Mathematical properties of weighted impact factors based on measures of prestige of the citing journals

The final publication is available at Springer via http://dx.doi.org/10.1007/s11192-015-1741-0An abstract construction for general weighted impact factors is introduced. We show that the classical weighted impact factors are particular cases of our model, but it can also be used for defining new impact measuring tools for other sources of information as repositories of datasets providing the mathematical support for a new family of altmet- rics. Our aim is to show the main mathematical properties of this class of impact measuring tools, that hold as consequences of their mathematical structure and does not depend on the definition of any given index nowadays in use. In order to show the power of our approach in a well-known setting, we apply our construction to analyze the stability of the ordering induced in a list of journals by the 2-year impact factor (IF2). We study the change of this ordering when the criterium to define it is given by the numerical value of a new weighted impact factor, in which IF2 is used for defining the weights. We prove that, if we assume that the weight associated to a citing journal increases with its IF2, then the ordering given in the list by the new weighted impact factor coincides with the order defined by the IF2. We give a quantitative bound for the errors committed. We also show two examples of weighted impact factors defined by weights associated to the prestige of the citing journal for the fields of MATHEMATICS and MEDICINE, GENERAL AND INTERNAL, checking if they satisfy the increasing behavior mentioned above.Ferrer Sapena, A.; Sánchez Pérez, EA.; González, LM.; Peset Mancebo, MF.; Aleixandre Benavent, R. (2015). Mathematical properties of weighted impact factors based on measures of prestige of the citing journals. Scientometrics. 105(3):2089-2108. https://doi.org/10.1007/s11192-015-1741-0S208921081053Ahlgren, P., & Waltman, L. (2014). The correlation between citation-based and expert-based assessments of publication channels: SNIP and SJR vs. Norwegian quality assessments. Journal of Informetrics, 8, 985–996.Aleixandre Benavent, R., Valderrama Zurián, J. C., & González Alcaide, G. (2007). Scientific journals impact factor: Limitations and alternative indicators. El Profesional de la Información, 16(1), 4–11.Altmann, K. G., & Gorman, G. E. (1998). The usefulness of impact factor in serial selection: A rank and mean analysis using ecology journals. Library Acquisitions-Practise and Theory, 22, 147–159.Arnold, D. N., & Fowler, K. K. (2011). Nefarious numbers. Notices of the American Mathematical Society, 58(3), 434–437.Beliakov, G., & James, S. (2012). Using linear programming for weights identification of generalized bonferroni means in R. In: Proceedings of MDAI 2012 modeling decisions for artificial intelligence. Lecture Notes in Computer Science, Vol. 7647, pp. 35–44.Beliakov, G., & James, S. (2011). Citation-based journal ranks: The use of fuzzy measures. Fuzzy Sets and Systems, 167, 101–119.Buela-Casal, G. (2003). Evaluating quality of articles and scientific journals. Proposal of weighted impact factor and a quality index. Psicothema, 15(1), 23–25.Dorta-Gonzalez, P., & Dorta-Gonzalez, M. I. (2013). Comparing journals from different fields of science and social science through a JCR subject categories normalized impact factor. Scientometrics, 95(2), 645–672.Dorta-Gonzalez, P., Dorta-Gonzalez, M. I., Santos-Penate, D. R., & Suarez-Vega, R. (2014). Journal topic citation potential and between-field comparisons: The topic normalized impact factor. Journal of Informetrics, 8(2), 406–418.Egghe, L., & Rousseau, R. (2002). A general frame-work for relative impact indicators. Canadian Journal of Information and Library Science, 27(1), 29–48.Gagolewski, M., & Mesiar, R. (2014). Monotone measures and universal integrals in a uniform framework for the scientific impact assessment problem. Information Sciences, 263, 166–174.Garfield, E. (2006). The history and meaning of the journal impact factor. JAMA, 295(1), 90–93.Habibzadeh, F., & Yadollahie, M. (2008). Journal weighted impact factor: A proposal. Journal of Informetrics, 2(2), 164–172.Klement, E., Mesiar, R., & Pap, E. (2010). A universal integral as common frame for Choquet and Sugeno integral. IEEE Transaction on Fuzzy System, 18, 178–187.Leydesdorff, L., & Opthof, T. (2010). Scopus’s source normalized impact per paper (SNIP) versus a journal impact factor based on fractional counting of citations. Journal of the American Society for Information Science and Technology, 61, 2365–2369.Li, Y. R., Radicchi, F., Castellano, C., & Ruiz-Castillo, J. (2013). Quantitative evaluation of alternative field normalization procedures. Journal of Informetrics, 7(3), 746–755.Moed, H. F. (2010). Measuring contextual citation impact of scientific journals. Journal of Informetrics, 4, 265–277.NISO. (2014). Alternative metrics initiative phase 1. White paper. http://www.niso.org/apps/group-public/download.php/13809/Altmetrics-project-phase1-white-paperOwlia, P., Vasei, M., Goliaei, B., & Nassiri, I. (2011). Normalized impact factor (NIF): An adjusted method for calculating the citation rate of biomedical journals. Journal of Biomedical Informatics, 44(2), 216–220.Pinski, G., & Narin, F. (1976). Citation influence for journal aggregates of scientific publications: Theory, with application to the literature of physics. Information Processing and Management, 12, 297–312.Pinto, A. C., & Andrade, J. B. (1999). Impact factor of scientific journals: What is the meaning of this parameter? Quimica Nova, 22, 448–453.Raghunathan, M. S., & Srinivas, V. (2001). Significance of impact factor with regard to mathematics journals. Current Science, 80(5), 605.Ruiz Castillo, J., & Waltman, L. (2015). Field-normalized citation impact indicators using algorithmically constructed classification systems of science. Journal of Informetrics, 9, 102–117.Saha, S., Saint, S., & Christakis, D. A. (2003). Impact factor: A valid measure of journal quality? Journal of the Medical Library Association, 91, 42–46.Torra, V., & Narukawa, Y. (2008). The h-index and the number of citations: Two fuzzy integrals. IEEE Transaction on Fuzzy System, 16, 795–797.Torres-Salinas, D., & Jimenez-Contreras, E. (2010). Introduction and comparative study of the new scientific journals citation indicators in journal citation reports and scopus. El Profesional de la Información, 19, 201–207.Waltman, L., & van Eck, N. J. (2008). Some comments on the journal weighted impact factor proposed by Habibzadeh and Yadollahie. Journal of Informetrics, 2(4), 369–372.Waltman, L., van Eck, N. J., van Leeuwen, T. N., & Visser, M. S. (2013). Some modifications to the SNIP journal impact indicator. Journal of Informetrics, 7, 272–285.Zitt, M. (2011). Behind citing-side normalization of citations: some properties of the journal impact factor. Scientometrics, 89, 329–344.Zitt, M., & Small, H. (2008). Modifying the journal impact factor by fractional citation weighting: The audience factor. Journal of the American Society for Information Science and Technology, 59, 1856–1860.Zyczkowski, K. (2010). Citation graph, weighted impact factors and performance indices. Scientometrics, 85(1), 301–315

Notch signaling during human T cell development

Notch signaling is critical during multiple stages of T cell development in both mouse and human. Evidence has emerged in recent years that this pathway might regulate T-lineage differentiation differently between both species. Here, we review our current understanding of how Notch signaling is activated and used during human T cell development. First, we set the stage by describing the developmental steps that make up human T cell development before describing the expression profiles of Notch receptors, ligands, and target genes during this process. To delineate stage-specific roles for Notch signaling during human T cell development, we subsequently try to interpret the functional Notch studies that have been performed in light of these expression profiles and compare this to its suggested role in the mouse

Incunabular Immunological Events in Prion Trafficking

While prions probably interact with the innate immune system immediately following infection, little is known about this initial confrontation. Here we investigated incunabular events in lymphotropic and intranodal prion trafficking by following highly enriched, fluorescent prions from infection sites to draining lymph nodes. We detected biphasic lymphotropic transport of prions from the initial entry site upon peripheral prion inoculation. Prions arrived in draining lymph nodes cell autonomously within two hours of intraperitoneal administration. Monocytes and dendritic cells (DCs) required Complement for optimal prion delivery to lymph nodes hours later in a second wave of prion trafficking. B cells constituted the majority of prion-bearing cells in the mediastinal lymph node by six hours, indicating intranodal prion reception from resident DCs or subcapsulary sinus macrophages or directly from follicular conduits. These data reveal novel, cell autonomous prion lymphotropism, and a prominent role for B cells in intranodal prion movement

Germinal center B cells recognize antigen through a specialized immune synapse architecture

B cell activation is regulated by B cell antigen receptor (BCR) signaling and antigen internalization in immune synapses. Using large-scale imaging across B cell subsets, we show that in contrast to naive and memory B cells, which gathered antigen towards the synapse center before internalization, germinal center (GC) B cells extracted antigen by a distinct pathway using small peripheral clusters. Both naive and GC B cell synapses required proximal BCR signaling, but GC cells signaled less through the protein kinase C-β (PKC-β)–NF-κB pathway and produced stronger tugging forces on the BCR, thereby more stringently regulating antigen binding. Consequently, GC B cells extracted antigen with better affinity discrimination than naive B cells, suggesting that specialized biomechanical patterns in B cell synapses regulate T-cell dependent selection of high-affinity B cells in GCs

Measurement of the inclusive and dijet cross-sections of b-jets in pp collisions at sqrt(s) = 7 TeV with the ATLAS detector

The inclusive and dijet production cross-sections have been measured for jets containing b-hadrons (b-jets) in proton-proton collisions at a centre-of-mass energy of sqrt(s) = 7 TeV, using the ATLAS detector at the LHC. The measurements use data corresponding to an integrated luminosity of 34 pb^-1. The b-jets are identified using either a lifetime-based method, where secondary decay vertices of b-hadrons in jets are reconstructed using information from the tracking detectors, or a muon-based method where the presence of a muon is used to identify semileptonic decays of b-hadrons inside jets. The inclusive b-jet cross-section is measured as a function of transverse momentum in the range 20 < pT < 400 GeV and rapidity in the range |y| < 2.1. The bbbar-dijet cross-section is measured as a function of the dijet invariant mass in the range 110 < m_jj < 760 GeV, the azimuthal angle difference between the two jets and the angular variable chi in two dijet mass regions. The results are compared with next-to-leading-order QCD predictions. Good agreement is observed between the measured cross-sections and the predictions obtained using POWHEG + Pythia. MC@NLO + Herwig shows good agreement with the measured bbbar-dijet cross-section. However, it does not reproduce the measured inclusive cross-section well, particularly for central b-jets with large transverse momenta.Comment: 10 pages plus author list (21 pages total), 8 figures, 1 table, final version published in European Physical Journal

Jet energy measurement with the ATLAS detector in proton-proton collisions at root s=7 TeV

The jet energy scale and its systematic uncertainty are determined for jets measured with the ATLAS detector at the LHC in proton-proton collision data at a centre-of-mass energy of √s = 7TeV corresponding to an integrated luminosity of 38 pb-1. Jets are reconstructed with the anti-kt algorithm with distance parameters R=0. 4 or R=0. 6. Jet energy and angle corrections are determined from Monte Carlo simulations to calibrate jets with transverse momenta pT≥20 GeV and pseudorapidities {pipe}η{pipe}<4. 5. The jet energy systematic uncertainty is estimated using the single isolated hadron response measured in situ and in test-beams, exploiting the transverse momentum balance between central and forward jets in events with dijet topologies and studying systematic variations in Monte Carlo simulations. The jet energy uncertainty is less than 2. 5 % in the central calorimeter region ({pipe}η{pipe}<0. 8) for jets with 60≤pT<800 GeV, and is maximally 14 % for pT<30 GeV in the most forward region 3. 2≤{pipe}η{pipe}<4. 5. The jet energy is validated for jet transverse momenta up to 1 TeV to the level of a few percent using several in situ techniques by comparing a well-known reference such as the recoiling photon pT, the sum of the transverse momenta of tracks associated to the jet, or a system of low-pT jets recoiling against a high-pT jet. More sophisticated jet calibration schemes are presented based on calorimeter cell energy density weighting or hadronic properties of jets, aiming for an improved jet energy resolution and a reduced flavour dependence of the jet response. The systematic uncertainty of the jet energy determined from a combination of in situ techniques is consistent with the one derived from single hadron response measurements over a wide kinematic range. The nominal corrections and uncertainties are derived for isolated jets in an inclusive sample of high-pT jets. Special cases such as event topologies with close-by jets, or selections of samples with an enhanced content of jets originating from light quarks, heavy quarks or gluons are also discussed and the corresponding uncertainties are determined. © 2013 CERN for the benefit of the ATLAS collaboration

A Regulatory Mechanism Involving TBP-1/Tat-Binding Protein 1 and Akt/PKB in the Control of Cell Proliferation

TBP-1 /Tat-Binding Protein 1 (also named Rpt-5, S6a or PSMC3) is a multifunctional protein, originally identified as a regulator of HIV-1-Tat mediated transcription. It is an AAA-ATPase component of the 19S regulative subunit of the proteasome and, as other members of this protein family, fulfils different cellular functions including proteolysis and transcriptional regulation. We and others reported that over expression of TBP-1 diminishes cell proliferation in different cellular contexts with mechanisms yet to be defined. Accordingly, we demonstrated that TBP-1 binds to and stabilizes the p14ARF oncosuppressor increasing its anti-oncogenic functions. However, TBP-1 restrains cell proliferation also in the absence of ARF, raising the question of what are the molecular pathways involved. Herein we demonstrate that stable knock-down of TBP-1 in human immortalized fibroblasts increases cell proliferation, migration and resistance to apoptosis induced by serum deprivation. We observe that TBP-1 silencing causes activation of the Akt/PKB kinase and that in turn TBP-1, itself, is a downstream target of Akt/PKB. Moreover, MDM2, a known Akt target, plays a major role in this regulation. Altogether, our data suggest the existence of a negative feedback loop involving Akt/PKB that might act as a sensor to modulate TBP-1 levels in proliferating cells

Stable Vascular Connections and Remodeling Require Full Expression of VE-Cadherin in Zebrafish Embryos

BACKGROUND: VE-cadherin is an endothelial specific, transmembrane protein, that clusters at adherens junctions where it promotes homotypic cell-cell adhesion. VE-cadherin null mutation in the mouse results in early fetal lethality due to altered vascular development. However, the mechanism of action of VE-cadherin is complex and, in the mouse embryo, it is difficult to define the specific steps of vascular development in which this protein is involved. METHODOLOGY AND PRINCIPAL FINDINGS: In order to study the role VE-cadherin in the development of the vascular system in a more suitable model, we knocked down the expression of the coding gene in zebrafish. The novel findings reported here are: 1) partial reduction of VE-cadherin expression using low doses of morpholinos causes vascular fragility, head hemorrhages and increase in permeability; this has not been described before and suggests that the total amount of the protein expressed is an important determinant of vascular stability; 2) concentrations of morpholinos which abrogate VE-cadherin expression prevent vessels to establish successful reciprocal contacts and, as a consequence, vascular sprouting activity is not inhibited. This likely explains the observed vascular hyper-sprouting and the presence of several small, collapsing vessels; 3) the common cardinal vein lacks a correct connection with the endocardium leaving the heart separated from the rest of the circulatory system. The lack of closure of the circulatory loop has never been described before and may explain some downstream defects of the phenotype such as the lack of a correct vascular remodeling. CONCLUSIONS AND SIGNIFICANCE: Our observations identify several steps of vascular development in which VE-cadherin plays an essential role. While it does not appear to regulate vascular patterning it is implicated in vascular connection and inhibition of sprouting activity. These processes require stable cell-cell junctions which are defective in absence of VE-cadherin. Notably, also partial modifications in VE-cadherin expression prevent the formation of a stable vasculature. This suggests that partial internalization or change of function of this protein may strongly affect vascular stability and organization