Institution
Royal Adelaide Hospital
Healthcare•Adelaide, South Australia, Australia•
About: Royal Adelaide Hospital is a healthcare organization based out in Adelaide, South Australia, Australia. It is known for research contribution in the topics: Population & Gastric emptying. The organization has 5830 authors who have published 10241 publications receiving 347876 citations. The organization is also known as: Adelaide Hospital & RAH.
Topics: Population, Gastric emptying, Transplantation, Medicine, Cancer
Papers published on a yearly basis
Papers
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TL;DR: The ability to detect oleic acid both orally and within the gastrointestinal tract is compromised in obese men, and oral and gastrointestinal responses to oleoic acid are related.
153 citations
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TL;DR: The aim of this Review is to comprehensively evaluate measures of disease activity in both ulcerative colitis and Crohn's disease, including clinical, endoscopic, histological and radiological assessment tools, as well as the use of biomarkers and quality of life evaluation.
Abstract: Therapeutic advances in the management of IBD have led to a paradigm shift in the assessment of IBD disease activity. Beyond clinical remission, objective assessment of inflammation is now critical to guiding subsequent therapy as part of a 'treat to target' strategy. Multiple domains of disease activity assessment in IBD exist, each of which has its merits, although none are perfect. The aim of this Review is to comprehensively evaluate measures of disease activity in both ulcerative colitis and Crohn's disease, including clinical, endoscopic, histological and radiological assessment tools, as well as the use of biomarkers and quality of life evaluation. A subjective appraisal of the best indices for use in clinical practice is provided, based on index validation, responsiveness and experience in clinical trials, international specialist opinion, and practicality and suitability for use in clinical practice. This Review aims to enable the reader to gain confidence in IBD disease activity assessment and to give ready access to the necessary tools.
153 citations
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TL;DR: It is suggested that Elovl2 will be critical in understanding if DHA synthesis can be increased by dietary means and the competition between ALA and 24:5n-3 for Fads2 may explain the decrease in DHA levels observed after certain intakes of dietary ALA have been exceeded.
Abstract: Background
Δ6-Desaturase (Fads2) is widely regarded as rate-limiting in the conversion of dietary α-linolenic acid (18:3n-3; ALA) to the long-chain omega-3 polyunsaturated fatty acid docosahexaenoic acid (22:6n-3; DHA). However, increasing dietary ALA or the direct Fads2 product, stearidonic acid (18:4n-3; SDA), increases tissue levels of eicosapentaenoic acid (20:5n-3; EPA) and docosapentaenoic acid (22:5n-3; DPA), but not DHA. These observations suggest that one or more control points must exist beyond ALA metabolism by Fads2. One possible control point is a second reaction involving Fads2 itself, since this enzyme catalyses desaturation of 24:5n-3 to 24:6n-3, as well as ALA to SDA. However, metabolism of EPA and DPA both require elongation reactions. This study examined the activities of two elongase enzymes as well as the second reaction of Fads2 in order to concentrate on the metabolism of EPA to DHA.
153 citations
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TL;DR: Transient LES relaxation and associated inhibition of the crural diaphragm was the major mechanism of reflux under conditions of low LES pressure induced by atropine, which does not predispose to reflux in normal healthy subjects.
152 citations
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TL;DR: Zoledronic acid inhibits osteoclast maturation indirectly by increasing OPG protein secretion and decreasing transmembrane RANKL expression in human osteoblasts, which seems to be related to the upregulation of the RankL sheddase, TACE.
Abstract: Bisphosphonates are used to prevent osteoclast-mediated bone loss. Zoledronic acid inhibits osteoclast maturation indirectly by increasing OPG protein secretion and decreasing transmembrane RANKL expression in human osteoblasts. The decreased transmembrane RANKL expression seems to be related to the upregulation of the RANKL sheddase, TACE.
Introduction: Bisphosphonates (BPs) exhibit high affinity for hydroxyapatite mineral in bone and are used extensively to treat malignancy-associated bone disease and postmenopausal bone loss by inhibiting osteoclast (OC)-mediated bone resorption.
Materials and Methods: We examined the effect of the most potent nitrogen-containing BP available, zoledronic acid (ZOL), on the expression of RANKL and osteoprotegerin (OPG), critical factors in the regulation of OC formation and activation, in primary osteoblast (OB)-like cells derived from human bone, using flow cytometry, ELISA, semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR), in situ immunofluorescence staining, and Western blotting.
Results: Our studies show that ZOL, while not significantly affecting RANKL or OPG gene expression, markedly increased OPG protein secretion and reduced transmembrane RANKL protein expression in OB-like cells. The reduction in transmembrane RANKL expression was preceded by a marked increase in the expression of the metalloprotease-disintegrin, TNF-α converting enzyme (TACE). In addition, the decreased transmembrane expression of RANKL could be partially reversed by a TACE inhibitor, TAPI-2.
Conclusions: Our studies indicate that ZOL, in addition to its direct effects on mature OCs, may inhibit the recruitment and differentiation of OCs by cleavage of transmembrane RANKL in OB-like cells by upregulating the sheddase, TACE.
152 citations
Authors
Showing all 5858 results
Name | H-index | Papers | Citations |
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Nicholas J. Talley | 158 | 1571 | 90197 |
John E. Morley | 154 | 1377 | 97021 |
Timothy P. Hughes | 145 | 831 | 91357 |
Christopher Hill | 144 | 1562 | 128098 |
John D. Potter | 137 | 795 | 75310 |
Daniel Thomas | 134 | 846 | 84224 |
Neville Owen | 127 | 700 | 74166 |
Linda Partridge | 118 | 491 | 56738 |
Michael Horowitz | 112 | 982 | 46952 |
Robert J. Norman | 103 | 755 | 45147 |
Craig S. Anderson | 101 | 650 | 49331 |
Helen E. Heslop | 97 | 523 | 36292 |
Philip J. Barter | 96 | 466 | 56118 |
Charles G. Mullighan | 94 | 435 | 37925 |
Prashanthan Sanders | 93 | 676 | 34146 |