diff --git a/content/15.results.md b/content/15.results.md
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@@ -253,7 +253,7 @@ After the construction of hybrid promoter, our engineered bacteria had the abili
 
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-**Figure 11 | Ultrasound approach tracks engineered bacteria.** [$^[10]$] Bourdeau *et al* [$^9$] genetically engineered bacteria to express what they term acoustic response genes (ARG), which encode the components of hollow structures called gas vesicles that scatter sound waves and generate an echo that can be detected by ultrasound.
+**Figure 11 | Ultrasound approach tracks engineered bacteria.** [$^{10}$] Bourdeau *et al* [$^9$] genetically engineered bacteria to express what they term acoustic response genes (ARG), which encode the components of hollow structures called gas vesicles that scatter sound waves and generate an echo that can be detected by ultrasound.
 
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@@ -327,8 +327,8 @@ Based on the above presentation, we successfully expressed vesicular proteins in
 
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-Though tumor-targeting and ultrasound-sensing has been achieved, controlled immunogenicity during in vivo delivery is still a problem. In order to avoid viremia as much as possible, we expect to mask epitopes of EcN before ultrasound imaging and achieve rapid clearance after diagnosis. Thus, we focused on engineering the capsular polysaccharide (CAP). CAP is a loose mucous substance located on the surface of the cell wall, protecting bacteria from environmental influences. It is worth mentioning that the thickness of CAP changes dynamically, and if not generated endogenously, its thickness will naturally become thinner. Harimoto *et al* [$^[11]$] have designed an inducible capsular polysaccharide (iCAP) system. They used the kfiC gene to regulate the expression of CAP. As an endogenous gene in EcN, kfiC encodes a glycotransferase essential in CAP biosynthesis, thus its expression determines the rate of CAP production, and then impacts the thickness of cellular outer layer.
-Based on the previous work, we designed the following circuit (**Fig. 16a**): kfiC under the control of ParaB (an arabinose-inducible promoter) would be transformed into EcN ∆asd ∆kfic. Prior to delivery, the bacteria would be induced by arabinose to start kfiC expression, and then encapsulation from CAP production, preparing it for host immune evasion and tumor focus localization. As CAP gradually degrades and cellular outer layer becomes thinner over time, the remaining bacteria in blood would be rapidly cleared, thus reducing long-term inflammatory response and toxicity risks (**Fig. 16b**) [$^[11]$].
+Though tumor-targeting and ultrasound-sensing has been achieved, controlled immunogenicity during in vivo delivery is still a problem. In order to avoid viremia as much as possible, we expect to mask epitopes of EcN before ultrasound imaging and achieve rapid clearance after diagnosis. Thus, we focused on engineering the capsular polysaccharide (CAP). CAP is a loose mucous substance located on the surface of the cell wall, protecting bacteria from environmental influences. It is worth mentioning that the thickness of CAP changes dynamically, and if not generated endogenously, its thickness will naturally become thinner. Harimoto *et al* [$^{11}$] have designed an inducible capsular polysaccharide (iCAP) system. They used the kfiC gene to regulate the expression of CAP. As an endogenous gene in EcN, kfiC encodes a glycotransferase essential in CAP biosynthesis, thus its expression determines the rate of CAP production, and then impacts the thickness of cellular outer layer.
+Based on the previous work, we designed the following circuit (**Fig. 16a**): kfiC under the control of ParaB (an arabinose-inducible promoter) would be transformed into EcN ∆asd ∆kfic. Prior to delivery, the bacteria would be induced by arabinose to start kfiC expression, and then encapsulation from CAP production, preparing it for host immune evasion and tumor focus localization. As CAP gradually degrades and cellular outer layer becomes thinner over time, the remaining bacteria in blood would be rapidly cleared, thus reducing long-term inflammatory response and toxicity risks (**Fig. 16b**) [$^{11}$].
 
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@@ -342,8 +342,8 @@ Based on the previous work, we designed the following circuit (**Fig. 16a**): kf
 
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-We tried to knockout the kfiC gene from the genome of EcN ∆asd in the same way as the asd gene (see Result 2.1), yet without success. A possible cause may be that both asd and kfiC genes are essential to bacterial cell wall synthesis, thus the absence of both would be fatal to both. We propose to change the output necessary gene of hybrid promoter to ThyA[$^[12]$]. ThyA encodes thymidylate synthase in E. coli, which is required in nucleotide biosynthesis pathways, and does not interfere with cell wall synthesis.
-Nevertheless, we demonstrated the feasibility of our iCAP system through modelling. By changing the elimination rate (k_e) in our MC model (see Dry Lab - Model), we were able to simulate an enrichment to the Tumor compartment as well as rapid clearance in other compartments with suitable elimination rates determined by CAP thickness.
+We tried to knockout the kfiC gene from the genome of EcN ∆asd in the same way as the asd gene (see Result 2.1), yet without success. A possible cause may be that both asd and kfiC genes are essential to bacterial cell wall synthesis, thus the absence of both would be fatal to both. We propose to change the output necessary gene of hybrid promoter to ThyA[$^{12}$]. ThyA encodes thymidylate synthase in E. coli, which is required in nucleotide biosynthesis pathways, and does not interfere with cell wall synthesis.
+Nevertheless, we demonstrated the feasibility of our iCAP system through modelling. By changing the elimination rate [$k_e$] in our MC model (see Dry Lab - Model), we were able to simulate an enrichment to the Tumor compartment as well as rapid clearance in other compartments with suitable elimination rates determined by CAP thickness.
 This design can be utilized to optimize therapeutic bacteria administration to maximize curative effects and minimize side effects. 
 
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