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Lethality was complete in Act::Gal4>UAS::dsCycG2 males and reached 86% in Act::Gal4>UAS::dsCycG2 females.
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Thirty-four TANK1+/+, sixty-six Tand1+/−, and thirty-five TANK1−/− mice were observed in 135 offspring from TANK1+/− intercrosses, consistent with Mendelian segregation and indicating that no lethality was associated with complete TANK1 inactivation.
However, even in C57BL/6 backcrossed mice where the penetrance of postnatal lethality is almost complete, Prokr2 null mice do have milk in their stomachs.
However, lethality was not prevented by complete inhibition of microthrombosis and consumptive coagulopathy with DEGR-Xa, an active site-modified, inactive derivative of Xa that binds to Va, and thus selectively and potently blocks thrombin generation by the prothrombinase complex [ 28].
First, while lethality with ET was evident before challenge was completed (<24 h), with LT the first death didn't occur until 24 h after challenge.
Nevertheless, complete protection against lethality was afforded by the treatment with the neuraminidase inhibitor peramivir given once daily for 5 days after the challenge (10 mg/kg/day).
If AMD was given after TNF, essentially no lethality was seen.
Cellular lethality was assessed by measurement of lactate dehydrogenase (LDH) 24 hrs later.
Pneumonia lethality was 49%.
Lethality was assayed daily for 8 d.
Per cent lethality was noted [ 12].
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