Institution
University of New South Wales
Education•Sydney, New South Wales, Australia•
About: University of New South Wales is a education organization based out in Sydney, New South Wales, Australia. It is known for research contribution in the topics: Population & Poison control. The organization has 51197 authors who have published 153634 publications receiving 4880608 citations. The organization is also known as: UNSW & UNSW Australia.
Topics: Population, Poison control, Health care, Mental health, Silicon
Papers published on a yearly basis
Papers
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University of New South Wales1, Garvan Institute of Medical Research2, Bankstown Lidcombe Hospital3, University of Queensland4, Baylor College of Medicine5, Ontario Institute for Cancer Research6, University of Newcastle7, Royal North Shore Hospital8, University of Sydney9, Life Technologies10, St. Vincent's Health System11, Royal Prince Alfred Hospital12, Fremantle Hospital13, Royal Adelaide Hospital14, University of Western Australia15, University of California, Los Angeles16, University Health Network17, Mayo Clinic18, University of Toronto19, Johns Hopkins University20, University of Verona21, University of California, San Francisco22, Houston Methodist Hospital23, Cancer Research UK24, Wellcome Trust Sanger Institute25, University of Minnesota26, Netherlands Cancer Institute27
TL;DR: It is found that frequent and diverse somatic aberrations in genes described traditionally as embryonic regulators of axon guidance, particularly SLIT/ROBO signalling, are also evident in murine Sleeping Beauty transposon-mediated somatic mutagenesis models of pancreatic cancer, providing further supportive evidence for the potential involvement ofAxon guidance genes in pancreatic carcinogenesis.
Abstract: Pancreatic cancer is a highly lethal malignancy with few effective therapies. We performed exome sequencing and copy number analysis to define genomic aberrations in a prospectively accrued clinical cohort (n = 142) of early (stage I and II) sporadic pancreatic ductal adenocarcinoma. Detailed analysis of 99 informative tumours identified substantial heterogeneity with 2,016 non-silent mutations and 1,628 copy-number variations. We define 16 significantly mutated genes, reaffirming known mutations (KRAS, TP53, CDKN2A, SMAD4, MLL3, TGFBR2, ARID1A and SF3B1), and uncover novel mutated genes including additional genes involved in chromatin modification (EPC1 and ARID2), DNA damage repair (ATM) and other mechanisms (ZIM2, MAP2K4, NALCN, SLC16A4 and MAGEA6). Integrative analysis with in vitro functional data and animal models provided supportive evidence for potential roles for these genetic aberrations in carcinogenesis. Pathway-based analysis of recurrently mutated genes recapitulated clustering in core signalling pathways in pancreatic ductal adenocarcinoma, and identified new mutated genes in each pathway. We also identified frequent and diverse somatic aberrations in genes described traditionally as embryonic regulators of axon guidance, particularly SLIT/ROBO signalling, which was also evident in murine Sleeping Beauty transposon-mediated somatic mutagenesis models of pancreatic cancer, providing further supportive evidence for the potential involvement of axon guidance genes in pancreatic carcinogenesis.
1,752 citations
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10 Dec 2015TL;DR: Countering the unavailability of network benchmark data set challenges, this paper examines a UNSW-NB15 data set creation which has a hybrid of the real modern normal and the contemporary synthesized attack activities of the network traffic.
Abstract: One of the major research challenges in this field is the unavailability of a comprehensive network based data set which can reflect modern network traffic scenarios, vast varieties of low footprint intrusions and depth structured information about the network traffic. Evaluating network intrusion detection systems research efforts, KDD98, KDDCUP99 and NSLKDD benchmark data sets were generated a decade ago. However, numerous current studies showed that for the current network threat environment, these data sets do not inclusively reflect network traffic and modern low footprint attacks. Countering the unavailability of network benchmark data set challenges, this paper examines a UNSW-NB15 data set creation. This data set has a hybrid of the real modern normal and the contemporary synthesized attack activities of the network traffic. Existing and novel methods are utilised to generate the features of the UNSWNB15 data set. This data set is available for research purposes and can be accessed from the link.
1,745 citations
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TL;DR: With a heightened awareness of these issues, informaticians can educate, design systems, implement, and conduct research in such a way that they might be able to avoid the unintended consequences of these subtle silent errors.
1,739 citations
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University of Cambridge1, Wellcome Trust Sanger Institute2, University of Melbourne3, Netherlands Cancer Institute4, University of Amsterdam5, University of Warwick6, Cancer Council Victoria7, University of Utah8, Columbia University9, Central Manchester University Hospitals NHS Foundation Trust10, Chapel Allerton Hospital11, Guy's and St Thomas' NHS Foundation Trust12, National Institute for Health Research13, University of Glasgow14, St George's, University of London15, Curie Institute16, Paris Descartes University17, Erasmus University Rotterdam18, Radboud University Nijmegen19, VU University Medical Center20, Cancer Prevention Institute of California21, Lunenfeld-Tanenbaum Research Institute22, University of Toronto23, Fox Chase Cancer Center24, Huntsman Cancer Institute25, Leipzig University26, German Cancer Research Center27, University of Cologne28, Hospital Clínico San Carlos29, Pomeranian Medical University30, Laval University31, University of New South Wales32, St. Vincent's Health System33, Peter MacCallum Cancer Centre34, QIMR Berghofer Medical Research Institute35, Medical University of Vienna36, Copenhagen University Hospital37, Karolinska Institutet38, Lund University39
TL;DR: To estimate age-specific risks of breast, ovarian, and contralateral breast cancer for mutation carriers and to evaluate risk modification by family cancer history and mutation location, a large cohort study recruited in 1997-2011 provides estimates of cancer risk based on BRCA1 and BRCa2 mutation carrier status.
Abstract: Importance: The clinical management of BRCA1 and BRCA2 mutation carriers requires accurate, prospective cancer risk estimates. Objectives: To estimate age-specific risks of breast, ovarian, and contralateral breast cancer for mutation carriers and to evaluate risk modification by family cancer history and mutation location. Design, Setting, and Participants: Prospective cohort study of 6036 BRCA1 and 3820 BRCA2 female carriers (5046 unaffected and 4810 with breast or ovarian cancer or both at baseline) recruited in 1997-2011 through the International BRCA1/2 Carrier Cohort Study, the Breast Cancer Family Registry and the Kathleen Cuningham Foundation Consortium for Research into Familial Breast Cancer, with ascertainment through family clinics (94%) and population-based studies (6%). The majority were from large national studies in the United Kingdom (EMBRACE), the Netherlands (HEBON), and France (GENEPSO). Follow-up ended December 2013; median follow-up was 5 years. Exposures: BRCA1/2 mutations, family cancer history, and mutation location. Main Outcomes and Measures: Annual incidences, standardized incidence ratios, and cumulative risks of breast, ovarian, and contralateral breast cancer. Results: Among 3886 women (median age, 38 years; interquartile range [IQR], 30-46 years) eligible for the breast cancer analysis, 5066 women (median age, 38 years; IQR, 31-47 years) eligible for the ovarian cancer analysis, and 2213 women (median age, 47 years; IQR, 40-55 years) eligible for the contralateral breast cancer analysis, 426 were diagnosed with breast cancer, 109 with ovarian cancer, and 245 with contralateral breast cancer during follow-up. The cumulative breast cancer risk to age 80 years was 72% (95% CI, 65%-79%) for BRCA1 and 69% (95% CI, 61%-77%) for BRCA2 carriers. Breast cancer incidences increased rapidly in early adulthood until ages 30 to 40 years for BRCA1 and until ages 40 to 50 years for BRCA2 carriers, then remained at a similar, constant incidence (20-30 per 1000 person-years) until age 80 years. The cumulative ovarian cancer risk to age 80 years was 44% (95% CI, 36%-53%) for BRCA1 and 17% (95% CI, 11%-25%) for BRCA2 carriers. For contralateral breast cancer, the cumulative risk 20 years after breast cancer diagnosis was 40% (95% CI, 35%-45%) for BRCA1 and 26% (95% CI, 20%-33%) for BRCA2 carriers (hazard ratio [HR] for comparing BRCA2 vs BRCA1, 0.62; 95% CI, 0.47-0.82; P=.001 for difference). Breast cancer risk increased with increasing number of first- and second-degree relatives diagnosed as having breast cancer for both BRCA1 (HR for ≥2 vs 0 affected relatives, 1.99; 95% CI, 1.41-2.82; P<.001 for trend) and BRCA2 carriers (HR, 1.91; 95% CI, 1.08-3.37; P=.02 for trend). Breast cancer risk was higher if mutations were located outside vs within the regions bounded by positions c.2282-c.4071 in BRCA1 (HR, 1.46; 95% CI, 1.11-1.93; P=.007) and c.2831-c.6401 in BRCA2 (HR, 1.93; 95% CI, 1.36-2.74; P<.001). Conclusions and Relevance: These findings provide estimates of cancer risk based on BRCA1 and BRCA2 mutation carrier status using prospective data collection and demonstrate the potential importance of family history and mutation location in risk assessment.
1,733 citations
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TL;DR: In this paper, the authors discuss recent developments in cognitive load theory related to the current view in instructional design that real-life tasks should be the driving force for complex learning, and provide guidelines for future research.
Abstract: Traditionally, Cognitive Load Theory (CLT) has focused on instructional methods to decrease extraneous cognitive load so that available cognitive resources can be fully devoted to learning. This article strengthens the cognitive base of CLT by linking cognitive processes to the processes used by biological evolution. The article discusses recent developments in CLT related to the current view in instructional design that real-life tasks should be the driving force for complex learning. First, the complexity, or intrinsic cognitive load, of such tasks is often high so that new methods are needed to manage cognitive load. Second, complex learning is a lengthy process requiring learners’ motivational states and levels of expertise development to be taken into account. Third, this perspective requires more advanced methods to measure expertise and cognitive load so that instruction can be flexibly adapted to individual learners’ needs. Experimental studies are reviewed to illustrate these recent developments. Guidelines for future research are provided.
1,731 citations
Authors
Showing all 51897 results
Name | H-index | Papers | Citations |
---|---|---|---|
Ronald C. Kessler | 274 | 1332 | 328983 |
Nicholas G. Martin | 192 | 1770 | 161952 |
John C. Morris | 183 | 1441 | 168413 |
Richard S. Ellis | 169 | 882 | 136011 |
Ian J. Deary | 166 | 1795 | 114161 |
Nicholas J. Talley | 158 | 1571 | 90197 |
Wolfgang Wagner | 156 | 2342 | 123391 |
Bruce D. Walker | 155 | 779 | 86020 |
Xiang Zhang | 154 | 1733 | 117576 |
Ian Smail | 151 | 895 | 83777 |
Rui Zhang | 151 | 2625 | 107917 |
Marvin Johnson | 149 | 1827 | 119520 |
John R. Hodges | 149 | 812 | 82709 |
Amartya Sen | 149 | 689 | 141907 |
J. Fraser Stoddart | 147 | 1239 | 96083 |