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No deaths occurred when intoxicated mice were treated with 80 µg of polyclonal goat anti-ricin antibodies by 6 h post-intoxication (Fig. 4B) but about 30% lethality were observed when antibodies were applied at 7 h post-intoxication.
In both environments, stunted seedlings and lethality were observed and postulated to be due to HN.
Taf4ahep−/− animals are born at Mendelian ratios and no prenatal abnormalities or lethality were observed (data not shown).
Analyses of rack1a, rack1b and rack1c double and triple mutants, however, revealed that rack1b and rack1c can enhance the rack1a mutant's developmental defects, and an extreme developmental defect and lethality were observed in rack1a rack1b rack1c triple mutant.
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An expressive difference in the predicted lethality was observed between the classic approach and the proposed model.
At the same time, in the control group of animals, lethality was observed in 11% of cases, and suppurative complications were observed in 100% of cases.
The result showed that the LD50 value of BtOH and EtOAc fractions could not be determined as no lethality was observed up to 40 g/kg (p.o). in mice.
Lethality was observed between days 2 4 after intoxication.
No lethality was observed in Dcas1/+ embryos (n = 613).
When the shRNA was ubiquitously induced by EIIa-Cre driver, embryonic lethality was observed.
Lethality is observed in a high proportion of heat shock treated embryos over-expressing menin [16].
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