a role for myostatin in insulin resistance. We evaluated the possible metabolic role of myostatin in patients with type 2 diabetes and healthy controls. DESIGN: 76 patients with type 2 diabetes and 92 control subjects were included in the study. They were matched for age, gender and BMI. Plasma samples and biopsies from the vastus lateralis muscle were obtained to assess plasma myostatin and expression of myostatin in skeletal muscle. RESULTS: Patients with type 2 diabetes had higher fasting glucose (8.9 versus 5.1 mmol/L, P<0.001), plasma insulin (68.2 versus 47.2 pmol/L, P<0.002) and HOMA2-IR (1.6 versus 0.9, P<0.0001) when compared to controls. Patients with type 2 diabetes had 1.4 (P<0.01) higher levels of muscle myostatin mRNA content than the control subjects. Plasma myostatin concentrations did not differ between patients with type 2 diabetes and controls. In healthy controls, muscle myostatin mRNA correlated with HOMA2-IR (r = 0.30, P<0.01), plasma IL-6 (r = 0.34, P<0.05) and VO2 max (r = -0.26, P<0.05), however, no correlations were observed in patients with type 2 diabetes. CONCLUSIONS: This study supports the idea that myostatin may have a negative effect on metabolism. However, the metabolic effect of myostatin appears to be overruled by other factors in patients with type 2 diabetes

HERV-W/MRSV envelope transcripts detection in blood of multiple sclerosis patients after Natalizumab treatment

FAPES

Relationships of Risk Factors for Pre-Eclampsia with Patterns of Occurrence of Isolated Gestational Proteinuria during Normal Term Pregnancy

&lt;p&gt;&lt;b&gt;Background:&lt;/b&gt; Isolated gestational proteinuria may be part of the pre-eclampsia disease spectrum. Confirmation of its association with established pre-eclampsia risk factors and higher blood pressure in uncomplicated pregnancies would support this concept.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Methods:&lt;/b&gt; Data from 11,651 women from the Avon Longitudinal Study of Parents and Children who had a term live birth but did not have pre-existing hypertension or diabetes or develop gestational diabetes or preeclampsia were used. Proteinuria was assessed repeatedly (median 12 measurements per woman) by dipstick and latent class analysis was used to identify subgroups of the population with different patterns of proteinuria in pregnancy.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Results:&lt;/b&gt; Higher maternal pre-pregnancy body mass index (BMI), younger age, nulliparity and twin pregnancy were independently associated with increased odds of any proteinuria in pregnancy. Women who experienced proteinuria showed five patterns: proteinuria in early pregnancy only (&lt;= 20 weeks gestation), and onset at 21-28 weeks, 29-32 weeks, 33-36 weeks and &gt;= 37 weeks gestation. There were higher odds of proteinuria onset after 33 weeks in obese women and after 37 weeks in nulliparous women compared with normal weight and multiparous women respectively. Smoking in pregnancy was weakly negatively associated with odds of proteinuria onset after 37 weeks. Twin pregnancies had higher odds of proteinuria onset from 29 weeks. In women with proteinuria onset after 33 weeks blood pressure was higher in early pregnancy and at the end of pregnancy.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Conclusions:&lt;/b&gt; Established pre-eclampsia risk factors were related to proteinuria occurrence in late gestation in healthy term pregnancies, supporting the hypothesis that isolated gestational proteinuria may represent an early manifestation of preeclampsia.&lt;/p&gt

Intrinsically determined cell death of developing cortical interneurons

Cortical inhibitory circuits are formed by GABAergic interneurons, a cell population that originates far from the cerebral cortex in the embryonic ventral forebrain. Given their distant developmental origins, it is intriguing how the number of cortical interneurons is ultimately determined. One possibility, suggested by the neurotrophic hypothesis1-5, is that cortical interneurons are overproduced, and then following their migration into cortex, excess interneurons are eliminated through a competition for extrinsically derived trophic signals. Here we have characterized the developmental cell death of mouse cortical interneurons in vivo, in vitro, and following transplantation. We found that 40% of developing cortical interneurons were eliminated through Bax- (Bcl-2 associated X-) dependent apoptosis during postnatal life. When cultured in vitro or transplanted into the cortex, interneuron precursors died at a cellular age similar to that at which endogenous interneurons died during normal development. Remarkably, over transplant sizes that varied 200-fold, a constant fraction of the transplanted population underwent cell death. The death of transplanted neurons was not affected by the cell-autonomous disruption of TrkB (tropomyosin kinase receptor B), the main neurotrophin receptor expressed by central nervous system (CNS) neurons6-8. Transplantation expanded the cortical interneuron population by up to 35%, but the frequency of inhibitory synaptic events did not scale with the number of transplanted interneurons. Together, our findings indicate that interneuron cell death is intrinsically determined, either cell-autonomously, or through a population-autonomous competition for survival signals derived from other interneurons

Plasma Elaidic Acid Level as Biomarker of Industrial Trans Fatty Acids and Risk of Weight Change: Report from the EPIC Study

Background Few epidemiological studies have examined the association between dietary trans fatty acids and weight gain, and the evidence remains inconsistent. The main objective of the study was to investigate the prospective association between biomarker of industrial trans fatty acids and change in weight within the large study European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Methods Baseline plasma fatty acid concentrations were determined in a representative EPIC sample from the 23 participating EPIC centers. A total of 1,945 individuals were followed for a median of 4.9 years to monitor weight change. The association between elaidic acid level and percent change of weight was investigated using a multinomial logistic regression model, adjusted by length of follow-up, age, energy, alcohol, smoking status, physical activity, and region. Results In women, doubling elaidic acid was associated with a decreased risk of weight loss (odds ratio (OR) = 0.69, 95% confidence interval (CI) = 0.55-0.88, p = 0.002) and a trend was observed with an increased risk of weight gain during the 5-year follow-up (OR = 1.23, 95% CI = 0.97-1.56, p = 0.082) (p-trend<.0001). In men, a trend was observed for doubling elaidic acid level and risk of weight loss (OR = 0.82, 95% CI = 0.66-1.01, p = 0.062) while no significant association was found with risk of weight gain during the 5-year follow-up (OR = 1.08, 95% CI = 0.88-1.33, p = 0.454). No association was found for saturated and cis-monounsaturated fatty acids. Conclusions These data suggest that a high intake of industrial trans fatty acids may decrease the risk of weight loss, particularly in women. Prevention of obesity should consider limiting the consumption of highly processed foods, the main source of industrially-produced trans fatty acids