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This finding was replicated in a second set of subjects using a double-blind task design.
We also examined the expression of Mer on dendritic cells in the second set of subjects by using another antibody panel.
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The present study is a two-stage analysis: we used a genome-wide genotyping array in the first set of subjects (stage 1) primarily to verify the homogeneity of our population by several statistical analysis like PCA, homogeneity test, and to perform imputation as a huge number of nucleotide variations were screened simultaneously.
In addition to this, and to further reduce the investigators ability to recall any measurements, the data collection protocol was staggered in the following way; subject 1 (first set of measurements), subject 2 (first set of measurements), subject 1 (second set of measurements), subject 2 (second set of measurements), etc.
In a second set of experiments subjects received the same breakfasts; ad libitum lunch was offered at the pre-determined moment.
To determine if the biologic responses seen in our military cohort apply to civilian trauma patients, we analyzed a second set of 18 subjects with 27 significant extremity wounds who underwent 49 surgical débridements.
In view of possible concerns over the accuracy of the result of the affine linear registration on the cerebellum, a second set of ROIs per subject excluding the cerebellar regions (n = 26) were calculated.
Next, we selected genes that had a fold change ≥ 1.25 in the same direction in all three data sets (i.e. first and second sets of CAC subjects in our study and in the CAD autopsy samples).
As the distribution of mutations types in the second set of clinically identified MFS subjects is unknown, they may not replicate the distribution of the two mutation classes in the original MFS subjects.
In the second set of experiments, specimens were subjected to an initial axial displacement in the elastic range followed by torsion load, maintaining initial axial displacement.
In a second set of experiments, preparations were subjected to pre-treatment with aCSF containing fluoxetine, a well-known SERT blocker known to increase 5-HT endogenous levels [22], prior to investigating the PBf responses to acidosis.
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