Institution
St Thomas' Hospital
Healthcare•London, United Kingdom•
About: St Thomas' Hospital is a healthcare organization based out in London, United Kingdom. It is known for research contribution in the topics: Population & Pregnancy. The organization has 12105 authors who have published 15596 publications receiving 624309 citations. The organization is also known as: St Thomas's Hospital & St. Thomas's.
Papers published on a yearly basis
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Royal Devon and Exeter Hospital1, University of Queensland2, Queen Mary University of London3, University of Exeter4, Northwestern University5, University of Oxford6, Wellcome Trust Centre for Human Genetics7, Statens Serum Institut8, Norwegian Institute of Public Health9, University of Bristol10, Erasmus University Rotterdam11, Children's Hospital of Philadelphia12, University of Copenhagen13, Copenhagen University Hospital14, University of Oulu15, St Thomas' Hospital16, Boston University17, QIMR Berghofer Medical Research Institute18, VU University Medical Center19, VU University Amsterdam20, Centre Hospitalier Universitaire de Sherbrooke21, University of Southampton22, Pompeu Fabra University23, University of Western Australia24, Newcastle University25, March of Dimes26, Cincinnati Children's Hospital Medical Center27, UCL Institute of Child Health28, Université de Sherbrooke29, University of Pennsylvania30, University of Helsinki31, University of Bergen32, University of Potsdam33, Jinan University34, University Hospital Southampton NHS Foundation Trust35, University of Ferrara36, University of Iowa37, Haukeland University Hospital38, University of Southern Denmark39, Charité40, Health Protection Agency41, Sahlgrenska University Hospital42, University of Crete43, Stanford University44, National Institute for Health Research45, Harvard University46, University of South Australia47
TL;DR: The identified associations indicate that genetic effects on maternal glucose, cytochrome P450 activity and gestational duration, and potentially on maternal blood pressure and immune function, are relevant for fetal growth.
Abstract: Genome-wide association studies (GWAS) of birth weight have focused on fetal genetics, while relatively little is known about the role of maternal genetic variation. We aimed to identify maternal genetic variants associated with birth weight that could highlight potentially relevant maternal determinants of fetal growth. We meta-analysed data on up to 8.7 million SNPs in up to 86,577 women of European descent from the Early Growth Genetics (EGG) Consortium and the UK Biobank. We used structural equation modelling (SEM) and analyses of mother-child pairs to quantify the separate maternal and fetal genetic effects. Maternal SNPs at 10 loci (MTNR1B, HMGA2, SH2B3, KCNAB1, L3MBTL3, GCK, EBF1, TCF7L2, ACTL9, CYP3A7) were associated with offspring birth weight at P<5x10-8. In SEM analyses, at least 7 of the 10 associations were consistent with effects of the maternal genotype acting via the intrauterine environment, rather than via effects of shared alleles with the fetus. Variants, or correlated proxies, at many of the loci had been previously associated with adult traits, including fasting glucose (MTNR1B, GCK and TCF7L2) and sex hormone levels (CYP3A7), and one (EBF1) with gestational duration. The identified associations indicate genetic effects on maternal glucose, cytochrome P450 activity and gestational duration, and potentially on maternal blood pressure and immune function, are relevant for fetal growth. Further characterization of these associations in mechanistic and causal analyses will enhance understanding of the potentially modifiable maternal determinants of fetal growth, with the goal of reducing the morbidity and mortality associated with low and high birth weights.
147 citations
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TL;DR: Central nervous system (CNS) involvement is one of the most prominent clinical manifestations of APS, and includes arterial and venous thrombotic events, psychiatric features and a variety of other non-thrombosis neurological syndromes.
Abstract: The antiphospholipid (Hughes) syndrome (APS) is characterized by arterial and/or venous thrombosis and pregnancy morbidity in the presence of anticardiolipin antibodies and/or lupus anticoagulant. APS can occur either as a primary disorder or secondary to a connective tissue disease, most frequently systemic lupus erythematosus. Central nervous system (CNS) involvement is one of the most prominent clinical manifestations of APS, and includes arterial and venous thrombotic events, psychiatric features and a variety of other non-thrombotic neurological syndromes. In this review we focus on the common and some of the less common CNS manifestations that have been reported in association with antiphospholipid antibodies.
147 citations
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TL;DR: In this article, the effects of three prostaglandin analogs, bimatoprost, latanoprost and travoprost on aqueous dynamics in the same subjects and to compare techniques of assessing outflow facility were studied.
147 citations
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TL;DR: Monoclonal aCL may recognize a cryptic epitope, which appears as a result of beta 2-GPI binding to anionic PLs or to polystyrene with carboxyl groups.
Abstract: Objective To elucidate the specificity of anticardiolipin antibodies (aCL) from patients with the antiphospholipid syndrome (APS) to various phospholipids (PLs), DNA, and beta 2-glycoprotein I (beta 2-GPI). Methods Five monoclonal aCL were established from peripheral blood lymphocytes of 3 patients with the APS. The reactivity of monoclonal aCL with various PLs, with DNA, and with beta 2-GPI was examined by enzyme-linked immunosorbent assay (ELISA). Results All of the monoclonal aCL bound to anionic PLs, only in the presence of beta 2-GPI. Neither monoclonal aCL nor beta 2-GPI bound to DNA. Monoclonal aCL bound to solid-phase beta 2-GPI on polystyrene ELISA plates that had carboxyl groups on their surface, but did not react with solid-phase beta 2-GPI on ordinary polystyrene plates. A mixture of beta 2-GPI and CL inhibited the binding of monoclonal aCL to beta 2-GPI, but CL or beta 2-GPI alone did not. Conclusion Monoclonal aCL may recognize a cryptic epitope, which appears as a result of beta 2-GPI binding to anionic PLs or to polystyrene with carboxyl groups.
146 citations
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TL;DR: The role of NGF in the peripheral sensitization of nociceptors and brain-derived neurotrophic factor (BDNF) as a central pain modulator is highlighted.
Abstract: Neurotrophic factors have an established developmental role in regulating the survival and specification of sensory neurons. However, these factors continue to exert an important influence on sensory neurons throughout the postnatal period and into adult life. In adulthood, approximately one-half of nociceptors are dependent on nerve growth factor (NGF) for trophic support, whereas the other half are sensitive to glial cell line-derived neurotrophic factor (GDNF). It is now known that many chronic pain states are maintained by widespread changes in the anatomy, neurochemistry, and function of the sensory nervous system both at the level of the primary sensory neuron and the dorsal horn of the spinal cord. Trophic factors appear to orchestrate many of these dynamic changes. This review highlights some of the key roles played by these molecules and in particular the role of NGF in the peripheral sensitization of nociceptors and brain-derived neurotrophic factor (BDNF) as a central pain modulator.
146 citations
Authors
Showing all 12132 results
Name | H-index | Papers | Citations |
---|---|---|---|
David J. Hunter | 213 | 1836 | 207050 |
Rory Collins | 162 | 489 | 193407 |
Steven Williams | 144 | 1375 | 86712 |
Geoffrey Burnstock | 141 | 1488 | 99525 |
Nick C. Fox | 139 | 748 | 93036 |
Christopher D.M. Fletcher | 138 | 674 | 82484 |
David A. Jackson | 136 | 1095 | 68352 |
Paul Harrison | 133 | 1400 | 80539 |
Roberto Ferrari | 133 | 1654 | 103824 |
David Taylor | 131 | 2469 | 93220 |
Keith Hawton | 125 | 657 | 55138 |
Nicole Soranzo | 124 | 316 | 74494 |
Roger Williams | 122 | 1455 | 72416 |
John C. Chambers | 122 | 645 | 71028 |
Derek M. Yellon | 122 | 638 | 54319 |