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: It is demonstrated that mucin misfolding and ER stress initiate colitis in mice, and that ER stress-related mucin depletion could be a fundamental component of the pathogenesis of human colitis and that clinical studies combining genetics, ER stressed pathology and relevant environmental epidemiology are warranted.
Abstract: Background
MUC2 mucin produced by intestinal goblet cells is the major component of the intestinal mucus barrier. The inflammatory bowel disease ulcerative colitis is characterized by depleted goblet cells and a reduced mucus layer, but the aetiology remains obscure. In this study we used random mutagenesis to produce two murine models of inflammatory bowel disease, characterised the basis and nature of the inflammation in these mice, and compared the pathology with human ulcerative colitis.
656 citations
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654 citations
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TL;DR: The cellular immune response to the human immunodeficiency virus, mediated by T lymphocytes, seems strong but fails to control the infection completely, and the failure of the latter to function efficiently facilitates the escape of virus from immune control and the collapse of the whole immune system.
Abstract: The cellular immune response to the human immunodeficiency virus, mediated by T lymphocytes, seems strong but fails to control the infection completely. In most virus infections, T cells either eliminate the virus or suppress it indefinitely as a harmless, persisting infection. But the human immunodeficiency virus undermines this control by infecting key immune cells, thereby impairing the response of both the infected CD4+ T cells and the uninfected CD8+ T cells. The failure of the latter to function efficiently facilitates the escape of virus from immune control and the collapse of the whole immune system.
653 citations
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TL;DR: Findings indicate a possible molecular basis for this HLA-disease association and support the candidacy of liver-stage-specific antigen-1 as a malaria vaccine component.
Abstract: The protective association between the human leukocyte antigen HLA-B53 and severe malaria was investigated by sequencing of peptides eluted from this molecule followed by screening of candidate epitopes from pre-erythrocytic-stage antigens of Plasmodium falciparum in biochemical and cellular assays. Among malaria-immune Africans, HLA-B53-restricted cytotoxic T lymphocytes recognized a conserved nonamer peptide from liver-stage-specific antigen-1 (LSA-1), but no HLA-B53-restricted epitopes were identified in other antigens. These findings indicate a possible molecular basis for this HLA-disease association and support the candidacy of liver-stage-specific antigen-1 as a malaria vaccine component.
652 citations
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TL;DR: It is shown that genes regulating cell death can be hypoxically induced and are overexpressed in clinical tumors and that BNIP3 is up-regulated in perinecrotic regions of the tumor.
Abstract: Solid tumors contain regions of hypoxia, a physiological stress that can activate cell death pathways and, thus, result in the selection of cells resistant to death signals and anticancer therapy. Bcl2/adenovirus EIB 19kD-interacting protein 3 (BNIP3) is a cell death factor that is a member of the Bcl-2 proapoptotic family recently shown to induce necrosis rather than apoptosis. Using cDNA arrays and serial analysis of gene expression, we found that hypoxia induces up-regulation of BNIP3 and its homologue, Nip3-like protein X. Analysis of human carcinoma cell lines showed that they are hypoxically regulated in many tumor types, as well as in endothelial cells and macrophages. Regulation was hypoxia inducible factor-1-dependent, and hypoxia inducible factor-1 expression was suppressed by von Hippel-Lindau protein in normoxic cells. Northern blotting and in situ hybridization analysis has revealed that these factors are highly expressed in human tumors compared with normal tissue and that BNIP3 is up-regulated in perinecrotic regions of the tumor. This study shows that genes regulating cell death can be hypoxically induced and are overexpressed in clinical tumors.
652 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 |