Institution
Charles University in Prague
Education•Prague, Czechia•
About: Charles University in Prague is a education organization based out in Prague, Czechia. It is known for research contribution in the topics: Population & Large Hadron Collider. The organization has 32392 authors who have published 74435 publications receiving 1804208 citations.
Topics: Population, Large Hadron Collider, Czech, Magnetization, Transplantation
Papers published on a yearly basis
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TL;DR: The precautionary principle suggests that possible role of toxoplasmosis as a triggering factor responsible for development of several clinical entities deserves much more attention and financial support both in everyday medical practice and future clinical research.
Abstract: Background: Toxoplasmosis is becoming a global health hazard as it infects 30–50% of the world human population. Clinically, the life-long presence of the parasite in tissues of a majority of infected individuals is usually considered asymptomatic. However, a number of studies show that this ‘asymptomatic infection’ may also lead to development of other human pathologies. Aims of the Study: The purpose of the study was to collect available geoepidemiological data on seroprevalence of toxoplasmosis and search for its relationship with mortality and disability rates in different countries. Methods and Findings: Prevalence data published between 1995–2008 for women in child-bearing age were collected for 88 countries (29 European). The association between prevalence of toxoplasmosis and specific disease burden estimated with age-standardized Disability Adjusted Life Year (DALY) or with mortality, was calculated using General Linear Method with Gross Domestic Product per capita (GDP), geolatitude and humidity as covariates, and also using nonparametric partial Kendall correlation test with GDP as a covariate. The prevalence of toxoplasmosis correlated with specific disease burden in particular countries explaining 23% of variability in disease burden in Europe. The analyses revealed that for example, DALY of 23 of 128 analyzed diseases and disease categories on the WHO list showed correlations (18 positive, 5 negative) with prevalence of toxoplasmosis and another 12 diseases showed positive trends (p,0.1). For several obtained significant correlations between the seroprevalence of toxoplasmosis and specific diseases/clinical entities, possible pathophysiological, biochemical and molecular explanations are presented. Conclusions: The seroprevalence of toxoplasmosis correlated with various disease burden. Statistical associations does not necessarily mean causality. The precautionary principle suggests however that possible role of toxoplasmosis as a triggering factor responsible for development of several clinical entities deserves much more attention and financial support both in everyday medical practice and future clinical research.
510 citations
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German Cancer Research Center1, Discovery Institute2, University of California, San Diego3, European Bioinformatics Institute4, University of Toronto5, Sanford-Burnham Institute for Medical Research6, Max Planck Society7, Semmelweis University8, Lund University9, Masaryk University10, Charles University in Prague11, University of Amsterdam12, University of Tübingen13, Cincinnati Children's Hospital Medical Center14, St. Jude Children's Research Hospital15, University of Hamburg16, University of Bonn17, Boston Children's Hospital18, University of Düsseldorf19, Heidelberg University20
TL;DR: GFI1 and GFI1B are identified as prominent medulloblastoma oncogenes and ‘enhancer hijacking’ is implicate as an efficient mechanism driving oncogene activation in a childhood cancer.
Abstract: Medulloblastoma is a highly malignant paediatric brain tumour currently treated with a combination of surgery, radiation and chemotherapy, posing a considerable burden of toxicity to the developing child. Genomics has illuminated the extensive intertumoral heterogeneity of medulloblastoma, identifying four distinct molecular subgroups. Group 3 and group 4 subgroup medulloblastomas account for most paediatric cases; yet, oncogenic drivers for these subtypes remain largely unidentified. Here we describe a series of prevalent, highly disparate genomic structural variants, restricted to groups 3 and 4, resulting in specific and mutually exclusive activation of the growth factor independent 1 family proto-oncogenes, GFI1 and GFI1B. Somatic structural variants juxtapose GFI1 or GFI1B coding sequences proximal to active enhancer elements, including super-enhancers, instigating oncogenic activity. Our results, supported by evidence from mouse models, identify GFI1 and GFI1B as prominent medulloblastoma oncogenes and implicate 'enhancer hijacking' as an efficient mechanism driving oncogene activation in a childhood cancer.
508 citations
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Felix Aharonian1, A. G. Akhperjanian1, Gisela Anton2, U. Barres de Almeida3 +165 more•Institutions (22)
TL;DR: In this article, the authors present a measurement of the cosmic-ray electron spectrum with H.E.S. starting at 340 GeV and show no indication of a structure in the electron spectrum, but rather a power-law spectrum with spectral index of 3.0 +- 0.1 (stat.) + − 0.3 (syst.) which steepens at about 1 TeV.
Abstract: The measurement of an excess in the cosmic-ray electron spectrum between 300 and 800 GeV by the ATIC experiment has - together with the PAMELA detection of a rise in the positron fraction up to 100 GeV - motivated many interpretations in terms of dark matter scenarios; alternative explanations assume a nearby electron source like a pulsar or supernova remnant. Here we present a measurement of the cosmic-ray electron spectrum with H.E.S.S. starting at 340 GeV. The H.E.S.S. data with their lower statistical errors show no indication of a structure in the electron spectrum, but rather a power-law spectrum with spectral index of 3.0 +- 0.1 (stat.) +- 0.3 (syst.) which steepens at about 1 TeV.
507 citations
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TL;DR: Therapy for SIBO must be complex, addressing all causes, symptoms and complications, and fully individualised, it should include treatment of the underlying disease, nutritional support and cyclical gastro-intestinal selective antibiotics.
Abstract: Human intestinal microbiota create a complex polymicrobial ecology. This is characterised by its high population density, wide diversity and complexity of interaction. Any dysbalance of this complex intestinal microbiome, both qualitative and quantitative, might have serious health consequence for a macro-organism, including small intestinal bacterial overgrowth syndrome (SIBO). SIBO is defined as an increase in the number and/or alteration in the type of bacteria in the upper gastrointestinal tract. There are several endogenous defence mechanisms for preventing bacterial overgrowth: gastric acid secretion, intestinal motility, intact ileo-caecal valve, immunoglobulins within intestinal secretion and bacteriostatic properties of pancreatic and biliary secretion. Aetiology of SIBO is usually complex, associated with disorders of protective antibacterial mechanisms (e.g. achlorhydria, pancreatic exocrine insufficiency, immunodeficiency syndromes), anatomical abnormalities (e.g. small intestinal obstruction, diverticula, fistulae, surgical blind loop, previous ileo-caecal resections) and/or motility disorders (e.g. scleroderma, autonomic neuropathy in diabetes mellitus, post-radiation enteropathy, small intestinal pseudo-obstruction). In some patients more than one factor may be involved. Symptoms related to SIBO are bloating, diarrhoea, malabsorption, weight loss and malnutrition. The gold standard for diagnosing SIBO is still microbial investigation of jejunal aspirates. Non-invasive hydrogen and methane breath tests are most commonly used for the diagnosis of SIBO using glucose or lactulose. Therapy for SIBO must be complex, addressing all causes, symptoms and complications, and fully individualised. It should include treatment of the underlying disease, nutritional support and cyclical gastro-intestinal selective antibiotics. Prognosis is usually serious, determined mostly by the underlying disease that led to SIBO.
506 citations
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TL;DR: Patients with lesions either to the right or to the left hippocampus were unimpaired on several memory tasks, including a spatial one, with a 30 min delay, designed to be analogous to the Morris water maze, suggesting that the parahippocampal cortex itself may play an important role in spatial memory.
506 citations
Authors
Showing all 32719 results
Name | H-index | Papers | Citations |
---|---|---|---|
Ronald C. Petersen | 178 | 1091 | 153067 |
P. Chang | 170 | 2154 | 151783 |
Vaclav Vrba | 141 | 1298 | 95671 |
Milos Lokajicek | 139 | 1511 | 98888 |
Christopher D. Manning | 138 | 499 | 147595 |
Yves Sirois | 137 | 1334 | 95714 |
Rupert Leitner | 136 | 1201 | 90597 |
Gerald M. Reaven | 133 | 799 | 80351 |
Roberto Sacchi | 132 | 1186 | 89012 |
S. Errede | 132 | 1481 | 98663 |
Mark Neubauer | 131 | 1252 | 89004 |
Peter Kodys | 131 | 1262 | 85267 |
Panos A Razis | 130 | 1287 | 90704 |
Vit Vorobel | 130 | 919 | 79444 |
Jehad Mousa | 130 | 1226 | 86564 |