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, Cytotoxic T cell, Immune system
Papers published on a yearly basis
Papers
More filters
••
TL;DR: Analysis of 13 clinically heterogeneous SMA families finds that 'chronic' childhood-onset SMA (including intermediate SMA or SMA type II, and KugelbergWelander or S MA type III) is genetically homogeneous, mapping to chromosomal region 5ql 1.3.
Abstract: SPINAL muscular atrophy (SMA) describes a group of heritable degenerative diseases that selectively affect the α-motor neuron. Childhood-onset SMAs rank second in frequency to cystic fibrosis among autosomal recessive disorders, and are the leading cause of heritable infant mortality. Predictions that genetic heterogeneity underlies the differences between types of SMA, together with the aggressive nature of the most-severe infantile form, make linkage analysis of SMA potentially complex. We have now analysed 13 clinically heterogeneous SMA families. We find that 'chronic' childhood-onset SMA (including intermediate SMA or SMA type II, and Kugelberg–Welander or SMA type III) is genetically homogeneous, mapping to chromosomal region 5ql 1.27#150;13.3.
539 citations
••
TL;DR: Ex vivo analysis shows that a population of CD4+ perforin+ T cells is present in the circulation at low numbers in healthy donors and is markedly expanded in donors with chronic viral infections, in particular HIV infection, at all stages of the disease, including early primary infection.
Abstract: The cytotoxic potential of CD8 + T cells and NK cells plays a crucial role in the immune response to pathogens. Although in vitro studies have reported that CD4 + T cells are also able to mediate perforin-mediated killing, the in vivo existence and relevance of cytotoxic CD4 + T cells have been the subject of debate. Here we show that a population of CD4 + perforin + T cells is present in the circulation at low numbers in healthy donors and is markedly expanded in donors with chronic viral infections, in particular HIV infection, at all stages of the disease, including early primary infection. Ex vivo analysis shows that these cells have cytotoxic potential mediated through the release of perforin. In comparison with more classical CD4 + T cells, this subset displays a distinct surface phenotype and functional profile most consistent with end-stage differentiated T cells and include Ag experienced CD4 + T cells. The existence of CD4 + cytotoxic T cells in vivo at relatively high levels in chronic viral infection suggests a role in the immune response.
539 citations
••
TL;DR: The utility of a new Multimodal Surface Matching (MSM) algorithm capable of driving alignment using a wide variety of descriptors of brain architecture, function and connectivity is demonstrated.
539 citations
••
TL;DR: This review focuses on three aspects: DNA repair mechanisms, cell cycle checkpoints, and apoptosis, and restricts coverage of the DNA repair field to base excision repair and DNA double-strand break repair.
Abstract: Cells are constantly under threat from the cytotoxic and mutagenic effects of DNA damaging agents. These agents can either be exogenous or formed within cells. Environmental DNA-damaging agents include UV light and ionizing radiation, as well as a variety of chemicals encountered in foodstuffs, or as air- and water-borne agents. Endogenous damaging agents include methylating species and the reactive oxygen species that arise during respiration. Although diverse responses are elicited in cells following DNA damage, this review focuses on three aspects: DNA repair mechanisms, cell cycle checkpoints, and apoptosis. Because the areas of nucleotide excision repair and mismatch repair have been covered extensively in recent reviews, we restrict our coverage of the DNA repair field to base excision repair and DNA double-strand break repair.
538 citations
••
TL;DR: A dual mechanism of activation is proposed in which the operation of an inducible activation domain is amplified by regulation of transcription factor abundance, most likely occurring through changes in protein stability.
537 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 |