Institution
Cardiff University
Education•Cardiff, United Kingdom•
About: Cardiff University is a education organization based out in Cardiff, United Kingdom. It is known for research contribution in the topics: Population & Context (language use). The organization has 34188 authors who have published 82643 publications receiving 3046531 citations. The organization is also known as: University of Cardiff & University College of South Wales and Monmouthshire.
Topics: Population, Context (language use), Catalysis, Galaxy, Poison control
Papers published on a yearly basis
Papers
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TL;DR: In this paper, the feasibility of using biosurfactants for the removal of heavy metals from sediments was evaluated using batch washing experiments, and it was shown that the metal removal process occurs through sorption of the surfactant on to the soil surface and complexation with the metal, detachment of the metal from the soil into the soil solution and hence association with surfactants micelles.
384 citations
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TL;DR: This study aims to investigate the effect of increasing quaternisation and therefore, positive charge on cell viability and transfection and found that higher toxicity was seen in polymeric chitosan derivatives over oligomeric chitOSan derivatives at similar degrees of trimethylation.
384 citations
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TL;DR: The impact of primordial magnetic fields (PMFs) on the CMB temperature and polarization spectra was investigated in this paper, with different bounds depending on the specific effect that is analysed.
Abstract: We predict and investigate four types of imprint of a stochastic background of primordial magnetic fields (PMFs) on the cosmic microwave background (CMB) anisotropies: the impact of PMFs on the CMB temperature and polarization spectra, related to their contribution to cosmological perturbations; the effect on CMB polarization induced by Faraday rotation; magnetically-induced non-Gaussianities and related non-zero bispectra; and the magnetically-induced breaking of statistical isotropy. We present constraints on the amplitude of PMFs derived from different combinations of Planck data products, depending on the specific effect that is analysed. Overall, Planck data constrain the amplitude of PMFs to less than a few nanogauss, with different bounds depending on the considered model. In particular, individual limits coming from the analysis of the CMB angular power spectra, using the Planck likelihood, are B1Mpc < 4:4 nG (where B1Mpc is the comoving field amplitude at a scale of 1 Mpc) at 95 % confidence level, assuming zero helicity, and B1Mpc < 5:6 nG when we consider a maximally helical field. For nearly scaleinvariant PMFs we obtain B1Mpc < 2:1 nG and B1Mpc < 0:7 nG if the impact of PMFs on the ionization history of the Universe is included in the analysis. From the analysis of magnetically-induced non-Gaussianity we obtain three different values, corresponding to three applied methods, all below 5 nG. The constraint from the magnetically-induced passive-tensor bispectrum is B1Mpc < 2:8 nG. A search for preferred directions in the magnetically-induced passive bispectrum yields B1Mpc < 4:5 nG, whereas the the compensated-scalar bispectrum gives B1Mpc < 3 nG. The analysis of the Faraday rotation of CMB polarization by PMFs uses the Planck power spectra in EE and BB at 70 GHz and gives B1Mpc < 1380 nG. In our final analysis, we consider the harmonic-space correlations produced by Alfv´ en waves, finding no significant evidence for the presence of these waves. Together, these results comprise a comprehensive set of constraints on possible PMFs with Planck data.
384 citations
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TL;DR: Genomic, cellular, and mouse modelling data are provided demonstrating that the polycomb group gene SUZ12 functions as tumour suppressor in PNS tumours, high-grade gliomas and melanomas by cooperating with mutations in NF1 and it is shown that SUZ 12 loss potentiates the effects of NF1 mutations by amplifying Ras-driven transcription through effects on chromatin.
Abstract: The polycomb repressive complex 2 (PRC2) exerts oncogenic effects in many tumour types1 However, loss-of-function mutations in PRC2 components occur in a subset of haematopoietic malignancies, suggesting that this complex plays a dichotomous and poorly understood role in cancer2, 3 Here we provide genomic, cellular, and mouse modelling data demonstrating that the polycomb group gene SUZ12 functions as tumour suppressor in PNS tumours, high-grade gliomas and melanomas by cooperating with mutations in NF1 NF1 encodes a Ras GTPase-activating protein (RasGAP) and its loss drives cancer by activating Ras4 We show that SUZ12 loss potentiates the effects of NF1 mutations by amplifying Ras-driven transcription through effects on chromatin Importantly, however, SUZ12 inactivation also triggers an epigenetic switch that sensitizes these cancers to bromodomain inhibitors Collectively, these studies not only reveal an unexpected connection between the PRC2 complex, NF1 and Ras, but also identify a promising epigenetic-based therapeutic strategy that may be exploited for a variety of cancers
384 citations
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TL;DR: Support for the majority of the previously implicated CNVs in schizophrenia is strengthened and routine CNV screening may be clinically appropriate given the high rate of known deleterious mutations in the disorder and the comorbidity associated with these heritable mutations.
Abstract: Background A number of copy number variants (CNVs) have been suggested as susceptibility factors for schizophrenia. For some of these the data remain equivocal, and the frequency in individuals with schizophrenia is uncertain. Aims To determine the contribution of CNVs at 15 schizophreniaassociated loci (a) using a large new data-set of patients with schizophrenia (n = 6882) and controls (n = 6316), and (b) combining our results with those from previous studies. Method We used Illumina microarrays to analyse our data. Analyses were restricted to 520 766 probes common to all arrays used in the different data-sets. Results
384 citations
Authors
Showing all 34629 results
Name | H-index | Papers | Citations |
---|---|---|---|
Rob Knight | 201 | 1061 | 253207 |
Stephen V. Faraone | 188 | 1427 | 140298 |
John J.V. McMurray | 178 | 1389 | 184502 |
David R. Williams | 178 | 2034 | 138789 |
John Hardy | 177 | 1178 | 171694 |
Dorret I. Boomsma | 176 | 1507 | 136353 |
Kay-Tee Khaw | 174 | 1389 | 138782 |
Anders Björklund | 165 | 769 | 84268 |
Edward T. Bullmore | 165 | 746 | 112463 |
Peter A. R. Ade | 162 | 1387 | 138051 |
Michael John Owen | 160 | 1110 | 135795 |
Gavin Davies | 159 | 2036 | 149835 |
Suvadeep Bose | 154 | 960 | 129071 |
Todd Adams | 154 | 1866 | 143110 |
John R. Hodges | 149 | 812 | 82709 |