Embryos from Nlrp2- deficient females had similar abnormal cleavage and fragmentation and arrested by blastocyst stage, irrespective of fertilization mode.

Pregnancies with transferred embryos from Nlrp2- deficient females produced smaller litters, stillbirths, and offspring with birth defects and growth abnormalities.

Intact females and estrogen-treated castrates demonstrated increased bcl-2 mRNA and protein expression compared with males and estrogen- deficient females, accompanied by a decrease in infarct size.

We found that G6PD- deficient females were significantly protected against uncomplicated malaria, but this protection was only seen when G6PD deficiency is described using enzyme activity.