Institution
Wellington Hospital
Healthcare•Wellington, New Zealand•
About: Wellington Hospital is a healthcare organization based out in Wellington, New Zealand. It is known for research contribution in the topics: Population & Intensive care. The organization has 1542 authors who have published 1717 publications receiving 41653 citations.
Papers published on a yearly basis
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TL;DR: In the Global Burden of Disease Study 2013 (GBD 2013) as mentioned in this paper, the authors estimated the quantities for acute and chronic diseases and injuries for 188 countries between 1990 and 2013.
4,510 citations
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TL;DR: Of 22 patients undergoing repeat open-heart surgery through a previous median sternotomy wound 11 were randomised to receive the serine proteinase inhibitor aprotinin in high dosage, seven of whom received only the single unit of their own blood taken before cardiopulmonary bypass.
632 citations
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TL;DR: In five families with mosaic variegated aneuploidy, including two with embryonal rhabdomyosarcoma, truncating and missense mutations of BUB1B are identified, which encodes BUBR1, a key protein in the mitotic spindle checkpoint.
Abstract: Mosaic variegated aneuploidy is a rare recessive condition characterized by growth retardation, microcephaly, childhood cancer and constitutional mosaicism for chromosomal gains and losses. In five families with mosaic variegated aneuploidy, including two with embryonal rhabdomyosarcoma, we identified truncating and missense mutations of BUB1B, which encodes BUBR1, a key protein in the mitotic spindle checkpoint. These data are the first to relate germline mutations in a spindle checkpoint gene with a human disorder and strongly support a causal link between aneuploidy and cancer development.
599 citations
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University College London1, Guy's and St Thomas' NHS Foundation Trust2, Glenfield Hospital3, Institute of Cancer Research4, St George's Hospital5, Wellington Hospital6, St James's University Hospital7, Leicester Royal Infirmary8, VU University Amsterdam9, Trinity College, Dublin10, Northern General Hospital11, University of London12
TL;DR: The data suggest that radical surgery in the form of EPP within trimodal therapy offers no benefit and possibly harms patients and a larger study is not feasible.
Abstract: Background The eff ects of extra-pleural pneumonectomy (EPP) on survival and quality of life in patients with malignant pleural mesothelioma have, to our knowledge, not been assessed in a randomised trial. We aimed to assess the clinical outcomes of patients who were randomly assigned to EPP or no EPP in the context of trimodal therapy in the Mesothelioma and Radical S urgery (MARS) feasibility study. Methods MARS was a multicentre randomised controlled trial in 12 UK hospitals. Patients aged 18 years or older who had pathologically confi rmed mesothelioma and were deemed fi t enough to undergo trimodal therapy were included. In a prerandomisation registration phase, all patients underwent induction platinum-based chemotherapy followed by clinical review. Af ter further consent, patients were randomly assigned (1:1) to EPP followed by postoperative hemithorax irradiation or to no EPP. Randomisation was done centrally with computer-generated permuted blocks stratifi ed by surgical centre. The main endpoints were feasibility of randomly assigning 50 patients in 1 year (results detailed in another report), proportion randomised who received treatment, proportion eligible (registered) who proceeded to randomisation, perioperative mortality, and quality of life. Patients and investigators were not masked to treatment allocation. This is the principal report of the MARS study; all patients have been recruited. Analyses were by intention to treat. This trial is registered, number ISRCTN95583524. Findings Between Oct 1, 2005, and Nov 3, 2008, 112 patients were registered and 50 were subsequently randomly assigned: 24 to EPP and 26 to no EPP. The main reasons for not proceeding to randomisation were disease progression (33 patients), inoperability (fi ve patients), and patient choice (19 patients). EPP was completed satisfactorily in 16 of 24 patients assigned to EPP; in fi ve patients EPP was not started and in three patients it was abandoned. Two patients in the EPP group died within 30 days and a further patient died without leaving hospital. One patient in the no EPP group died perioperatively af ter receiving EPP off trial in a non-MARS centre. The hazard ratio [HR] for overall survival between the EPP and no EPP groups was 1·90 (95% CI 0·92–3·93; exact p=0·082), and after adjustment for sex, histological subtype, stage, and age at randomisation the HR was 2·75 (1·21–6·26; p=0·016). Median survival was 14·4 months (5·3–18·7) for the EPP group and 19·5 months (13·4 to time not yet reached) for the no EPP group. Of the 49 randomly assigned patients who consented to quality of life assessment (EPP n=23; no EPP n=26), 12 patients in the EPP group and 19 in the no EPP group completed the quality of life questionnaires. Although median quality of life scores were lower in the EPP group than the no EPP group, no signifi cant diff erences between groups were reported in the quality of life analyses. There were ten serious adverse events reported in the EPP group and two in the no EPP group. Interpretation In view of the high morbidity associated with EPP in this trial and in other non-randomised studies a larger study is not feasible. These data, although limited, suggest that radical surgery in the form of EPP within trimodal therapy off ers no benefi t and possibly harms patients.
588 citations
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TL;DR: Autosomal recessive primary microcephaly is a potential model in which to research genes involved in human brain growth and neuroepithelial expression of the genes during prenatal neurogenesis and protein localization to the spindle poles of mitotic cells is found, suggesting that a centrosomal mechanism controls neuron number in the developing mammalian brain.
Abstract: Autosomal recessive primary microcephaly is a potential model in which to research genes involved in human brain growth. We show that two forms of the disorder result from homozygous mutations in the genes CDK5RAP2 and CENPJ. We found neuroepithelial expression of the genes during prenatal neurogenesis and protein localization to the spindle poles of mitotic cells, suggesting that a centrosomal mechanism controls neuron number in the developing mammalian brain.
547 citations
Authors
Showing all 1546 results
Name | H-index | Papers | Citations |
---|---|---|---|
Rinaldo Bellomo | 147 | 1714 | 120052 |
Neil Pearce | 107 | 729 | 105762 |
Richard Beasley | 90 | 621 | 45696 |
Graeme Eisenhofer | 89 | 534 | 30487 |
Martin H.N. Tattersall | 80 | 373 | 22761 |
Brian R. Davidson | 75 | 557 | 21214 |
Beverley J. Hunt | 74 | 380 | 27474 |
Philip Robinson | 68 | 443 | 16164 |
Keith Grimwood | 63 | 346 | 12640 |
Mark Weatherall | 62 | 380 | 12480 |
Stephen R. Holdsworth | 62 | 253 | 11442 |
Peter G. Tipping | 59 | 139 | 10404 |
David Lamb | 56 | 399 | 13856 |
Peter M. Ellis | 54 | 321 | 13579 |
Avijit Lahiri | 53 | 273 | 9923 |