## 3 Results
### Metabolite Variance across Multiwell Fluidic System to Ascertain Sites of Generated Cell Byproducts
#### 3.8.1 Trending Relevance
NEF stimulates GSH activity in wells 3 (*), 4 (*), 5 and (*), is non-significant in wells 6-7, induces again in wells 8 (*), 9 (*), and 10 (*), then falls below DMSO control in well 11 (*). For Studies 9-12, GSH trending responses are summarized in Table 8.  
\begin{table}
\begin{tabular}{c c c} \hline \hline  & Trending Chart (system wide): & Discloses a bell curve response having inferior function at upstream well 3 (0.4-fold \(\Delta\)), maximum functions in midstream wells 6–9 (1.3-fold \(\Delta\)), and diminishing function at downstream well 11 (0.7-fold \(\Delta\)); Figure 11(a2). \\ \cline{2-3}
**Study 5** & Variability Chart (adjacentwell): & Confirms irregularities in upstream well 4 (process shift = direct ASA influence), and midstream wells 6–9 (special cause or generated metabolite = indirect ASA influence) given that well 5 has lower functions; Figure 11(a3). \\ \cline{2-3}  & Blended Data (Figure 11(a1–a3)): & Infers ASA directly and indirectly stimulate CYP3A4 activity in HepaRG cells. \\ \hline  & Trending Chart (system wide): & Discloses an exponential growth curve response, Figure 11(b2), revealing rat hepatocyte CYP3A4 functions 7.5\(\times\) to 33.1\(\times\) are higher than HepaRG functions, ranges being 3.0-to-43.0 fold versus 0.4-to-1.3 fold, respectively. \\ \cline{2-3}
**Study 6** & Variability Chart (adjacent well): & Confirms irregularities having partitioned influences. Influence-1, well 3, being unchanged and replicates DMSO control functions (i.e., no direct ASA influence = no process shift). Influence-2, wells 4–9, have upregulated CYP3A4 at 1.5-to-7.0-fold ranges (i.e., special cause A (e.g., metabolite A = indirect ASA influence)). Influence-3, wells 10–11, have top-heavy upregulated CYP3A4 with 20-to-40-fold ranges (i.e., special cause A† (e.g., additional cell generating impacts = indirect ASA influence)); Figure 11(b3). \\ \cline{2-3}  & Blended Data (Figure 11(b1–b3)): & Infers ASA endogenous metabolites stimulate CYP3A4 induction in rat hepatocytes, i.e., wells 4–11. \\ \hline  & Trending Chart (system wide): & Discloses NEF outcomes with fold levels 0.9–1.0-fold below the DMSO vehicle control. A marginal rise is evident at wells 7–8; Figure 11(c2). \\ \cline{2-3}
**Study 7** & Variability Chart (adjacent well): & Confirms activity as minimal, no irregularity across the entire uchannel (i.e., a process shift \\ \cline{2-3} NEF on HepaRG cells & (adjacent well): & as direct NEF exposure inhibits CYP3A4 functions); Figure 11(c3). \\ \cline{2-3}  & Blended Data (Figure 11(c1–c3)): & Infers that NEF directly impedes CYP3A4 in HepaRG cells. \\ \hline  & Trending Chart (system wide): & Discloses three notable cell-function influencers; Influence-1 with upstream wells 3–6 at fold levels 0.6–1.0 below the DMSO vehicle control, Influence-2 shows wells 9–10 at fold levels 2.3-to-8.3-fold above DMSO control, Influence-3 displays downstream well 11 at 1.9-fold above the DMSO control; Figure 11(d2). \\ \cline{2-3}
**Study 8** & & Confirms irregularities in upstream wells 4–6 (i.e., process shift = direct NEF influence), highly irregular in downstream wells 9–10 (i.e., special cause or generated metabolite = indirect NEF influence), and a decline in downstream well 11 (i.e., unusual outcome = tertiary indirect NEF influence); Figure 11(d3). \\ \cline{2-3}  & Blended Data (Figure 11(d1–d3)): & Infers NEF has direct, indirect, and tertiary influences on CYP3A4 mutable responses in rat hepatocytes. \\ \hline  & Trending Chart (system wide): & Discloses a delayed exponential growth curve with inferior functions upstream and midstream (0.2–0.6-fold \(\Delta\)) and ramping at downstream well 11 (1.19-fold \(\Delta\)). Only well 11 resides in \(\pm\)3\(\sigma\) DMSO boundary limits; Figure 12(a2). \\ \cline{2-3}
**Study 9** & & Variability Chart (adjacentwell): & Confirms functions remain similar across the entire uchannel (not well 11), inferring direct ASA exposure induces a process shift; Figure 12(a3).