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Joshua H. Wong, Jonathan Dukes, Robert E. Levy, Brandon Sos, Sara E. Mason, Tina S. Fong, Ethan J. Weiss
Published in Volume 118, Issue 8
J Clin Invest. 2008; 118(8):2969–2978 doi:10.1172/JCI34957
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Figure 3
pGH administration rescues the whole-blood clotting defect in lit mice and shortens clotting times in WT female mice, while cGH administration prolongs the clotting time in WT male mice.

Blood was collected and prepared as in Figure 1. (A) Whole-blood clotting times (mean ± SEM) were significantly shorter in male (filled squares) versus female (open circles) litm/+ mice not receiving GH (–pGH); *P < 0.01. Mean clotting times were significantly longer in male and female litm/m –pGH versus litm/+ –pGH mice; ***P < 0.001, ANOVA with Bonferroni’s post-hoc test. Clotting times were shortened to male litm/+ –pGH levels (and were significantly shorter than those in litm/+ –pGH females) in male and female litm/m mice receiving pGH (+pGH); ***P < 0.001. (B and C) WT male and female mice were given an identical dose of GH (28 μg/g body weight) or vehicle either divided into twice-daily doses over 7 days (pGH) (B) or as a continuous infusion (cGH) (C). The clotting times of female animals receiving pGH (WT +pGH) (B) were shortened relative to those of animals not receiving GH (WT –pGH), with no effect on male animals. Whole-blood clotting times (mean ± SEM) were significantly shorter in male (filled squares) than female (open circles) WT –cGH mice in both groups. The clotting times of male animals receiving cGH (WT +cGH) (C) were prolonged relative to those of animals receiving vehicle control (WT –cGH), with no effect on female animals. *P < 0.05, ***P < 0.001, ANOVA with Bonferroni’s post-hoc test.