231 research outputs found

    Extreme Energy Cosmic Rays: Bottom-up vs. Top-down scenarii

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    We present an overview on extreme energy cosmic rays (EECR) and the fundamental physics connected with them. The top-down and bottom-up scenarii are contrasted. We summarize the essential features underlying the top-down scenarii for EECR, namely, the lifetime and the mass {\bf imposed} to the heavy relics whatever they be: topological and non-topological solitons, X-particles, cosmic defects, microscopic black-holes, fundamental strings. An unified formula for the quantum decay rate of all these objects was provided in hep-ph/0202249. The key point in the top-down scenarii is the necessity to {\bf adjust} the lifetime of the heavy object to the age of the universe. The natural lifetimes of such heavy objects are, however, microscopic times associated to the GUT energy scale (sim 10^{-28} sec. or shorter); such heavy objects could have been abundantly formed by the end of inflation and it seems natural they decayed shortly after being formed. The arguments produced to {\bf fine tune} the relics lifetime to the age of the universe are critically analyzed. The annihilation scenario (`Wimpzillas') is analyzed too. Top-down scenarii based on networks of topological defects are strongly disfavored at the light of the recent CMB anisotropy observations. We discuss the acceleration mechanisms of cosmic rays,their possible astrophysical sources and the main open physical problems and difficulties in the context of bottom-up scenarii, and we conclude by outlining the expectations from future observatories like EUSO and where the theoretical effort should be placed.Comment: LaTex, 16 pages, 2 .eps figures. The annihilation scenario (Wimpzillas) is included and the discussion on gamma ray bursts improved. Based on lectures at the Fourth International Workshop on `New Worlds in Astroparticle Physics' in Faro, Portugal, September 2002, at the 9th Course on Astrofundamental Physics of the Chalonge School, Palermo, Italia, September 2002 and at the SOWG EUSO meeting, Roma, Italia, November 200

    An empirical investigation of dance addiction

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    Although recreational dancing is associated with increased physical and psychological well-being, little is known about the harmful effects of excessive dancing. The aim of the present study was to explore the psychopathological factors associated with dance addiction. The sample comprised 447 salsa and ballroom dancers (68% female, mean age: 32.8 years) who danced recreationally at least once a week. The Exercise Addiction Inventory (Terry, Szabo, & Griffiths, 2004) was adapted for dance (Dance Addiction Inventory, DAI). Motivation, general mental health (BSI-GSI, and Mental Health Continuum), borderline personality disorder, eating disorder symptoms, and dance motives were also assessed. Five latent classes were explored based on addiction symptoms with 11% of participants belonging to the most problematic class. DAI was positively associated with psychiatric distress, borderline personality and eating disorder symptoms. Hierarchical linear regression model indicated that Intensity (ß=0.22), borderline (ß=0.08), eating disorder (ß=0.11) symptoms, as well as Escapism (ß=0.47) and Mood Enhancement (ß=0.15) (as motivational factors) together explained 42% of DAI scores. Dance addiction as assessed with the Dance Addiction Inventory is associated with indicators of mild psychopathology and therefore warrants further research

    Role of BRCA gene dysfunction in breast and ovarian cancer predisposition

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    Tumor suppressor genes that perform apparently generic cellular functions nonetheless cause tissue-specific syndromes in the human population when they are mutated in the germline. The two major hereditary breast/ovarian cancer predisposition genes, BRCA1 and BRCA2, appear to participate in a common pathway that is involved in the control of homologous recombination and in the maintenance of genomic integrity. How might such functions translate into the specific suppression of cancers of the breast and ovarian epithelia? Recent advances in the study of BRCA1 and BRCA2, discussed herein, have provided new opportunities to address this question

    Genomic Profiling of Advanced-Stage Oral Cancers Reveals Chromosome 11q Alterations as Markers of Poor Clinical Outcome

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    Identifying oral cancer lesions associated with high risk of relapse and predicting clinical outcome remain challenging questions in clinical practice. Genomic alterations may add prognostic information and indicate biological aggressiveness thereby emphasizing the need for genome-wide profiling of oral cancers. High-resolution array comparative genomic hybridization was performed to delineate the genomic alterations in clinically annotated primary gingivo-buccal complex and tongue cancers (n = 60). The specific genomic alterations so identified were evaluated for their potential clinical relevance. Copy-number changes were observed on chromosomal arms with most frequent gains on 3q (60%), 5p (50%), 7p (50%), 8q (73%), 11q13 (47%), 14q11.2 (47%), and 19p13.3 (58%) and losses on 3p14.2 (55%) and 8p (83%). Univariate statistical analysis with correction for multiple testing revealed chromosomal gain of region 11q22.1–q22.2 and losses of 17p13.3 and 11q23–q25 to be associated with loco-regional recurrence (P = 0.004, P = 0.003, and P = 0.0003) and shorter survival (P = 0.009, P = 0.003, and P 0.0001) respectively. The gain of 11q22 and loss of 11q23-q25 were validated by interphase fluorescent in situ hybridization (I-FISH). This study identifies a tractable number of genomic alterations with few underlying genes that may potentially be utilized as biological markers for prognosis and treatment decisions in oral cancers

    Author Correction: Comprehensive analysis of chromothripsis in 2,658 human cancers using whole-genome sequencing (Nature Genetics, (2020), 52, 3, (331-341), 10.1038/s41588-019-0576-7)

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    Correction to: Nature Genetics, published online 05 February 2020. In the published version of this paper, the members of the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium were listed in the Supplementary Information; however, these members should have been included in the main paper. The original Article has been corrected to include the members and affiliations of the PCAWG Consortium in the main paper; the corrections have been made to the HTML version of the Article but not the PDF version. Additional corrections to affiliations have been made to the PDF and HTML versions of the original Article for consistency of information between the PCAWG list and the main paper
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