Figure 3.
Modeling serum tryptase levels based on genotype improves clinical utility. (A) Normalized (left) and total (right) read counts for reads aligning exactly to the 39-bp consensus sequences that identify β-, αWT-, and αDUP-tryptase. (B) BST levels among individuals with conserved 4n tryptase copy number (combined from TPSAB1 and TPSB2). (C) Regression analysis of relative expression levels of αDUP-tryptase (y-axis) and αWT-tryptase (x-axis) transcripts. (D) Prediction intervals for BST levels based on TPSAB1 replication number. (E) Prevalence of HαT, clonal MCD, and those without either among individuals referred with BST levels above the predicted upper limit of normal (>11.4 ng/mL). ∗P < .01; ∗∗P < .005; ∗∗∗P < .0001.

Modeling serum tryptase levels based on genotype improves clinical utility. (A) Normalized (left) and total (right) read counts for reads aligning exactly to the 39-bp consensus sequences that identify β-, αWT-, and αDUP-tryptase. (B) BST levels among individuals with conserved 4n tryptase copy number (combined from TPSAB1 and TPSB2). (C) Regression analysis of relative expression levels of αDUP-tryptase (y-axis) and αWT-tryptase (x-axis) transcripts. (D) Prediction intervals for BST levels based on TPSAB1 replication number. (E) Prevalence of HαT, clonal MCD, and those without either among individuals referred with BST levels above the predicted upper limit of normal (>11.4 ng/mL). ∗P < .01; ∗∗P < .005; ∗∗∗P < .0001.

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