Institution
King's College London
Education•London, United Kingdom•
About: King's College London is a education organization based out in London, United Kingdom. It is known for research contribution in the topics: Population & Mental health. The organization has 43107 authors who have published 113125 publications receiving 4498103 citations. The organization is also known as: King's & KCL.
Papers published on a yearly basis
Papers
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897 citations
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TL;DR: Empirical evidence suggests that efforts aimed at reducing bullying victimization in childhood and adolescence should be strongly supported and research on explanatory mechanisms involved in the development of mental health problems in bullied youths is needed.
Abstract: Bullying victimization is a topic of concern for youths, parents, school staff and mental health practitioners. Children and adolescents who are victimized by bullies show signs of distress and adjustment problems. However, it is not clear whether bullying is the source of these difficulties. This paper reviews empirical evidence to determine whether bullying victimization is a significant risk factor for psychopathology and should be the target of intervention and prevention strategies. Research indicates that being the victim of bullying (1) is not a random event and can be predicted by individual characteristics and family factors; (2) can be stable across ages; (3) is associated with severe symptoms of mental health problems, including self-harm, violent behaviour and psychotic symptoms; (4) has long-lasting effects that can persist until late adolescence; and (5) contributes independently to children's mental health problems. This body of evidence suggests that efforts aimed at reducing bullying victimization in childhood and adolescence should be strongly supported. In addition, research on explanatory mechanisms involved in the development of mental health problems in bullied youths is needed.
896 citations
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TL;DR: There appears to considerable redundancy among the oral microbiota and a focus on functional rather than phylogenetic diversity may be required in order to fully understand host-microbiome interactions.
895 citations
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TL;DR: A small beneficial effect of memantine at six months in moderate to severe AD is suggested and the statistical significance of these benefits could be overturned by data from two unpublished studies which are known to show no significant effect.
Abstract: Background
Memantine, a low affinity antagonist to glutamate NMDA receptors, may prevent excitatory neurotoxicity in dementia.
Objectives
To determine efficacy and safety of memantine for people with Alzheimer's disease (AD), vascular (VD) and mixed dementia.
Search methods
The Specialized Register of the Cochrane Dementia and Cognitive Improvement Group was searched on 8 February 2006. This register contains references from all major healthcare databases and many ongoing trial databases and is updated regularly. In addition, the search engines Copernic and Google were used to identify unpublished trials through inspection of the websites of licensing bodies like the FDA , EMEA and NICE and of companies' websites (Lundbeck, Merz, Forest, Suntori etc) and clinical trials registries.
Selection criteria
Double-blind, parallel group, placebo-controlled, randomized trials of memantine in people with dementia.
Data collection and analysis
Data were pooled where possible. Intention-to-treat (ITT) and observed case (OC) analyses are reported.
Main results
1. Moderate to severe AD. Two out of three six month studies show a small beneficial effect of memantine. Pooled data indicate a beneficial effect at six months on cognition (2.97 points on the 100 point SIB, 95% CI 1.68 to 4.26, P < 0.00001), activities of daily living (1.27 points on the 54 point ADCS-ADLsev, 95% CI 0.44 to 2.09, P = 0.003) and behaviour (2.76 points on the 144 point NPI, 95% CI 0.88 to 4.63, P=0.004), supported by clinical impression of change (0.28 points on the 7 point CIBIC+, 95% CI 0.15 to 0.41, P < 0.0001).
2. Mild to moderate AD. Pooled data from three unpublished studies indicate a marginal benefical effect at six months on ITT cognition (0.99 points on the 70 point ADAS-Cog, 95% CI 0.21 to 1.78, P = 0.01) which was barely detectable clinically (0.13 CIBIC+ points, 95% CI 0.01 to 0.25, P = 0.03) but no effect on behaviour, activities of daily living or OC analysis of cognition.
3. Mild to moderate vascular dementia. Pooled data from two six month studies indicated a small beneficial effect of memantine on cognition (1.85 ADAS-Cog points, 95% CI 0.88 to 2.83, P = 0.0002), and behaviour (0.84 95% CI 0.06 to 0.91, P = 0.03) but this was not supported by clinical global measures.
4. Patients taking memantine were slightly less likely to develop agitation (134/1739, 7.7% versus 175/1873, 9.3% OR 0.78, 95% CI 0.61 to 0.99, P = 0.04). This effect was slightly larger, but still small, in moderate to severe AD (58/506 [12%] vs 88/499 [18%]; OR = 0.6, 95% CI 0.42 to 0.86, P = 0.005). There is no evidence either way about whether it has an effect on agitation which is already present.
5. Memantine is well tolerated.
Authors' conclusions
Memantine has a small beneficial effect at six months in moderate to severe AD. In patients with mild to moderate dementia, the small beneficial effect on cognition was not clinically detectable in those with vascular dementia and was detectable in those with AD. Memantine is well tolerated.
895 citations
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University of Basel1, Swiss Tropical and Public Health Institute2, Fudan University3, University of Melbourne4, University of California, San Francisco5, Wellcome Trust Sanger Institute6, Veterinary Laboratories Agency7, King's College London8, University of Ghana9, Centers for Disease Control and Prevention10, Addis Ababa University11, Imperial College London12, National Institute for Medical Research13
TL;DR: Coalescent analyses indicate that MTBC emerged about 70,000 years ago, accompanied migrations of anatomically modern humans out of Africa and expanded as a consequence of increases in human population density during the Neolithic period, consistent with MTBC displaying characteristics indicative of adaptation to both low and high host densities.
Abstract: Tuberculosis caused 20% of all human deaths in the Western world between the seventeenth and nineteenth centuries and remains a cause of high mortality in developing countries. In analogy to other crowd diseases, the origin of human tuberculosis has been associated with the Neolithic Demographic Transition, but recent studies point to a much earlier origin. We analyzed the whole genomes of 259 M. tuberculosis complex (MTBC) strains and used this data set to characterize global diversity and to reconstruct the evolutionary history of this pathogen. Coalescent analyses indicate that MTBC emerged about 70,000 years ago, accompanied migrations of anatomically modern humans out of Africa and expanded as a consequence of increases in human population density during the Neolithic period. This long coevolutionary history is consistent with MTBC displaying characteristics indicative of adaptation to both low and high host densities.
894 citations
Authors
Showing all 43962 results
Name | H-index | Papers | Citations |
---|---|---|---|
Cyrus Cooper | 204 | 1869 | 206782 |
David Miller | 203 | 2573 | 204840 |
Rob Knight | 201 | 1061 | 253207 |
Mark I. McCarthy | 200 | 1028 | 187898 |
Michael Rutter | 188 | 676 | 151592 |
Eric Boerwinkle | 183 | 1321 | 170971 |
Terrie E. Moffitt | 182 | 594 | 150609 |
Kenneth S. Kendler | 177 | 1327 | 142251 |
John Hardy | 177 | 1178 | 171694 |
Dorret I. Boomsma | 176 | 1507 | 136353 |
Barry Halliwell | 173 | 662 | 159518 |
Feng Zhang | 172 | 1278 | 181865 |
Simon Baron-Cohen | 172 | 773 | 118071 |
Phillip A. Sharp | 172 | 614 | 117126 |
Yang Yang | 171 | 2644 | 153049 |