Institution
University of Newcastle
Education•Newcastle, New South Wales, Australia•
About: University of Newcastle is a education organization based out in Newcastle, New South Wales, Australia. It is known for research contribution in the topics: Population & Health care. The organization has 19211 authors who have published 51893 publications receiving 1694726 citations. The organization is also known as: Newcastle University.
Topics: Population, Health care, Context (language use), Poison control, Randomized controlled trial
Papers published on a yearly basis
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University of Queensland1, University of Glasgow2, QIMR Berghofer Medical Research Institute3, Garvan Institute of Medical Research4, Baylor College of Medicine5, University of Utah6, South Australia Pathology7, University of Adelaide8, Harvard University9, Campbelltown Hospital10, St. Vincent's Health System11, University of New South Wales12, University of Newcastle13, Royal North Shore Hospital14, Royal Prince Alfred Hospital15, University of Sydney16, Fiona Stanley Hospital17, Royal Adelaide Hospital18, Princess Alexandra Hospital19, University of Western Australia20, Beatson West of Scotland Cancer Centre21, Southern General Hospital22, Dresden University of Technology23, University of Texas MD Anderson Cancer Center24, Memorial Sloan Kettering Cancer Center25, Johns Hopkins University School of Medicine26, University of Verona27, Mayo Clinic28, University of Melbourne29
TL;DR: Detailed genomic analysis of 456 pancreatic ductal adenocarcinomas identified 32 recurrently mutated genes that aggregate into 10 pathways: KRAS, TGF-β, WNT, NOTCH, ROBO/SLIT signalling, G1/S transition, SWI-SNF, chromatin modification, DNA repair and RNA processing.
Abstract: Integrated genomic analysis of 456 pancreatic ductal adenocarcinomas identified 32 recurrently mutated genes that aggregate into 10 pathways: KRAS, TGF-β, WNT, NOTCH, ROBO/SLIT signalling, G1/S transition, SWI-SNF, chromatin modification, DNA repair and RNA processing. Expression analysis defined 4 subtypes: (1) squamous; (2) pancreatic progenitor; (3) immunogenic; and (4) aberrantly differentiated endocrine exocrine (ADEX) that correlate with histopathological characteristics. Squamous tumours are enriched for TP53 and KDM6A mutations, upregulation of the TP63∆N transcriptional network, hypermethylation of pancreatic endodermal cell-fate determining genes and have a poor prognosis. Pancreatic progenitor tumours preferentially express genes involved in early pancreatic development (FOXA2/3, PDX1 and MNX1). ADEX tumours displayed upregulation of genes that regulate networks involved in KRAS activation, exocrine (NR5A2 and RBPJL), and endocrine differentiation (NEUROD1 and NKX2-2). Immunogenic tumours contained upregulated immune networks including pathways involved in acquired immune suppression. These data infer differences in the molecular evolution of pancreatic cancer subtypes and identify opportunities for therapeutic development.
2,443 citations
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TL;DR: The aim of the twenty‐year follow-up survey was to determine the Incidence and natural history of thyroid disease in this cohort.
Abstract: Summary
BACKGROUND AND OBJECTIVE The original Whlckham Survey documented the prevalence of thyroid disorders in a randomly selected sample of 2779 adults which matched the population of Great Britain in age, sex and social class. The aim of the twenty-year follow-up survey was to determine the Incidence and natural history of thyroid disease in this cohort.
DESIGN, PATIENTS AND MEASUREMENTS Subjects were traced at follow-up via the Electoral Register, General Practice registers, Gateshead Family Health Services Authority register and Office of Population Censuses and Surveys. Eight hundred and twenty-five subjects (30% of the sample) had died and, In addition to death certificates, two-thirds had Information from either hospital/General Practitioner notes or post-mortem reports to document morbidity prior to death. Of the 1877 known survivors, 96% participated in the follow-up study and 91 % were tested for clinical, biochemical and Immunological evidence of thyroid dysfunction.
RESULTS Outcomes in terms of morbidity and mortality were determined for over 97% of the original sample. The mean Incidence (with 95% confidence Intervals) of spontaneous hypothyroidism in women was 3.5/1000 survivors/year (2.8-4.5) rising to 4.1/1000 survivors/year (3.3-5.0) for all causes of hypothyroidism and in men was 0.6/1000 survivors/year (0.3-1.2). The mean incidence of hyperthyroidism In women was 0.8/1000 survivors/year (0.5.1.4) and was negligible in men. Similar incidence rates were calculated for the deceased subjects. An estimate of the probability of the development of hypothyroidism and hyperthyroidism at a particular time, i.e. the hazard rate, showed an Increase with age In hypothyroidism but no age relation in hyperthyroidism.
The frequency of goitre decreased with age with 10% of women and 2% of men having a goitre at follow-up, as compared to 23% and 5% in the same subjects respectively at the first survey. The presence of a goitre at either survey was not associated with any clinical or biochemical evidence of thyroid dysfunction. In women, an association was found between the development of a goitre and thyroid-antibody status at follow-up, but not initially.
The risk of having developed hypothyroidism at follow-up was examined with respect to risk factors Identified at first survey. The odds ratios (with 95% confidence Intervals) of developing hypothyroidism with (a) raised serum TSH alone were 8 (3-20) for women and 44 (19-104) for men; (b) positive anti-thyroid antibodies alone were 8 (5-15) for women and 25 (10-63) for men; (c) both raised serum TSH and positive anti-thyroid antibodies were 38 (22-65) for women and 173 (81-370) for men. A loglt model Indicated that Increasing values of serum TSH above 2mU/l at first survey Increased the probability of developing hypothyroidism which was further Increased in the presence of anti-thyroid antibodies. Neither a positive family history of any form of thyroid disease nor parity of women at first survey was associated with Increased risk of developing hypothyroidism. Fasting cholesterol and triglyceride levels at first survey when corrected for age showed no association with the development of hypothyroidism In women.
CONCLUSIONS This historical cohort study has provided Incidence data for thyroid disease over a twenty-year period for a representative cross-sectional sample of the population, and has allowed the determination of the importance of prognostic risk factors for thyroid disease Identified twenty years earlier.
2,134 citations
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TL;DR: It is suggested here that oxidative stress is an important modulator of telomeres loss and that telomere-driven replicative senescence is primarily a stress response.
2,125 citations
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Vanderbilt University1, University of Texas MD Anderson Cancer Center2, University of Pennsylvania3, University of Colorado Denver4, New York University5, University of South Florida6, Peter MacCallum Cancer Centre7, Baylor University Medical Center8, University of Pittsburgh9, Harvard University10, University of Newcastle11, University of California, Los Angeles12, Hoffmann-La Roche13, Veterans Health Administration14, Plexxikon15
TL;DR: Vemurafenib induces clinical responses in more than half of patients with previously treated BRAF V600-mutant metastatic melanoma, and the median overall survival in this study with a long follow-up was approximately 16 months.
Abstract: Approximately 50% of melanomas harbor activating (V600) mutations in the serine– threonine protein kinase B-RAF (BRAF). The oral BRAF inhibitor vemurafenib (PLX4032) frequently produced tumor regressions in patients with BRAF V600– mutant metastatic melanoma in a phase 1 trial and improved overall survival in a phase 3 trial. METHODS We designed a multicenter phase 2 trial of vemurafenib in patients with previously treated BRAF V600–mutant metastatic melanoma to investigate the efficacy of vem urafenib with respect to overall response rate (percentage of treated patients with a tumor response), duration of response, and overall survival. The primary end point was the overall response rate as ascertained by the independent review committee; overall survival was a secondary end point. RESULTS A total of 132 patients had a median follow-up of 12.9 months (range, 0.6 to 20.1). The confirmed overall response rate was 53% (95% confidence interval [CI], 44 to 62; 6% with a complete response and 47% with a partial response), the median duration of response was 6.7 months (95% CI, 5.6 to 8.6), and the median progression-free survival was 6.8 months (95% CI, 5.6 to 8.1). Primary progression was observed in only 14% of patients. Some patients had a response after receiving vemurafenib for more than 6 months. The median overall survival was 15.9 months (95% CI, 11.6 to 18.3). The most common adverse events were grade 1 or 2 arthralgia, rash, photosensitivity, fatigue, and alopecia. Cutaneous squamous-cell carcinomas (the majority, keratoacanthoma type) were diagnosed in 26% of patients. CONCLUSIONS Vemurafenib induces clinical responses in more than half of patients with previously treated BRAF V600–mutant metastatic melanoma. In this study with a long follow-up, the median overall survival was approximately 16 months. (Funded by Hoffmann–La Roche; ClinicalTrials.gov number, NCT00949702.)
1,986 citations
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TL;DR: Partial least squares structural equation modeling (PLS-SEM) has become a popular method for estimating path models with latent variables and their relationships as discussed by the authors, and a common goal of PLSSEM analyses is to identify key success factors and sources of competitive advantage for important target constructs such as customer satisfaction, customer loyalty, behavioral intentions, and user behavior.
Abstract: Partial least squares structural equation modeling (PLS-SEM) has become a popular method for estimating path models with latent variables and their relationships. A common goal of PLS-SEM analyses is to identify key success factors and sources of competitive advantage for important target constructs such as customer satisfaction, customer loyalty, behavioral intentions, and user behavior. Building on an introduction of the fundamentals of measurement and structural theory, this chapter explains how to specify and estimate path models using PLS-SEM. Complementing the introduction of the PLS-SEM method and the description of how to evaluate analysis results, the chapter also offers an overview of complementary analytical techniques. A PLS-SEM application of the widely recognized corporate reputation model illustrates the method.
1,842 citations
Authors
Showing all 19437 results
Name | H-index | Papers | Citations |
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Graham A. Colditz | 261 | 1542 | 256034 |
Martin White | 196 | 2038 | 232387 |
David W. Bates | 159 | 1239 | 116698 |
Nicholas J. Talley | 158 | 1571 | 90197 |
David Cameron | 154 | 1586 | 126067 |
Stephen J. O'Brien | 153 | 1062 | 93025 |
David J. Brooks | 152 | 1056 | 94335 |
Rui Zhang | 151 | 2625 | 107917 |
David Goldstein | 141 | 1301 | 101955 |
Graeme J. Hankey | 137 | 844 | 143373 |
Peter M. Rothwell | 134 | 779 | 67382 |
John F. Thompson | 132 | 1420 | 95894 |
Peter A. Jones | 130 | 513 | 81683 |
David Smith | 129 | 2184 | 100917 |
Christopher G. Maher | 128 | 940 | 73131 |