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. 2001 Jan 23;98(3):1059–1064. doi: 10.1073/pnas.031573498

Table 2.

Resistance to indomethacin-induced fetal DA closure and neonatal mortality results from the deficiency of COX-2

Offspring genotype Fetal DA closure,* % incidence Neonatal survival, % incidence
COX-1(+/+)/COX-2(+/+) 100 (6/6) 0 (0/7)
COX-1(+/−)/COX-2(+/+) 100 (5/5) 0 (0/5)
COX-1(−/−)/COX-2(+/+) 100 (6/6) 0 (0/8)
COX-1(+/+)/COX-2(+/−) 100 (6/6) 0 (0/6)
COX-1(+/−)/COX-2(+/−) 100 (6/6) 0 (0/8)
COX-1(−/−)/COX-2(+/−) 100 (8/8) 0 (0/14)
COX-1(+/+)/COX-2(−/−) 0 (0/6) 100 (5/5)
COX-1(+/−)/COX-2(−/−) 0 (0/6) 100 (7/7)
COX-1(−/−)/COX-2(−/−) 0 (0/6) 100 (12/12)
*

Indomethacin-induced fetal DA closure was determined on gestation day 18.5 after maternal indomethacin administration 4 h prior to Cesarean delivery. In parentheses are number closed/number analyzed. 

Neonatal survival after maternal indomethacin administration was determined after Cesarean delivery on gestation day 19.5. The surviving pups were sacrificed 5 h after birth. In parentheses are number alive/number born.