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. 2008 Feb 6;105(6):2111–2116. doi: 10.1073/pnas.0710228105

Table 1.

Dicer mutant mice are defective in cardiac function

Genotypes Heart rate, bpm IVSd, mm IVSs, mm LVPWd, mm LVPWs, mm LVIDd, mm LVIDs, mm FS, %
+/+ (n = 10) 555.9 ± 42.33 0.348 ± 0.06 0.604 ± 0.12 0.355 ± 0.07 0.624 ± 0.13 1.248 ± 0.13 0.696 ± 0.15 44.63 ± 8.86
−/− (n = 7) 278.6 ± 64.38 0.40 ± 0.12 0.57 ± 0.15 0.571 ± 0.10 0.713 ± 0.10 1.517 ± 0.25 1.287 ± 0.16 19.77 ± 5.31
+/− (n = 8) 537.4 ± 48.28 0.335 ± 0.05 0.573 ± 0.09 0.295 ± 0.04 0.567 ± 0.17 1.306 ± 0.16 0.756 ± 0.16 42.34 ± 8.52
P value <0.0001 0.296 0.629 0.0001 0.170 0.01 <0.0001 <0.0001

Echocardiographic analyses of P0 wild-type (+/+), Dicer heterozygous (+/-), and homozygous (-/-) mutant mice. Values were quantified from five independent M-mode measurements. IVSd, interventricular septal thickness at end diastole; IVSs, interventricular septal thickness at end systole; LVPWd, left ventricular posterior wall thickness at end diastole; LVPWs, left ventricular posterior wall thickness at end systole; LVIDd, left ventricular internal diameter at end diastole; LVIDs, left ventricular internal diameter at end systole; and FS, fractional shortening.