Institution
Maastricht University
Education•Maastricht, Limburg, Netherlands•
About: Maastricht University is a education organization based out in Maastricht, Limburg, Netherlands. It is known for research contribution in the topics: Population & Health care. The organization has 19263 authors who have published 53291 publications receiving 2266866 citations. The organization is also known as: Universiteit Maastricht & UM.
Papers published on a yearly basis
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TL;DR: Cryotransmission electron microscopy has found that template-directed calcium carbonate formation starts with the formation of prenucleation clusters, which aggregation leads to the nucleation of amorphous nanoparticles in solution.
Abstract: Biogenic calcium carbonate forms the inorganic component of seashells, otoliths, and many marine skeletons, and its formation is directed by an ordered template of macromolecules. Classical nucleation theory considers crystal formation to occur from a critical nucleus formed by the assembly of ions from solution. Using cryotransmission electron microscopy, we found that template-directed calcium carbonate formation starts with the formation of prenucleation clusters. Their aggregation leads to the nucleation of amorphous nanoparticles in solution. These nanoparticles assemble at the template and, after reaching a critical size, develop dynamic crystalline domains, one of which is selectively stabilized by the template. Our findings have implications for template-directed mineral formation in biological as well as in synthetic systems.
764 citations
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TL;DR: The role of drinking-water nitrate exposure as a risk factor for specific cancers, reproductive outcomes, and other chronic health effects must be studied more thoroughly before changes to the regulatory level for nitrate in drinking water can be considered.
Abstract: Human alteration of the nitrogen cycle has resulted in steadily accumulating nitrate in our water resources. The U.S. maximum contaminant level and World Health Organization guidelines for nitrate in drinking water were promulgated to protect infants from developing methemoglobinemia, an acute condition. Some scientists have recently suggested that the regulatory limit for nitrate is overly conservative; however, they have not thoroughly considered chronic health outcomes. In August 2004, a symposium on drinking-water nitrate and health was held at the International Society for Environmental Epidemiology meeting to evaluate nitrate exposures and associated health effects in relation to the current regulatory limit. The contribution of drinking-water nitrate toward endogenous formation of N-nitroso compounds was evaluated with a focus toward identifying subpopulations with increased rates of nitrosation. Adverse health effects may be the result of a complex interaction of the amount of nitrate ingested, the concomitant ingestion of nitrosation cofactors and precursors, and specific medical conditions that increase nitrosation. Workshop participants concluded that more experimental studies are needed and that a particularly fruitful approach may be to conduct epidemiologic studies among susceptible subgroups with increased endogenous nitrosation. The few epidemiologic studies that have evaluated intake of nitrosation precursors and/or nitrosation inhibitors have observed elevated risks for colon cancer and neural tube defects associated with drinking-water nitrate concentrations below the regulatory limit. The role of drinking-water nitrate exposure as a risk factor for specific cancers, reproductive outcomes, and other chronic health effects must be studied more thoroughly before changes to the regulatory level for nitrate in drinking water can be considered.
760 citations
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TL;DR: The effects of menarche and menopause on breast cancer risk might not be acting merely by lengthening women's total number of reproductive years, and endogenous ovarian hormones are more relevant for oestrogen receptor-positive disease than for ostrogens receptor-negative disease and for lobular than for ductal tumours.
Abstract: BACKGROUND:Menarche and menopause mark the onset and cessation, respectively, of ovarian activity associated with reproduction, and affect breast cancer risk. Our aim was to assess the strengths of their effects and determine whether they depend on characteristics of the tumours or the affected women.METHODS:Individual data from 117 epidemiological studies, including 118 964 women with invasive breast cancer and 306 091 without the disease, none of whom had used menopausal hormone therapy, were included in the analyses. We calculated adjusted relative risks (RRs) associated with menarche and menopause for breast cancer overall, and by tumour histology and by oestrogen receptor expression.FINDINGS:Breast cancer risk increased by a factor of 1·050 (95% CI 1·044-1·057; p<0·0001) for every year younger at menarche, and independently by a smaller amount (1·029, 1·025-1·032; p<0·0001), for every year older at menopause. Premenopausal women had a greater risk of breast cancer than postmenopausal women of an identical age (RR at age 45-54 years 1·43, 1·33-1·52, p<0·001). All three of these associations were attenuated by increasing adiposity among postmenopausal women, but did not vary materially by women's year of birth, ethnic origin, childbearing history, smoking, alcohol consumption, or hormonal contraceptive use. All three associations were stronger for lobular than for ductal tumours (p<0·006 for each comparison). The effect of menopause in women of an identical age and trends by age at menopause were stronger for oestrogen receptor-positive disease than for oestrogen receptor-negative disease (p<0·01 for both comparisons).INTERPRETATION:The effects of menarche and menopause on breast cancer risk might not be acting merely by lengthening women's total number of reproductive years. Endogenous ovarian hormones are more relevant for oestrogen receptor-positive disease than for oestrogen receptor-negative disease and for lobular than for ductal tumours.
759 citations
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University of Manchester1, Imperial College London2, Central Manchester University Hospitals NHS Foundation Trust3, Ford Motor Company4, Harvard University5, King's College London6, University Medical Center Groningen7, University of Cambridge8, University of Oxford9, The Royal Marsden NHS Foundation Trust10, University of Leeds11, University of Michigan12, European Organisation for Research and Treatment of Cancer13, Institute of Cancer Research14, University College London15, United States Military Academy16, VU University Amsterdam17, University of Wisconsin-Madison18, Maastricht University19, Institut Gustave Roussy20, Robarts Research Institute21, Memorial Sloan Kettering Cancer Center22, Newcastle University23, University of Leicester24, Mount Vernon Hospital25, Johns Hopkins University26, Hofstra University27, University of Birmingham28, University of Antwerp29, Duke University30, Brighton and Sussex Medical School31, University of Sheffield32, University of Texas at Austin33
TL;DR: Experts assembled to review, debate and summarize the challenges of IB validation and qualification produced 14 key recommendations for accelerating the clinical translation of IBs, which highlight the role of parallel (rather than sequential) tracks of technical validation, biological/clinical validation and assessment of cost-effectiveness.
Abstract: Imaging biomarkers (IBs) are integral to the routine management of patients with cancer. IBs used daily in oncology include clinical TNM stage, objective response and left ventricular ejection fraction. Other CT, MRI, PET and ultrasonography biomarkers are used extensively in cancer research and drug development. New IBs need to be established either as useful tools for testing research hypotheses in clinical trials and research studies, or as clinical decision-making tools for use in healthcare, by crossing 'translational gaps' through validation and qualification. Important differences exist between IBs and biospecimen-derived biomarkers and, therefore, the development of IBs requires a tailored 'roadmap'. Recognizing this need, Cancer Research UK (CRUK) and the European Organisation for Research and Treatment of Cancer (EORTC) assembled experts to review, debate and summarize the challenges of IB validation and qualification. This consensus group has produced 14 key recommendations for accelerating the clinical translation of IBs, which highlight the role of parallel (rather than sequential) tracks of technical (assay) validation, biological/clinical validation and assessment of cost-effectiveness; the need for IB standardization and accreditation systems; the need to continually revisit IB precision; an alternative framework for biological/clinical validation of IBs; and the essential requirements for multicentre studies to qualify IBs for clinical use.
758 citations
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TL;DR: Coronary pressure–derived fractional flow reserve (FFR) is an invasive index of stenosis severity that is a reliable substitute for noninvasive stress testing and identifies stenoses with hemodynamic significance.
Abstract: Background—PTCA of a coronary stenosis without documented ischemia at noninvasive stress testing is often performed, but its benefit is unproven. Coronary pressure–derived fractional flow reserve (FFR) is an invasive index of stenosis severity that is a reliable substitute for noninvasive stress testing. A value of 0.75 identifies stenoses with hemodynamic significance. Methods and Results—In 325 patients for whom PTCA was planned and who did not have documented ischemia, FFR of the stenosis was measured. If FFR was >0.75, patients were randomly assigned to deferral (deferral group; n=91) or performance (performance group; n=90) of PTCA. If FFR was <0.75, PTCA was performed as planned (reference group; n=144). Clinical follow-up was obtained at 1, 3, 6, 12, and 24 months. Event-free survival was similar between the deferral and performance groups (92% versus 89% at 12 months and 89% versus 83% at 24 months) but was significantly lower in the reference group (80% at 12 months and 78% at 24 months). In addi...
757 citations
Authors
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Name | H-index | Papers | Citations |
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Edward Giovannucci | 206 | 1671 | 179875 |
Julie E. Buring | 186 | 950 | 132967 |
Aaron R. Folsom | 181 | 1118 | 134044 |
John J.V. McMurray | 178 | 1389 | 184502 |
Alvaro Pascual-Leone | 165 | 969 | 98251 |
Lex M. Bouter | 158 | 767 | 103034 |
David T. Felson | 153 | 861 | 133514 |
Walter Paulus | 149 | 809 | 86252 |
Michael Conlon O'Donovan | 142 | 736 | 118857 |
Randy L. Buckner | 141 | 346 | 110354 |
Philip Scheltens | 140 | 1175 | 107312 |
Anne Tjønneland | 139 | 1345 | 91556 |
Ewout W. Steyerberg | 139 | 1226 | 84896 |
James G. Herman | 138 | 410 | 120628 |
Andrew Steptoe | 137 | 1003 | 73431 |