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John L. Adams Matthias Schonlau José J. Escarce Meredith Kilgore Michael Schoenbaum Dana P. Goldman 《Health services & outcomes research methodology》2003,4(3):151-167
In order to better inform study design decisions when sampling patients within and across health care providers we develop a simulation-based approach for designing complex multi-stage samples. The approach explores the tradeoff between competing design goals such as precision of estimates, coverage of the target population and cost.We elicit a number of sensible candidate designs, evaluate these designs with respect to multiple sampling goals, investigate their tradeoffs, and identify the design that is the best compromise among all goals. This approach recognizes that, in the practice of sampling, precision of the estimates is not the only important goal, and that there are tradeoffs with coverage and cost that should be explicitly considered. One can easily add other goals. We construct a sample frame with all phase III clinical cancer treatment trials that are conducted by cooperative oncology groups of the National Cancer Institute from October 1, 1998 through December 31, 1999. Simulation results for our study suggest sampling a different number of trials and institutions than initially considered.Simulations of different study designs can uncover efficiency gains both in terms of improved precision of the estimates and in terms of improved coverage of the target population. Simulations enable us to explore the tradeoffs between competing sampling goals and to quantify these efficiency gains. This is true even for complex designs where the stages are not strictly nested in one another. 相似文献
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Functional neuromuscular stimulation (FNS) has been used in upper extremity neuroprostheses to provide grasp and release for
quadriplegic individuals. The goal of this project was to determine the electrode/muscle input/output characteristics with
the greatest influence on the grasp output. This was evaluated by simulating the grasp synthesis procedure, using a model
of the electrode/muscle output as a function of stimulus level and joint angle. The parameters of this model were determined
from experimental data from 112 electrodes. The grasp output for 500 different modelled pairs of electrodes were analysed,
with each pair consisting of a thumb flexor and a thumb extensor. The simulation results indicate that the most influential
electrode input/output characteristics are the output stiffness, defined as the change in force output for a unit change in
joint angle at a constant level of stimulation, and the length dependency mean-squared error. Recruitment gain was found to
be of secondary influence on the grasp output, and the threshold, force direction and non-linearity of the stimulus level
to force relationship were found to have little influence on the grasp output. These results establish criteria for electrode
selection and implantation for use in upper extremity FNS. 相似文献
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doublecortin is the major gene causing X-linked subcortical laminar heterotopia (SCLH) 总被引:12,自引:0,他引:12
des Portes V; Francis F; Pinard JM; Desguerre I; Moutard ML; Snoeck I; Meiners LC; Capron F; Cusmai R; Ricci S; Motte J; Echenne B; Ponsot G; Dulac O; Chelly J; Beldjord C 《Human molecular genetics》1998,7(7):1063-1070
Subcortical laminar heterotopia (SCLH), or 'double cortex', is a cortical
dysgenesis disorder associated with a defect in neuronal migration.
Clinical manifestations are epilepsy and mental retardation. This disorder,
which mainly affects females, can be inherited in a single pedigree with
lissencephaly, a more severe disease which affects the male individuals.
This clinical entity has been described as X- SCLH/LIS syndrome. Recently
we have demonstrated that the doublecortin gene, which is localized on the
X chromosome, is implicated in this disorder. We have now performed a
systematic mutation analysis of doublecortin in 11 unrelated females with
SCLH (one familial and 10 sporadic cases) and have identified mutations in
10/11 cases. The sequence differences include nonsense, splice site and
missense mutations and these were found throughout the gene. These results
provide strong evidence that loss of function of doublecortin is the major
cause of SCLH. The absence of phenotype-genotype correlations suggests that
X-inactivation patterns of neuronal precursor cells are likely to
contribute to the variable clinical severity of this disorder in females.
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