Institution
London Clinic
Healthcare•London, United Kingdom•
About: London Clinic is a healthcare organization based out in London, United Kingdom. It is known for research contribution in the topics: Cancer & Survival rate. The organization has 279 authors who have published 301 publications receiving 9614 citations.
Papers published on a yearly basis
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Beth Israel Deaconess Medical Center1, University of Wisconsin-Madison2, University of Southampton3, Mayo Clinic4, Peking University5, Seoul National University Hospital6, Institut Gustave Roussy7, Anschutz Medical Campus8, Rhode Island Hospital9, Harvard University10, University Health Network11, London Clinic12, University of Wisconsin Hospital and Clinics13, University of Pisa14, Wayne State University15, University of California, Los Angeles16, University of California, Davis17, Albert Einstein Medical Center18
TL;DR: This updated consensus document provides a framework that will facilitate the clearest communication among investigators regarding ablative technologies and improve the precision of communications in this field, leading to more accurate comparison of technologies and results, and ultimately to improved patient outcomes.
Abstract: The main objective of this document is to improve precision in communication in the field of image-guided tumor ablation that leads to more accurate comparison of technologies and results and ultimately to improved patient outcomes.
1,001 citations
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TL;DR: The authors' finding of isolated nerve fibres that express substance P deep within diseased intervertebral discs and their association with pain suggests an important role for nerve growth into the interverTEbral disc in the pathogenesis of chronic low back pain.
917 citations
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TL;DR: The results of an extensive analysis of computerized tomography scans using Simplant software demonstrate that an objective scale of bone density based on the Houndsfield scale, can be established and that there is a strong correlation between bone density value and subjective quality score.
Abstract: Dental implants are subject to masticatory loads of varying magnitude. Implant performance is closely related to load transmission at the bone-to-implant interface where bone quality will be highly variable. The type and architecture of bone is known to influence its load bearing capacity and it has been demonstrated that poorer quality bone is associated with higher failure rates. To date, bone classifications have only provided rough subjective methods for pre-operative assessment, which can prove unreliable. The results of an extensive analysis of computerized tomography scans using Simplant software (Columbia Scientific Inc., Columbia, MD, USA) demonstrate that an objective scale of bone density based on the Houndsfield scale, can be established and that there is a strong correlation between bone density value and subjective quality score (P = 0.002) as well as between the bone density score and the region of the mouth (P < 0.001).
416 citations
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TL;DR: Findings show that nociceptive nerve ingrowth into painful IVD is causally linked with NGF production by blood vessels growing into the IVD, from adjacent vertebral bodies.
Abstract: Following a previous description of nociceptive nerve fibre growth into usually aneural inner parts of painful intervertebral disc (IVD), this study has investigated whether nociceptive nerve ingrowth into painful IVD is stimulated by local production of neurotrophins. Immunohistochemistry and in situ hybridization have been used to investigate expression of the candidate neurotrophin, nerve growth factor (NGF), and its high- and low-affinity receptors trk-A and p75, respectively, in painful IVD excised for the management of low back pain. IVD from patients with back pain were of two types: those that when examined by discography reproduced the patient symptoms (pain level IVD) and those that did not (non-pain level IVD). Microvascular blood vessels accompanied nerve fibres growing into pain level IVD and these expressed NGF. The adjacent nerves expressed the high-affinity NGF receptor trk-A. These vessels entered the normally avascular IVD through the discal end plates. NGF expression was not identified in non-pain level or control IVD. Some non-pain level IVD had vessels within them, which entered through the annulus fibrosus. These did not express NGF nor did nerves accompany them. These findings show that nociceptive nerve ingrowth into painful IVD is causally linked with NGF production by blood vessels growing into the IVD, from adjacent vertebral bodies.
415 citations
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TL;DR: The elevated alveolar-arterial oxygen difference that is seen in subjects who are in conditions of extreme hypoxia may represent a degree of subclinical high-altitude pulmonary edema or a functional limitation in pulmonary diffusion.
Abstract: Background: The level of environmental hypobaric hypoxia that affects climbers at the summit of Mount Everest (8848 m [29,029 ft]) is close to the limit of tolerance by humans. We performed direct field measurements of arterial blood gases in climbers breathing ambient air on Mount Everest. Methods: We obtained samples of arterial blood from 10 climbers during their ascent to and descent from the summit of Mount Everest. The partial pressures of arterial oxygen (PaO2) and carbon dioxide (PaCO2), pH, and hemoglobin and lactate concentrations were measured. The arterial oxygen saturation (SaO2), bicarbonate concentration, base excess, and alveolar-arterial oxygen difference were calculated. Results: PaO2 fell with increasing altitude, whereas SaO2 was relatively stable. The hemoglobin concentration increased such that the oxygen content of arterial blood was maintained at or above sea-level values until the climbers reached an elevation of 7100 m (23,294 ft). In four samples taken at 8400 m (27,559 ft) - at which altitude the barometric pressure was 272 mm Hg (36.3 kPa) - the mean PaO2 in subjects breathing ambient air was 24.6 mm Hg (3.28 kPa), with a range of 19.1 to 29.5 mm Hg (2.55 to 3.93 kPa). The mean PaCO2 was 13.3 mm Hg (1.77 kPa), with a range of 10.3 to 15.7 mm Hg (1.37 to 2.09 kPa). At 8400 m, the mean arterial oxygen content was 26% lower than it was at 7100 m (145.8 ml per liter as compared with 197.1 ml per liter). The mean calculated alveolar-arterial oxygen difference was 5.4 mm Hg (0.72 kPa). Conclusions: The elevated alveolar-arterial oxygen difference that is seen in subjects who are in conditions of extreme hypoxia may represent a degree of subclinical high-altitude pulmonary edema or a functional limitation in pulmonary diffusion. Copyright © 2009 Massachusetts Medical Society.
397 citations
Authors
Showing all 281 results
Name | H-index | Papers | Citations |
---|---|---|---|
Sergio Giralt | 109 | 1024 | 48513 |
John F. DiPersio | 98 | 708 | 47154 |
Ann F. Chambers | 88 | 297 | 27266 |
Allan Donner | 82 | 284 | 30079 |
Issa F. Khouri | 71 | 399 | 17746 |
G. M. Besser | 71 | 286 | 15583 |
Prokar Dasgupta | 68 | 721 | 17482 |
Gordon Stamp | 61 | 147 | 14639 |
John A. Collins | 61 | 205 | 13451 |
Binith Cheeran | 35 | 64 | 4633 |
Daniel Martin | 34 | 158 | 4469 |
Alice Gillams | 27 | 48 | 5681 |
J. M. A. Northover | 27 | 44 | 4558 |
Michael Potter | 24 | 89 | 1974 |
John E. Biaglow | 24 | 59 | 1775 |