Institution
John Radcliffe Hospital
Healthcare•Oxford, Oxfordshire, United Kingdom•
About: John Radcliffe Hospital is a healthcare organization based out in Oxford, Oxfordshire, United Kingdom. It is known for research contribution in the topics: Population & Antigen. The organization has 14491 authors who have published 23670 publications receiving 1459015 citations.
Topics: Population, Antigen, Transplantation, Gene, Immune system
Papers published on a yearly basis
Papers
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TL;DR: In human cells, it is reported that WRN co-localizes and physically interacts with the critical telomere maintenance protein TRF2, and this interaction is mediated by the RecQ conserved C-terminal region of WRN.
395 citations
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TL;DR: Young offspring of pregnancies complicated by preeclampsia already have increased blood pressure and BMI, a finding that may need to be considered in future primary prevention strategies for cardiovascular disease.
Abstract: BACKGROUND AND OBJECTIVE: Preeclampsia is an independent cardiovascular risk factor for the mother, and recent studies reveal that offspring of affected pregnancies also may have an increased cardiovascular risk. Our objective was to examine evidence for increased cardiovascular risk factors in children exposed to preeclampsia in utero.
METHODS: We performed a systematic review and meta-analysis on studies reporting traditional cardiovascular risk factors in those exposed to preeclampsia compared to controls. Information was extracted on the classic cardiovascular risk factors, including blood pressure, lipid profile, glucose metabolism, and BMI from articles published between 1948 and August 2011 in Medline and Embase.
RESULTS: Eighteen studies provided cumulated data on 45 249 individuals. In utero exposure to preeclampsia was associated with a 2.39 mm Hg (95% confidence interval: 1.74–3.05; P < .0001) higher systolic and a 1.35 mm Hg (95% confidence interval: 0.90–1.80; P < .00001) higher diastolic blood pressure during childhood and young adulthood. BMI was increased by 0.62 kg/m2 ( P < .00001). Associations were similar in children and adolescents, for different genders, and with variation in birth weight. There was insufficient evidence to identify consistent variation in lipid profile or glucose metabolism.
CONCLUSIONS: Young offspring of pregnancies complicated by preeclampsia already have increased blood pressure and BMI, a finding that may need to be considered in future primary prevention strategies for cardiovascular disease.
* Abbreviations:
CI — : confidence interval
393 citations
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TL;DR: Potential mechanisms underlying the syndromes of uncomplicated and severe vivax malaria, identifying key areas for future research are discussed.
393 citations
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TL;DR: The data indicate that the two mutations have arisen independently since the divergence of African and non African populations and both have attained high frequencies.
Abstract: We have previously identified, in three British families having an index child with frequent infections, a point mutation (GGC-->GAC) in codon 54 of exon 1 of the gene for the human lectin mannose binding protein (MBP). This was associated with low serum levels of this complement activating protein and would be anticipated to impair opsonization of mannose rich microorganisms. We now report a second point mutation (GGA-->GAA) in Gambians from West Africa, involving codon 57 of exon 1. By substituting carboxylic acids for axial glycines in the translated proteins both mutations would be expected to disrupt the secondary structure of the collagenous triple helix of the 96 kDa MBP subunits. In the Gambians the codon 57 mutation was studied by PCR, sequence analysis and restriction analysis and found to be remarkably common (frequency of the mutant gene 0.29 in adults and 0.23 in newborns) whereas the codon 54 mutation was very rare (frequency 0.003). However, the codon 54 mutation was frequent in both a British Caucasian and a Hong Kong Chinese population (frequency of the mutant gene 0.17 and 0.11 respectively). It was predicted that both homozygous and heterozygous individuals would have profoundly reduced serum levels of the protein and this was confirmed by immunoassay as was the reduced capacity of such sera to activate complement through the MBP initiated classical pathway. Our data indicate that the two mutations have arisen independently since the divergence of African and non African populations and both have attained high frequencies.
392 citations
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TL;DR: The leukocyte populations that can promote immune tolerance after cell or solid-organ transplantation are discussed, including regulatory T cells, B cells and macrophages, as well as myeloid-derived suppressor cells, dendritic cells and mesenchymal stromal cells.
Abstract: Establishing immune tolerance in transplant recipients is essential for promoting the long-term survival of an allograft and for preventing the development of harmful graft-versus-host responses. This Review considers the clinical potential of manipulating different immunosuppressive cell populations, including regulatory T cells, B cells and macrophages, in the setting of transplantation. Immune regulation is fundamental to any immune response to ensure that it is appropriate for the perceived threat to the host. Following cell and organ transplantation, it is essential to control both the innate immune response triggered by the injured tissue and the adaptive immune response stimulated by mismatched donor and recipient histocompatibility antigens to enable the transplant to survive and function. Here, we discuss the leukocyte populations that can promote immune tolerance after cell or solid-organ transplantation. Such populations include regulatory T cells, B cells and macrophages, as well as myeloid-derived suppressor cells, dendritic cells and mesenchymal stromal cells. We consider the potential of these regulatory immune cells to develop and function in transplant recipients and their potential use as cellular therapies to promote long-term graft function.
392 citations
Authors
Showing all 14542 results
Name | H-index | Papers | Citations |
---|---|---|---|
Douglas G. Altman | 253 | 1001 | 680344 |
Salim Yusuf | 231 | 1439 | 252912 |
David J. Hunter | 213 | 1836 | 207050 |
Mark I. McCarthy | 200 | 1028 | 187898 |
Stuart H. Orkin | 186 | 715 | 112182 |
Richard Peto | 183 | 683 | 231434 |
Ralph M. Steinman | 171 | 453 | 121518 |
Adrian L. Harris | 170 | 1084 | 120365 |
Rory Collins | 162 | 489 | 193407 |
Nicholas J. White | 161 | 1352 | 104539 |
David W. Johnson | 160 | 2714 | 140778 |
David Cella | 156 | 1258 | 106402 |
Edmund T. Rolls | 153 | 612 | 77928 |
Martin A. Nowak | 148 | 591 | 94394 |
Kypros H. Nicolaides | 147 | 1302 | 87091 |