## 4 Discussion  
Previous studies have already addressed the characteristics of normal body tissues or lesions in T1 images by external parameters, but there is a lack of data regarding the SI changes of GBCA due to TE. Furthermore, GBCAs have been used clinically for the purpose of T1 enhancement without detailed information regarding the relationship between the parameters and response of gadolinium. However, the experiments in this study indicated that the extent of signal enhancement in T1 imaging is affected by TE. First, as shown in Figure 5c, the phantom study examined the effect of TE on signal enhancement between water and fat. Specifically, as the TE was decreased, there was almost no change in SSI1, but there was a gradual increase in FSI1. This is because the energy transfer efficiency in fat, which is a carbon-based macromolecule, was better than that of saline in a free water state. The CPFS graph in Figure 5d shows how changing TE affected the contrast between free water and fat. In terms of contrast enhancement, as shown in Figure 5b, AST increased with decreasing TE. Likewise, as shown in Table 4 and Figure 5a, RSP was earlier for shorter TE, meaning that the visible contrast enhancement response formed more rapidly. Decreasing TE was also associated with increased MPSI and earlier formation of the MPP. Consequently, EPMS also increased with decreasing TE, as shown in Figure 5d. In order to compare the improvement in contrast enhancement between different concentrations, we quantified the improvement and expressed this as EP; as shown in Figure 5e, decreasing TE was associated with a shift in the peak of the graph toward higher concentrations. In particular, signal enhancement was greatest at TE 7 msec, which means that the GBCA response was faster at TE 7 msec, resulting in greater signal enhancement. In other words, the phantom study demonstrated that diagnostically useful contrast enhancement can be achieved by decreasing TE. We also conducted a clinical study for direct comparisons with brain images, and obtained the following results. First, as seen in Figure 6, the GBCA signal enhancement at low concentrations was visibly increased in the clinical phantom as TE was decreased. Indeed, the ASTM graph in Figure 7a demonstrates increasing SI with decreasing TE. In order to compare the free water SI of saline in the clinical phantom and CSF in the body, we produced the graph in Figure 7b. Little difference was observed between the values at all TEs, with both measures varying in the range 120-130 a.u. In other words, the SI in free water was similar in the clinical phantom to that in the body. The SI in the brain parenchyma was higher than in free water, as shown by the SBP in Figure 7b, and FSI2 was even higher than SBP. Here, SBP and FSI2, with a constant molecular weight, showed an increase in signal with decreasing TE, whereas there was little change in the CSF signal. Usually, when GBCA is delivered into the body, it mixes with the blood, resulting in a decrease in GBCA concentration over time. Based on this principle, each container in the clinical phantom can be considered to represent a mass or cancer. We obtained the contrasts between each phantom container and the brain images in Figure 6 as percentages, and compared the effect of TE on contrast enhancement in each container with that of the brain parenchyma, in order to quantify this contrast. For this purpose, we calculated EPSS and EPSC, as well as their corresponding averages, AEPSS and AEPSC, and have displayed these measures in both Table 4 and Figure 7c. Figure 7c shows a gradual increase in AEPSS and AEPSC with decreasing TE. Thus, if the phantom is considered to represent a tumor, given the  
Figure 7: Graphs of SI changes in the clinical study. **(a)** changes in SI at different concentrations and ASTM by TE; **(b)** changes in SSI\({}^{1}\), SSI\({}^{2}\), FSI\({}^{2}\), SBP, SC, and MPSI, by TE; **(c)** changes in EPSS, AEPSS, EPSC, and AEPSC by TE.