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Furthermore, Pfirrmann et al. [3] evaluated 44 patients with a cam FAI and observed a sensitivity, specificity, and accuracy of 22 30, 95, and 57 61 %, respectively.
The produced sensor paper was tested for sensitivity using different ammonia concentrations and we observed a sensitivity lower limit at 63 ppm.
24 Our results confirm the inadequacy of biopsy, where we observed a sensitivity of just over 12% in detecting MVI.
Using miR-483-5p miR-483-5p miR-483-5prved AUCensitivity of 62.2% and a specificity of 58.0.600ata not showe).
We also assessed sensitivity to topotecan, a topoisomerase 1 inhibitor, and observed a sensitivity of ATMIN-null MEFs to this agent (Supplementary Fig. 6A and B).
At a cut point of four, where sensitivity and specificity most closely intersected, we observed a sensitivity of 0.66, and specificity of 0.61.
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We, therefore, observe a sensitivity of more than 99%.
It should be noted however that we did not observe a sensitivity of ATMIN-null MEFs to the DNA double-strand break-inducing agent NCS (Supplementary Fig. 5C).
Given a prevalence of 5%, if we observe a sensitivity of 90% this cohort size will give a 95% confidence interval for this sensitivity of 84.0 to 94.3, and a specificity of 91%.
In the former assay we did not observe a sensitivity of ATMIN-deficient cells to either the alkylating agent methyl methanesulfonate (MMS) or hydroxyurea (HU), that induces replication stress by depleting the pool of deoxynucleotides via inhibition of ribonucleotide reductase (Supplementary Fig. 4).
(2002) also described sensitivity of UHRF1-deficient cells to genotoxic agents, although they observed a greater sensitivity to IR and UVC.
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