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Toggle의학논문 번역에 대해서 알아 보겠습니다(한영번역)
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의학논문 번역(한국어 원본)Blood vessel의 deformation은 stenosis 이후 영역보다 stenosis 이전 에서 크게 발생하며 이는 stenosis를 지나면서 pressure이 강하되며 이에 따라 stenosis 이후에서 vessel wall의 expansion이 상대적으로 적게 발생하기 때문이다. Stenosis가 시작되는 부분에서 radial directional strain은 0.20, 0.50, 1.25 MPa의 elastic modulus를 가지는 FSI model에 대해 각각 0.021, 0.010, 0.004 로 발생하며 2-way FSI method의 특성으로 blood vessel wall의 motion이 매시간 내부 flow와 interaction을 하기 때문에 maximum strain은 elastic modulus에 정비례하지 않는다. 또한 각 FSI model에서 maximum deformation이 발생되는 즉, 최대로 expansion되는 peak time은 각 model에 대해 t/tp = 0.16, 0.15, 0.14로 vessel wall이 유연할수록 blood vessel의 vibration period가 길어 졌다. |
의학논문 번역(영어 번역본)The deformation of blood vessels occurs on larger scale in areas past the stenosis than before it, since pressure rises at the stenosis and hence the expansion of the vessel wall is relatively smaller past the stenosis. At the point where stenosis begins, the radial directional of 0.021, 0.010, and 0.004 occurred in the FSI models with elastic moduli of 0.20, 0.50, and 1.25 MPa respectively. As the motion of the blood vessel wall interacts with the internal flow at every moment in the 2-way FSI method, the maximum strain is not proportional to the elastic modulus. Also, the moment of maximum deformation, or peak expansion, was t/tp = 0.16, 0.15, and 0.14 for each model, and the more flexible the vessel wall, the longer the vibration period of the blood vessel. These differences in vessel elasticity induced periodic differences in blood flow, as well as differences in axial velocities, pressures, and WSS. Fig. 5 shows the time history of the axial velocity profile in stenosis when angular velocity is 4 rev/s. As the elastic modulus decreases, the change period for axial velocity became longer and the magnitude of the peak velocity became greater. In the rigid wall model, a peak velocity of 0.804 m/s occurred at t/tp = 0.16 which is the inlet pulsatile’s peak time, but in the FSI model with the elastic modulus of 0.2 MPa, the peak occurred at t/tp = 0.20, when the velocity reached 0.939 m/s, or 17% greater than that in the rigid body model. This is because the pulsatile profile remains homogenous in all sections in the rigid body model, but in the FSI model the vibration of the wall affects blood flow. In particular, when the vessel contracts, the vessel’s area decreases, thereby increasing velocity inside the vessel. Vessel walls directly affected by pressure had identical periods as the pressure. Fig. 6(a) shows that in the FSI model with the elastic modulus of 0.5 MPa, the change periods of pressure and area are the same. But periodic differences occurred for pressure due to the differences in the elastic modulus. Fig 6(b) presents the time history of average pressure distribution at 1D downstream from stenosis when angular velocity is 4 rev/s, showing that pressure and periodic differences decreased after passing through stenosis. The period of pressure became shorter when elastic modulus became smaller, as was the case with axial velocity, but the maximum magnitude tended to decrease. The material properties of blood vessels also affected the WSS distribution. Fig. 7 shows the time history of WSS distribution at 4 downstream locations. In order to account for the asymmetric flow of stenosed artery, the average WSS of the radial tangent at each location was used. Negative WSS means that there was backflow, and the change of a negative value to positive or vice versa indicates a fluid separation point or a reattachment point near the wall. Near the wall at 1D downstream, which is immediately after the stenosis, there was backflow at all times due to the effect of the stenosis, and in subsequent sections generally fluid recirculation zones (FRZ) developed, where the flow stops or reverses, until systole (t/tp = 0.40). Compared to the rigid wall model, in the case of the FSI model the change period of WSS differed according to the vessel vibration period, because of the differences in internal flow caused by the differing vibration period which depends on the vessel’s elasticity. As can be seen in Fig 7(b), in the FSI model with the least elasticity (E = 0.20 MPa), the blood vessel’s vibration period was the longest, and therefore the change period for WSS was also the longest. Moreover, the greater the vessel elasticity, the shorter the vibration period of WSS. These changes in WSS led to differences in the direction and the size of WSS, as well as differences in the time of FRZ formation and disappearance. The fact that the minimum WSS in the rigid body model shown in Fig. 7(c) was -2.55 Pa whereas it was -4.65 Pa, or 1.8 times greater, in the FSI model (E = 0.50 MPa) further illustrates this process. FRZs, where flow stops or reverses, are created as the result of stenosis, and these form or disintegrate depending on the radial velocity-axial velocity ratio (Sung et al., 2009). Fig. 8 shows the FRZ and the axial velocity profiles of blood vessel when elastic modulus was 0.5 MPa and angular velocity 6 rev/s. The black area indicates the FRZ, and the jet velocity profile, shaped like a piston, appears behind the stenosis in flow acceleration phase. However, the size of the FRZ changed according to the vessel’s elastic modulus. In general, as elastic modulus decreased, the size of the FRZ tended to decrease also. Fig. 9(a) shows the FRZ in the FSI models with elastic moduli of 0.50 MPa and 0.20 MPa and in the rigid wall model, during diastole (t/tp = 0.16) in blood vessel with an angular velocity of 4 rev/s. The black area in the figure represents the FRZ, which decreases in size as elastic modulus decreases. Fig. 9(b) shows the FRZ in the FSI model with elastic modulus of 0.2 MPa and in the rigid wall model, during systole (t/tp = 0.40). It can be seen that the size of the FRZ becomes smaller in the FSI model even during systole (t/tp = 0.40) when the FRZ reaches its maximum size. This means that wall expansion increases as blood vessel becomes more flexible, leading to the reduction of reversal or stagnation of blood flow after passing through stenosis. Hence, the difference in the characteristics of blood flow in the rigid body model and the FSI model stems from the presence or the absence of vessel wall motion as a factor. In addition, there were differences in blood flow depending on the vessel elasticity, which directly influences the vessel wall motion. |
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이상 중앙대학교에서 의뢰한 의학논문 번역(한영번역)의 일부를 살펴 보았습니다.