Institution
University of Queensland
Education•Brisbane, Queensland, Australia•
About: University of Queensland is a education organization based out in Brisbane, Queensland, Australia. It is known for research contribution in the topics: Population & Poison control. The organization has 51138 authors who have published 155721 publications receiving 5717659 citations. The organization is also known as: UQ & The University of Queensland.
Papers published on a yearly basis
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TL;DR: The technologies of encapsulation of polyphenols, including spray drying, coacervation, liposome entrapment, inclusion complexation, cocrystallization, nanoencapsulation, freeze drying, yeast encapsulation and emulsion, are discussed in this paper.
Abstract: Research on and the application of polyphenols, have recently attracted great interest in the functional foods, nutraceutical and pharmaceutical industries, due to their potential health benefits to humans. However, the effectiveness of polyphenols depends on preserving the stability, bioactivity and bioavailability of the active ingredients. The unpleasant taste of most phenolic compounds also limits their application. The utilization of encapsulated polyphenols, instead of free compounds, can effectively alleviate these deficiencies. The technologies of encapsulation of polyphenols, including spray drying, coacervation, liposome entrapment, inclusion complexation, cocrystallization, nanoencapsulation, freeze drying, yeast encapsulation and emulsion, are discussed in this review. Current research, developments and trends are also discussed.
1,220 citations
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TL;DR: This model shows follicle numbers decline bi-exponentially rather than as a simple exponential function of age, as had been assumed, with a first exponential rate parameter of -0.097 and a second of - 0.237, and predicts the impact of step reductions of follicles numbers on the prospective span of menstrual life was predicted.
Abstract: Menopause is triggered by the number of ovarian follicles falling below a threshold number and is irreversible because oogonial stem cells disappear after birth. Since it is the result of programmed disappearance of a limited store of follicles, menopause can be predicted using mathematical models based on total follicle counts at different ages. Our model shows follicle numbers decline bi-exponentially rather than as a simple exponential function of age, as had been assumed, with a first exponential rate parameter of -0.097 and a second of -0.237. The change occurred when numbers had fallen to the critical figure of 25,000 at age 37.5 years. The unexpectedly faster rate of ovarian ageing afterwards lowers the follicle population to 1000 at approximately 51 years, and was adopted as the menopausal threshold because it corresponds to the median age of menopause in the general population. Had the earlier rate persisted menopause would not be expected until 71 years. The impact of step reductions of follicle numbers on the prospective span of menstrual life was predicted by the model. A reduction by 50% before age 30 years resulted in the threshold being reached at 44 years and 0.6 year later for every subsequent year until age 37.5 years after which it is reached at 48 years. A reduction of 90% in childhood before age 14 years could result in menopause as early as 27 years, with increments of 0.6 year per year afterwards until after 37.5 years when it is expected at age 41 years.(ABSTRACT TRUNCATED AT 250 WORDS)
1,219 citations
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TL;DR: The distribution of the 1,25-dihydroxyvitamin D3 receptor (VDR), and 1α-hydroxylase (1α-OHase), the enzyme responsible for the formation of the active vitamin in the human brain, was reported for the first time.
1,209 citations
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University of Alabama at Birmingham1, University of Hohenheim2, College of Health Sciences, Bahrain3, Jimma University4, University of Queensland5, Queensland Government6, Mekelle University7, Institute for Health Metrics and Evaluation8, University of Cartagena9, Komfo Anokye Teaching Hospital10, University of Manitoba11, University of Gondar12, University of São Paulo13, Aga Khan University14, New Generation University College15, Public Health Foundation of India16, Duy Tan University17, Centers for Disease Control and Prevention18, Bielefeld University19, Swiss Tropical and Public Health Institute20, Imperial College London21, University of Basel22, Baylor College of Medicine23, Boston Children's Hospital24, Yonsei University25, Tehran University of Medical Sciences26, Jordan University of Science and Technology27, University of London28, University of Melbourne29, Aintree University Hospitals NHS Foundation Trust30, University of Liverpool31, Martin Luther University of Halle-Wittenberg32, United Nations Population Fund33, Iran University of Medical Sciences34, University of Ulm35, University of Sydney36, University of Porto37, University of British Columbia38, A.T. Still University39, Golestan University40, Harvard University41, Marshall University42, Case Western Reserve University43, University of KwaZulu-Natal44, AIIMS, New Delhi45, Utkal University46, Haramaya University47, Queensland University of Technology48, Jagiellonian University Medical College49, Wrocław Medical University50, Hanoi Medical University51, Johns Hopkins University52, National Research University – Higher School of Economics53, Norwegian Institute of Public Health54, University of Bergen55, University of Tromsø56, Karolinska Institutet57, Kyoto University58, Jackson State University59, Wuhan University60, University of Washington61
TL;DR: In this article, the authors report results of the Global Burden of Disease (GBD) 2015 study on primary liver cancer incidence, mortality, and disability-adjusted life-years (DALYs) for 195 countries or territories from 1990 to 2015, and present global, regional, and national estimates on the burden of liver cancer attributable to hepatitis B virus (HBV) and hepatitis C virus (HCV) infection and alcohol, and an “other” group that encompasses residual causes.
Abstract: Importance Liver cancer is among the leading causes of cancer deaths globally. The most common causes for liver cancer include hepatitis B virus (HBV) and hepatitis C virus (HCV) infection and alcohol use. Objective To report results of the Global Burden of Disease (GBD) 2015 study on primary liver cancer incidence, mortality, and disability-adjusted life-years (DALYs) for 195 countries or territories from 1990 to 2015, and present global, regional, and national estimates on the burden of liver cancer attributable to HBV, HCV, alcohol, and an “other” group that encompasses residual causes. Design, Settings, and Participants Mortality was estimated using vital registration and cancer registry data in an ensemble modeling approach. Single-cause mortality estimates were adjusted for all-cause mortality. Incidence was derived from mortality estimates and the mortality-to-incidence ratio. Through a systematic literature review, data on the proportions of liver cancer due to HBV, HCV, alcohol, and other causes were identified. Years of life lost were calculated by multiplying each death by a standard life expectancy. Prevalence was estimated using mortality-to-incidence ratio as surrogate for survival. Total prevalence was divided into 4 sequelae that were multiplied by disability weights to derive years lived with disability (YLDs). DALYs were the sum of years of life lost and YLDs. Main Outcomes and Measures Liver cancer mortality, incidence, YLDs, years of life lost, DALYs by etiology, age, sex, country, and year. Results There were 854 000 incident cases of liver cancer and 810 000 deaths globally in 2015, contributing to 20 578 000 DALYs. Cases of incident liver cancer increased by 75% between 1990 and 2015, of which 47% can be explained by changing population age structures, 35% by population growth, and −8% to changing age-specific incidence rates. The male-to-female ratio for age-standardized liver cancer mortality was 2.8. Globally, HBV accounted for 265 000 liver cancer deaths (33%), alcohol for 245 000 (30%), HCV for 167 000 (21%), and other causes for 133 000 (16%) deaths, with substantial variation between countries in the underlying etiologies. Conclusions and Relevance Liver cancer is among the leading causes of cancer deaths in many countries. Causes of liver cancer differ widely among populations. Our results show that most cases of liver cancer can be prevented through vaccination, antiviral treatment, safe blood transfusion and injection practices, as well as interventions to reduce excessive alcohol use. In line with the Sustainable Development Goals, the identification and elimination of risk factors for liver cancer will be required to achieve a sustained reduction in liver cancer burden. The GBD study can be used to guide these prevention efforts.
1,208 citations
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Christopher Newton-Cheh1, Christopher Newton-Cheh2, Toby Johnson3, Toby Johnson4 +359 more•Institutions (64)
TL;DR: In this paper, the association between systolic or diastolic blood pressure and common variants in eight regions near the CYP17A1 (P = 7 × 10(-24)), CYP1A2(P = 1 × 10-23), FGF5 (P=1 × 10 -21), SH2B3(P= 3 × 10−18), MTHFR(MTHFR), c10orf107(P), ZNF652(ZNF652), PLCD3 (P,P = 5 × 10 −9),
Abstract: Elevated blood pressure is a common, heritable cause of cardiovascular disease worldwide. To date, identification of common genetic variants influencing blood pressure has proven challenging. We tested 2.5 million genotyped and imputed SNPs for association with systolic and diastolic blood pressure in 34,433 subjects of European ancestry from the Global BPgen consortium and followed up findings with direct genotyping (N ≤ 71,225 European ancestry, N ≤ 12,889 Indian Asian ancestry) and in silico comparison (CHARGE consortium, N = 29,136). We identified association between systolic or diastolic blood pressure and common variants in eight regions near the CYP17A1 (P = 7 × 10(-24)), CYP1A2 (P = 1 × 10(-23)), FGF5 (P = 1 × 10(-21)), SH2B3 (P = 3 × 10(-18)), MTHFR (P = 2 × 10(-13)), c10orf107 (P = 1 × 10(-9)), ZNF652 (P = 5 × 10(-9)) and PLCD3 (P = 1 × 10(-8)) genes. All variants associated with continuous blood pressure were associated with dichotomous hypertension. These associations between common variants and blood pressure and hypertension offer mechanistic insights into the regulation of blood pressure and may point to novel targets for interventions to prevent cardiovascular disease.
1,205 citations
Authors
Showing all 52145 results
Name | H-index | Papers | Citations |
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Graham A. Colditz | 261 | 1542 | 256034 |
George Davey Smith | 224 | 2540 | 248373 |
David J. Hunter | 213 | 1836 | 207050 |
Daniel Levy | 212 | 933 | 194778 |
Christopher J L Murray | 209 | 754 | 310329 |
Matthew Meyerson | 194 | 553 | 243726 |
Luigi Ferrucci | 193 | 1601 | 181199 |
Nicholas G. Martin | 192 | 1770 | 161952 |
Paul M. Thompson | 183 | 2271 | 146736 |
Jie Zhang | 178 | 4857 | 221720 |
Alan D. Lopez | 172 | 863 | 259291 |
Ian J. Deary | 166 | 1795 | 114161 |
Steven N. Blair | 165 | 879 | 132929 |
Carlos Bustamante | 161 | 770 | 106053 |
David W. Johnson | 160 | 2714 | 140778 |