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1.
Tim Holland 《The Hastings Center report》2023,53(1):50-51
This letter responds to the article “On the Authority of Advance Euthanasia Directives for People with Severe Dementia: Reflections on a Dutch Case,” by Henri Wijsbek and Thomas Nys, in the September-October 2022 issue of the Hastings Center Report. 相似文献
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Thomas Asendorf Robin Henderson Heinz Schmidli Tim Friede 《Statistics in medicine》2019,38(9):1503-1528
In some diseases, such as multiple sclerosis, lesion counts obtained from magnetic resonance imaging (MRI) are used as markers of disease progression. This leads to longitudinal, and typically overdispersed, count data outcomes in clinical trials. Models for such data invariably include a number of nuisance parameters, which can be difficult to specify at the planning stage, leading to considerable uncertainty in sample size specification. Consequently, blinded sample size re-estimation procedures are used, allowing for an adjustment of the sample size within an ongoing trial by estimating relevant nuisance parameters at an interim point, without compromising trial integrity. To date, the methods available for re-estimation have required an assumption that the mean count is time-constant within patients. We propose a new modeling approach that maintains the advantages of established procedures but allows for general underlying and treatment-specific time trends in the mean response. A simulation study is conducted to assess the effectiveness of blinded sample size re-estimation methods over fixed designs. Sample sizes attained through blinded sample size re-estimation procedures are shown to maintain the desired study power without inflating the Type I error rate and the procedure is demonstrated on MRI data from a recent study in multiple sclerosis. 相似文献
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Katherine M. Duszynski Nicole L. Pratt John W. Lynch Jesia G. Berry Michael S. Gold 《Vaccine》2019,37(2):280-288
Objective
To determine whether differences in combination DTaP vaccine types at 2, 4 and 6?months of age were associated with mortality (all-cause or non-specific), within 30?days of vaccination.Design
Observational nationwide cohort study.Setting
Linked population data from the Australian Childhood Immunisation Register and National Death Index.Participants
Australian infants administered a combination trivalent, quadrivalent or hexavalent DTaP vaccine (DTaP types) between January 1999 and December 2010 at 2, 4 and 6?months as part of the primary vaccination series. The study population included 2.9, 2.6, & 2.3?million children in the 2, 4 and 6?month vaccine cohorts, respectively.Main outcome measures
Infants were evaluated for the primary outcome of all-cause mortality within 30?days. A secondary outcome was non-specific mortality (unknown cause of death) within 30?days of vaccination. Non-specific mortality was defined as underlying or other cause of death codes, R95 ‘Sudden infant death syndrome’, R96 ‘Other sudden death, cause unknown’, R98 ‘Unattended death’, R99 ‘Other ill-defined and unspecified cause of mortality’ or where no cause of death was recorded.Results
The rate of 30?day all-cause mortality was low and declined from 127.4 to 59.3 deaths per 100,000 person-years between 2 and 6?month cohorts. When compared with trivalent DTaP vaccines, no elevated risk in all-cause or non-specific mortality was seen with any quadrivalent or hexavalent DTaP vaccines, for any cohort.Conclusion
Use of routine DTaP combination vaccines with differing disease antigens administered during the first six months of life is not associated with infant mortality. 相似文献8.
Ronny Redlich Ilona Schneider Nicole Kerkenberg Nils Opel Jonas Bauhaus Verena Enneking Jonathan Repple Elisabeth J. Leehr Dominik Grotegerd Claas Khler Katharina Frster Katharina Dohm Susanne Meinert Tim Hahn Harald Kugel Kathrin Schwarte Christiane Schettler Katharina Domschke Volker Arolt Walter Heindel Bernhard T. Baune Weiqi Zhang Christa Hohoff Udo Dannlowski 《Human brain mapping》2020,41(3):594-604
Epigenetic alterations of the brain‐derived neurotrophic factor (BDNF) gene have been associated with psychiatric disorders in humans and with differences in amygdala BDNF mRNA levels in rodents. This human study aimed to investigate the relationship between the functional BDNF‐Val66Met polymorphism, its surrounding DNA methylation in BDNF exon IX, amygdala reactivity to emotional faces, and personality traits. Healthy controls (HC, n = 189) underwent functional MRI during an emotional face‐matching task. Harm avoidance, novelty seeking and reward dependence were measured using the Tridimensional Personality Questionnaire (TPQ). Individual BDNF methylation profiles were ascertained and associated with several BDNF single nucleotide polymorphisms surrounding the BDNF‐Val66Met, amygdala reactivity, novelty seeking and harm avoidance. Higher BDNF methylation was associated with higher amygdala reactivity (x = 34, y = 0, z = ?26, t(166) = 3.00, TFCE = 42.39, p(FWE) = .045), whereby the BDNF‐Val66Met genotype per se did not show any significant association with brain function. Furthermore, novelty seeking was negatively associated with BDNF methylation (r = ?.19, p = .015) and amygdala reactivity (r = ?.17, p = .028), while harm avoidance showed a trend for a positive association with BDNF methylation (r = .14, p = .066). The study provides first insights into the relationship among BDNF methylation, BDNF genotype, amygdala reactivity and personality traits in humans, highlighting the multidimensional relations among genetics, epigenetics, and neuronal functions. The present study suggests a possible involvement of epigenetic BDNF modifications in psychiatric disorders and related brain functions, whereby high BDNF methylation might reduce BDNF mRNA expression and upregulate amygdala reactivity. 相似文献
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