3% vs 9.2 ± 1.7%, P = .001; Figure 3B). The average number of cells with caspase-3 expression in the treatment group increased significantly compared to that of the control one [(82.6 ± 3.5) × 103 and (21.4 ± 2.3) × 103, respectively; Figure 3A]. All mice were alive during the whole experiment. In the preparatory Venetoclax study, we observed the tumor slices under the TEM and calculated the mean sizes of gaps between vascular endothelial cells (865 ± 5.2 nm; range, 630-1325 nm) for 20 xenograft tumors. This result indicated that average gap sizes between tumor vascular endothelial cells were larger than our NB mean sizes (586 ± 6.0 nm) in our mouse model.

As the time line in Figure 2 showed, we processed the following experiment and observed that there were no statistical differences in the average weights of mice within four groups on day 0 (P = .76) and day 7 (P = .79). As for tumor sizes, the data indicated no differences among four groups

from day 0 to day 7 during the whole treatment process (P = .98; Figure 4A). Histologic analysis showed that there were no significant differences in the percentage of necrotic areas of samples between treatment (TI and T2) and control groups (C1 and C2; P = .21). At the end of treatment, anti–Her-2 therapy response was investigated by IHC analyses of Her-2 and caspase-3 expression in excised tumors. The data showed that the percentages of Her-2–positive expression in mouse tumors in the two treatment groups

(TI and T2; 54.5% click here and 66.7%) were lower than the control ones (91.2% and 80%, respectively; Progesterone Figure 6B). This indicated that there was effective treatment in mouse xenograft models (T1 and T2 groups) and the trastuzumab treatment also induced apoptosis cells in these tumors. Thus, the percentages of caspase-3–positive expression in mouse samples in the two treatment groups (TI and T2) were higher than those of the control groups (C1 and C2; 90.0% and 83.3% vs 66.7% and 70%, respectively; Figure 6A). The ultrasound contrast imaging detected NB signals in in vivo models after 60 minutes from the injection of NB through the mouse tail vein, and this process was carried out under different time points (days 0, 3, 5, and 8; Figure 5A). Then, ultrasound imaging software analyses indicated that the average mean intensities of targeted bubbles in ROIs ( Figure 5B) in the T1 group were significantly higher than those in the other three groups (T2, C1, and C2; P = .001; Figure 4C). However, there were no differences within the three groups (T2, C1, and C2 groups), when one group was compared to other three groups (T2 vs T1 + C1 + C2, P = .74; C1 vs T1 + T2 + C2, P = .51, and C2 vs T1 + T2 + C1, P = .33, respectively). As for peak intensities of intratumor microbubble perfusion, they were also higher in the T1 group than those in the other groups (T2, C1, and C2; P = .00), but there were no differences within T2, C1, and C2 groups (P = .43, .96, and .42, respectively; Figure 4B).