Citescore of publications indexed in Scopus: an implementation of panel data

This article is intended to establish the variables that explain the behavior of the CiteScore metrics from 2014 to 2016, for journals indexed in Scopus in 2017. With this purpose, journals with a CiteScore value greater than 11 were selected in any of the periods, that is to say, 133 journals. For the data analysis, a model of standard corrected errors for panel was used, from which a coefficient of determination of 77% was obtained. From the results, it was possible to state that journals of arts and humanities; business; administration and accounting; economics, econometrics, and finance; immunology and microbiology; medicine and social sciences, have the greatest impact.Corporación Universitaria Minuto de Dios, Fundación Universitaria Konrad Lorenz, Universidad de La Habana, Universidad de la Costa

Delayed and Accelerated Aging Share Common Longevity Assurance Mechanisms

Mutant dwarf and calorie-restricted mice benefit from healthy aging and unusually long lifespan. In contrast, mouse models for DNA repair-deficient progeroid syndromes age and die prematurely. To identify mechanisms that regulate mammalian longevity, we quantified the parallels between the genome-wide liver expression profiles of mice with those two extremes of lifespan. Contrary to expectation, we find significant, genome-wide expression associations between the progeroid and long-lived mice. Subsequent analysis of significantly over-represented biological processes revealed suppression of the endocrine and energy pathways with increased stress responses in both delayed and premature aging. To test the relevance of these processes in natural aging, we compared the transcriptomes of liver, lung, kidney, and spleen over the entire murine adult lifespan and subsequently confirmed these findings on an independent aging cohort. The majority of genes showed similar expression changes in all four organs, indicating a systemic transcriptional response with aging. This systemic response included the same biological processes that are triggered in progeroid and long-lived mice. However, on a genome-wide scale, transcriptomes of naturally aged mice showed a strong association to progeroid but not to long-lived mice. Thus, endocrine and metabolic changes are indicative of “survival” responses to genotoxic stress or starvation, whereas genome-wide associations in gene expression with natural aging are indicative of biological age, which may thus delineate pro- and anti-aging effects of treatments aimed at health-span extension

Persistent fetal γ-globin expression in adult transgenic mice following deletion of two silencer elements located 3′ to the human Aγ-globin gene

Natural deletions of the human γ-globin gene cluster lead to specific syndromes characterized by increased production of fetal hemoglobin in adult life and provide a useful model to delineate novel cis-acting elements involved in the developmental control of hemoglobin switching. A hypothesis accounting for these phenotypic features assumes that silencers located within the Aγ-to δ-gene region are deleted in hereditary persistence of fetal hemoglobin (HPFH) and δβ-thalassemias, leading to failure of switching. In the present study, we sought to clarify the in vivorole of two elements, termed Enh and F, located 3′ to the Aγ-globin, in silencing the fetal genes. To this end, we generated three transgenic lines using cosmid constructs containing the full length of the globin locus control region (LCR) linked to the 3.3-kb Aγ-gene lacking both the Enh and F elements. The Enh/F deletion resulted in high levels of Aγ-globin gene expression in adult mice in all single copy lines, whereas, the LCR-Aγ single copy lines which retain the Enh and F elements exhibited complete normal switching of the fetal Aγ-gene. Our study documents directly for the first time the in vivorole of these two gene-proximal negative regulatory elements in silencing the fetal globin gene in the perinatal period, and thus these data may permit their eventual exploitation in therapeutic approaches for thalassemias. © 2009 The Feinstein Institute for Medical Research

Persistent Fetal γ-Globin Expression in Adult Transgenic Mice following Deletion of Two Silencer Elements Located 3′ to the Human Aγ-Globin Gene

Natural deletions of the human γ-globin gene cluster lead to specific syndromes characterized by increased production of fetal hemoglobin in adult life and provide a useful model to delineate novel cis-acting elements involved in the developmental control of hemoglobin switching. A hypothesis accounting for these phenotypic features assumes that silencers located within the Aγ-to δ-gene region are deleted in hereditary persistence of fetal hemoglobin (HPFH) and δβ-thalassemias, leading to failure of switching. In the present study, we sought to clarify the in vivo role of two elements, termed Enh and F, located 3′ to the Aγ-globin, in silencing the fetal genes. To this end, we generated three transgenic lines using cosmid constructs containing the full length of the globin locus control region (LCR) linked to the 3.3-kb Aγ-gene lacking both the Enh and F elements. The Enh/F deletion resulted in high levels of Aγ-globin gene expression in adult mice in all single copy lines, whereas, the LCR-Aγ single copy lines which retain the Enh and F elements exhibited complete normal switching of the fetal Aγ-gene. Our study documents directly for the first time the in vivo role of these two gene-proximal negative regulatory elements in silencing the fetal globin gene in the perinatal period, and thus these data may permit their eventual exploitation in therapeutic approaches for thalassemias