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These three factors accounted for 52% of maternal mortality variation between countries.
Mortality variations after emergency surgery were less pronounced for 1 yr-RSMR than for in-RSMR.
However, the performance difference between the best- and worst-fitting model was not large as measured by the proportion of daily mortality variation (i.e., deviance) explained: 27.9% for the SSC model and 24.7% for the deviation from maximum temperature model.
Cosinor analysis was performed for a visual demonstration of mortality variations between seasons.
The significant Genotype*Load interaction represents genetic variation for mortality tolerance.
We also found genetic variation for mortality tolerance in the acute phase of infection (Model C; Table 7; Genotype*Load: p < 0.001), but not in the chronic phase (Model C; Table 7; Genotype*Load: p = 0.909).
There is significant geographic variation for both mortality and hospital costs.
Marked variation for infant mortality and the characteristics of industrialization was observed among the 66 sub-regions of Poland.
We found genetic variation for resistance, mortality tolerance, and fecundity tolerance in the acute phase of the infection, but only for resistance in the chronic phase.
The six additional study clinics were not included in the calculation of the coefficient of variation for 18-month mortality.
The presence of genetic variation for fecundity and mortality tolerance is contrary to simple theoretical models, and we show that context dependence and non-independence between defense strategies may be maintaining this variation.
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