Institution
University of Otago
Education•Dunedin, New Zealand•
About: University of Otago is a education organization based out in Dunedin, New Zealand. It is known for research contribution in the topics: Population & Poison control. The organization has 21668 authors who have published 53810 publications receiving 1835189 citations. The organization is also known as: Otago University & otago.ac.nz.
Papers published on a yearly basis
Papers
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TL;DR: Data suggest that the base following the stop codon influences translational termination efficiency as part of a larger termination signal in the expression of mammalian genes.
Abstract: The base following stop codons in mammalian genes is strongly biased, suggesting that it might be important for the termination event. This proposal has been tested experimentally both in vivo by using the human type I iodothyronine deiodinase mRNA and the recoding event at the internal UGA codon and in vitro by measuring the ability of each of the 12 possible 4-base stop signals to direct the eukaryotic polypeptide release factor to release a model peptide, formylmethionine, from the ribosome. The internal UGA in the deiodinase mRNA is used as a codon for incorporation of selenocysteine into the protein. Changing the base following this UGA codon affected the ratio of termination to selenocysteine incorporation in vivo at this codon: 1:3 (C or U) and 3:1 (A or G). These UGAN sequences have the same order of efficiency of termination as was found with the in vitro termination assay (4th base: A approximately G >> C approximately U). The efficiency of in vitro termination varied in the same manner over a 70-fold range for the UAAN series and over an 8-fold range for the UGAN and UAGN series. There is a correlation between the strength of the signals and how frequently they occur at natural termination sites. Together these data suggest that the base following the stop codon influences translational termination efficiency as part of a larger termination signal in the expression of mammalian genes.
276 citations
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TL;DR: It is demonstrated that germline mutation of the E‐cadherin gene is a common cause of hereditary diffuse gastric cancer and a role for these mutations in the incidence of breast cancer is suggested.
Abstract: To extend earlier observations of germline E-cadherin mutations in kindreds with an inherited susceptibility to diffuse gastric cancer, we searched for germline E-cadherin mutations in five further families affected predominantly by diffuse gastric cancer and one family with a history of diffuse gastric cancer and early-onset breast cancer. Heterozygous inactivating mutations were found in the E-cadherin gene in each of these families. No mutation hotspots were identified. These results demonstrate that germline mutation of the E-cadherin gene is a common cause of hereditary diffuse gastric cancer and suggest a role for these mutations in the incidence of breast cancer. Hum Mutat 14:249–255, 1999. © 1999 Wiley-Liss, Inc.
276 citations
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University of Toronto1, University of Washington2, Stanford University3, University of Leeds4, University College Dublin5, Tufts University6, University of Utah7, University of Queensland8, University of Rochester9, University of Otago10, University of Sheffield11, University of Cagliari12, Federal University of Rio de Janeiro13, King's College London14, VU University Amsterdam15, LSU Health Sciences Center New Orleans16, Maastricht University17, Harvard University18, Hospital Italiano de Buenos Aires19
TL;DR: A psoriatic arthritis (PsA) module was convened at OMERACT 8 in order to achieve consensus on the core domains that should be included in randomized controlled trials and longitudinal observational cohorts of subjects with PsA.
Abstract: A psoriatic arthritis (PsA) module was convened at OMERACT 8 in order to achieve consensus on the core domains that should be included in randomized controlled trials and longitudinal observational cohorts of subjects with PsA. Following a plenary session at which current status of measures used to assess PsA were reviewed, and discussion at breakout groups, the group achieved consensus on 6 core domains: peripheral joint activity, skin activity, pain, patient global assessment, physical function, and health-related quality of life. In addition the following domains were considered important but not mandatory: spinal disease, dactylitis, enthesitis, fatigue, nail disease, radiography, physician global assessment, and acute-phase reactants. A research agenda was proposed to include development and validation of instruments for the domains where none existed, and in particular further research was recommended for the following areas: magnetic resonance imaging and ultrasound of joints, enthesitis, skin and synovial tissue analysis, and "participation."
276 citations
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TL;DR: The aim was to determine whether a low FODMAP diet improves symptoms in IBS patients.
Abstract: SummaryBackground and aim
Current treatment for irritable bowel syndrome (IBS) is suboptimal. Fermentable oligo-, di-, mono-saccharides and polyols (FODMAPs) may trigger gastrointestinal symptoms in IBS patients. Our aim was to determine whether a low FODMAP diet improves symptoms in IBS patients.
Methods
Irritable bowel syndrome patients, who had performed hydrogen/methane breath testing for fructose and lactose malabsorption and had received dietary advice regarding the low FODMAP diet, were included. The effect of low FODMAP diet was prospectively evaluated using a symptom questionnaire. Furthermore, questions about adherence and satisfaction with symptom improvement, dietary advice and diet were assessed.
Results
Ninety patients with a mean follow up of 15.7 months were studied. Most symptoms including abdominal pain, bloating, flatulence and diarrhoea significantly improved (p 0.27, p < 0.011). Most patients (72.1%) were satisfied with their symptoms.
Conclusions
The low FODMAP diet shows efficacy for IBS patients. The current strategy of breath testing and dietary advice provides a good basis to understand and adhere to the diet.
276 citations
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TL;DR: This review systematically analyzed various aspects that explain the limited clinical progress yet achieved and reviewed results from over one hundred publications to construct patterns of factors that can influence the transition of EPR based anticancer nanomedicine to the clinic.
275 citations
Authors
Showing all 21953 results
Name | H-index | Papers | Citations |
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David Miller | 203 | 2573 | 204840 |
Terrie E. Moffitt | 182 | 594 | 150609 |
Tien Yin Wong | 160 | 1880 | 131830 |
Grant W. Montgomery | 157 | 926 | 108118 |
Ichiro Kawachi | 149 | 1216 | 90282 |
David M. Fergusson | 127 | 474 | 55992 |
Carlos A. Camargo | 125 | 1283 | 69143 |
Philip H Butler | 125 | 970 | 71999 |
Francis V. Chisari | 123 | 322 | 54772 |
Michael P. Murphy | 120 | 601 | 53338 |
Guy S. Salvesen | 116 | 337 | 75598 |
Mitch Dowsett | 114 | 478 | 62453 |
Valerie Beral | 114 | 471 | 53729 |
Gordon Dougan | 114 | 715 | 55037 |
Christopher A. Hunter | 113 | 633 | 52559 |