More recently, 23 commercial field trials (n = 6,660,569 pigs) were summarized and the frequency of dead pigs, nonambulatory pigs, and total transport losses at the processing plant were 0.25, 0.44, and 0.69% respectively.
This is thought to be because of the frequency of dead animals, which can be an important source of food.
Mortality rates were calculated by determining the frequency of dead worms relative to the total counted.
Here, the frequency of dead 7-AAD+ cells increased moderately over 96 hours (Figure 2A) whereas per cell ex vivo binding of DAB4 increased marginally (Figure 2B).
Anaemic homozygous embryos were still detected at 13.5 dpc, but in reduced numbers (the frequency of dead embryos was 10%) and they showed no signs of tissue necrosis.
Given the frequency of dead and dying homozygous embryos at 14.5 dpc (45%), we analysed mutant embryos at 14.5 dpc (if still alive) and 13.5 dpc.
Most dead cells showed ROS generation in each leaf sample, and no significant difference in the frequency of dead cells with ROS was observed between leaf samples of the WT and type III necrosis lines (Fig. 6C).
In this setting, the frequency of dead cells was significantly decreased in LAPTM5 siRNA-transfected GOTO cells, compared with that in control siRNA-transfected GOTO cells (p = 0.035 for Baf.A1; p = 0.022 for ALLN) (Figure 3G).
In contrast, chemotherapy not only markedly increased the frequency of dead tumor cells (Figure 2A) but also produced a cumulative increase in DAB4 binding to each dead tumor cell (Figure 2B), and suggested that DNA-damaging drugs induced tumor cell expression of La in vivo.
In control tumors during the 96-hour observation period, the frequency of dead 7-AAD+ cells increased from 26±3 to 46±2% (Figure 2A) in parallel with the increase in DAB4 tumor accumulation from 17±1 to 34±4% of the injected dose per gram of tumor tissue (see Figure S2 online).
