Institution
Erasmus University Medical Center
Healthcare•Rotterdam, Zuid-Holland, Netherlands•
About: Erasmus University Medical Center is a healthcare organization based out in Rotterdam, Zuid-Holland, Netherlands. It is known for research contribution in the topics: Population & Medicine. The organization has 8162 authors who have published 11395 publications receiving 517117 citations.
Topics: Population, Medicine, Cancer, Transplantation, Breast cancer
Papers published on a yearly basis
Papers
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TL;DR: The parallel analysis of IgG Fab and Fc, as set up in this paper, will be important for unraveling roles of these glycans in (auto)immunity, which may be mediated via recognition by human lectins or modulation of antigen binding.
212 citations
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TL;DR: The estimated current and future number of annual TAVI candidates in 27 European countries, the USA and Canada and Northern-American annually and the incidence rate of severe AS has major implications for health care resource planning in the 29 individual countries are estimated.
Abstract: Aims The number of transcatheter aortic valve implantation (TAVI) procedures is rapidly increasing. This has a major
impact on health care resource planning. However, the annual numbers of TAVI candidates per country are unknown. The aim of this study was to estimate current and future number of annual TAVI candidates in 27
European countries, the USA and Canada.
Methods
and results
Systematic literature searches and meta-analyses were performed on aortic stenosis (AS) epidemiology and
decision-making in severe symptomatic AS. The incidence rate of severe AS was determined. Findings were combined with population statistics and integrated into a model employing Monte Carlo simulations to predict the annual number of TAVI candidates. Various future scenarios and sensitivity analyses were explored. Data from 37
studies (n = 26 402) informed the model. The calculated incidence rate of severe AS was 4.4&/year [95% confidence interval (95% CI) 3.0–6.1&] in patients >_65 years. AS-related symptoms were present in 68.3% (95% CI
60.8–75.9%) of patients with severe AS. Despite having severe symptomatic AS, 41.6% (95% CI 36.9–46.3%) did
not undergo surgical aortic valve replacement. Of the non-operated patients, 61.7% (95% CI 42.0–81.7%) received
TAVI. The model predicted 114 757 (95% CI 69 380–172 799) European and 58 556 (95% CI 35 631–87 738)
Northern-American TAVI candidates annually.
Conclusion Currently, approximately 180 000 patients can be considered potential TAVI candidates in the European Union and
in Northern-America annually. This number might increase up to 270 000 if indications for TAVI expand to lowrisk patients. These findings have major implications for health care resource planning in the 29 individual
countries.
212 citations
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TL;DR: Data from the collective EBMT experience support the hypothesis that autologous HSCT can alter disease progression in severe autoimmune disease.
Abstract: Experimental data and early phase I/II studies suggest that high-dose chemotherapy followed by autologous hematopoietic stem cell transplantation (HSCT) can arrest progression of severe autoimmune diseases. We have evaluated the toxicity and disease response in 473 patients with severe autoimmune disease treated with autologous HSCT between 1995 and 2003, from 110 centers participating in the European Group for Blood and Marrow Transplantation (EBMT) autoimmune disease working party database. Survival, transplant-related mortality, treatment response and disease progression were assessed. In all, 420 patients (89%; 86+/-4% at 3 years, median follow-up 20 months) were alive, 53 (11%) had died from transplant-related mortality (N=31; 7+/-3% at 3 years) or disease progression (N=22; 9+/-4% at 3 years). Of 370 patients, 299 evaluable for response (81%) showed a treatment response, which was sustained in 213 (71% of responders). Response was associated with disease (P 40 years, RR0.29 (0.11-0.82)). Disease progression was associated with disease (P<0.001) and conditioning intensity (high intensity, RR1; intermediate intensity, RR1.81 (0.96-3.42)); low intensity, RR2.34 (1.074-5.11)). These data from the collective EBMT experience support the hypothesis that autologous HSCT can alter disease progression in severe autoimmune disease.
212 citations
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TL;DR: It is shown that an E-box-mediated circadian rhythm ofNRF2 protein is essential in regulating the rhythmic expression of antioxidant genes involved in glutathione redox homeostasis in the mouse lung, revealing a pivotal role for the circadian control of the NRF2/glutathione pathway in combating oxidative/fibrotic lung damage.
Abstract: The disruption of the NRF2 (nuclear factor erythroid-derived 2-like 2)/glutathione-mediated antioxidant defense pathway is a critical step in the pathogenesis of several chronic pulmonary diseases and cancer. While the mechanism of NRF2 activation upon oxidative stress has been widely investigated, little is known about the endogenous signals that regulate the NRF2 pathway in lung physiology and pathology. Here we show that an E-box-mediated circadian rhythm of NRF2 protein is essential in regulating the rhythmic expression of antioxidant genes involved in glutathione redox homeostasis in the mouse lung. Using an in vivo bleomycin-induced lung fibrosis model, we reveal a clock “gated” pulmonary response to oxidative injury, with a more severe fibrotic effect when bleomycin was applied at a circadian nadir in NRF2 levels. Timed administration of sulforaphane, an NRF2 activator, significantly blocked this phenotype. Moreover, in the lungs of the arrhythmic ClockΔ19 mice, the levels of NRF2 and the reduced glutathione are constitutively low, associated with increased protein oxidative damage and a spontaneous fibrotic-like pulmonary phenotype. Our findings reveal a pivotal role for the circadian control of the NRF2/glutathione pathway in combating oxidative/fibrotic lung damage, which might prompt new chronotherapeutic strategies for the treatment of human lung diseases, including idiopathic pulmonary fibrosis.
212 citations
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TL;DR: The EMC-92-gene signature is better or comparable to previously published signatures and contributes to risk assessment in clinical trials and could provide a tool for treatment choices in high-risk MM patients.
Abstract: There is a strong need to better predict the survival of patients with newly diagnosed multiple myeloma (MM). As gene expression profiles (GEPs) reflect the biology of MM in individual patients, we built a prognostic signature based on GEPs. GEPs obtained from newly diagnosed MM patients included in the HOVON65/GMMG-HD4 trial (n=290) were used as training data. Using this set, a prognostic signature of 92 genes (EMC-92-gene signature) was generated by supervised principal component analysis combined with simulated annealing. Performance of the EMC-92-gene signature was confirmed in independent validation sets of newly diagnosed (total therapy (TT)2, n=351; TT3, n=142; MRC-IX, n=247) and relapsed patients (APEX, n=264). In all the sets, patients defined as high-risk by the EMC-92-gene signature show a clearly reduced overall survival (OS) with a hazard ratio (HR) of 3.40 (95% confidence interval (CI): 2.19-5.29) for the TT2 study, 5.23 (95% CI: 2.46-11.13) for the TT3 study, 2.38 (95% CI: 1.65-3.43) for the MRC-IX study and 3.01 (95% CI: 2.06-4.39) for the APEX study (P<0.0001 in all studies). In multivariate analyses this signature was proven to be independent of the currently used prognostic factors. The EMC-92-gene signature is better or comparable to previously published signatures. This signature contributes to risk assessment in clinical trials and could provide a tool for treatment choices in high-risk MM patients.
211 citations
Authors
Showing all 8309 results
Name | H-index | Papers | Citations |
---|---|---|---|
Albert Hofman | 267 | 2530 | 321405 |
André G. Uitterlinden | 199 | 1229 | 156747 |
Patrick W. Serruys | 186 | 2427 | 173210 |
Cornelia M. van Duijn | 183 | 1030 | 146009 |
Tien Yin Wong | 160 | 1880 | 131830 |
Monique M.B. Breteler | 159 | 546 | 93762 |
Marjo-Riitta Järvelin | 156 | 923 | 100939 |
Fernando Rivadeneira | 146 | 628 | 86582 |
Ewout W. Steyerberg | 139 | 1226 | 84896 |
J. Wouter Jukema | 124 | 785 | 61555 |
Bart W. Koes | 124 | 730 | 57630 |
Albert D. M. E. Osterhaus | 124 | 955 | 83678 |
Jan K. Buitelaar | 123 | 1004 | 61880 |
Frits R. Rosendaal | 122 | 763 | 69043 |
Johan P. Mackenbach | 120 | 783 | 56705 |