Arterial stiffness is well accepted as a reliable indicator of arterial disease. Increase in carotid arterial stiffness has been associated with carotid arterial disease, e.g., atherosclerotic plaque, thrombosis, stenosis, etc. Several methods for carotid arterial stiffness assessments have been proposed. In this study, in-vivo noninvasive assessment using applanation tonometry and an ultrasound-based motion estimation technique was applied in seven healthy volunteers (age 28 ± 3.6 years old) to determine pressure and wall displacement in the left common carotid artery (CCA), respectively. The carotid pressure was obtained using a calibration method by assuming that the mean and diastolic blood pressures remained constant throughout the arterial tree. The regional carotid arterial wall displacement was estimated using a 1D cross-correlation technique on the ultrasound radio frequency (RF) signals acquired at a frame rate of 505–1010 Hz. Young’s moduli were estimated under two different assumptions: (i) a linear elastic two-parallel spring model and (ii) a two-dimensional, nonlinear, hyperelastic model. The circumferential stress (σθ) and strain (εθ) relationship was then established in humans in vivo. A slope change in the circumferential stress-strain curve was observed and defined as a transition point. The Young’s moduli of the elastic lamellae (E1), elastin-collagen fibers (E2) and collagen fibers (E3) and the incremental Young’s moduli before (E0≤εθ<ε0T) and after the transition point (EεθT≤εθ) were determined from the first and second approach, respectively, to describe the contribution of the complex mechanical interaction of the different arterial wall constituents. The average E1, E2 and E3 from seven healthy volunteers were found to be equal to 0.15 ± 0.04, 0.89 ± 0.27 and 0.75 ± 0.29 MPa, respectively. The average E0≤εθ<εθTInt and EεθT≤εθInt of the intact wall (both the tunica adventitia and tunica media layers) were found to be equal to 0.16 ± 0.04 MPa and 0.90 ± 0.25 MPa, respectively. The average E0≤εθ<εθTAd and EεθT≤εθAd of the tunica adventitia were found to be equal to 0.18 ± 0.05 MPa and 0.84 ± 0.22 MPa, respectively. The average EεθT≤εθMe and EεθT≤εθMe of the tunica media were found to be equal to 0.19 ± 0.05 MPa and 0.90 ± 0.25 MPa, respectively. The stiffness of the carotid artery increased with strain during the systolic phase of cardiac cycle. In conclusion, the feasibility of measuring the regional stress-strain relationship and stiffness of the normal human carotid artery noninvasively was demonstrated in human in vivo.

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-With increasing concern about environmental degradation, it is desirable to decrease energy consumption in all sectors. Drying has been reported to account for anywhere from 12 to 20% of the energy consumption in the industrial sector. Drying processes are one of the most energy intensive unit operations. There are a number of approaches to reduce energy consumption in dryers. This paper reviews some novel strategies used to decrease energy consumption in drying operations. Drying conditions can be modified or the drying equipments can be modified to increase overall efficiencies. Hybrid drying techniques can also be used, such as combining vacuum or convective drying with electro-technologies (microwave, radio frequency, infrared heating). There is much debate on how to define drying and energy efficiencies. Some techniques to determine these efficiencies can be misleading when the goal is to take a holistic approach to determining energy consumption.

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Arterial stiffness has been shown to be a good indicator of the arterial wall diseases. However, a single parameter is insufficient to describe the complex stress-strain relationship of a multi-component, non-linear tissue such as the aorta. We therefore propose a new approach to measure the stress-strain relationship locally in vivo and present a noninvasively, clinically relevant parameter describing the mechanical interaction between aortic wall constituents. The slope change of the circumferential stress-strain curve was hypothesized as a contribution of elastin and collagen, which was noninvasively defined in the term of strain using only radial aortic wall acceleration, i.e., transition strain false(εθTfalse). Two-spring parallel was employed as the phenomenological model and three Young's moduli were accordingly evaluated, i.e., corresponding to the: elastic lamellae (E1), elastin-collagen fibers (E2) and collagen fibers (E3). Our study performed on normal and Angiotensin II (AngII)-treated mouse abdominal aortas using aortic pressure from catheterization and local aortic wall diameters from a cross-correlation technique on the radio frequency (RF) ultrasound signal at 30 MHz and frame rate of 8 kHz. Using our technique, transition strain and three Young’s moduli in both normal and pathological aortas were mapped in 2D. In the results, the slope change of the circumferential stress-strain curve was first observed in vivo under physiologic conditions. The transition strain was identified at the lower strain level in the AngII-treated case, i.e., 0.029±0.006 of normal and 0.012±0.004 of AngII-treated aortas. E1, E2 and E3 were 69.7±18.6, 214.5±65.8 and 144.8±55.2 kPa for normal aortas, respectively, and 222.1±114.8, 775.0±586.4 and 552.9±519.1 kPa for AngII-treated aortas, respectively. This is because of the alteration of structures and content of the wall constituents, the degradation of elastic lamella and collagen formation due to AngII treatment. While such values illustrate the alteration of structure and content of the wall constituents related to AngII treatment, limitations regarding physical assumptions (isotropic linear elastic) should be kept in mind. The transition strain, however, was shown to be an aortic pressure waveform independent parameter that can be clinically relevant and noninvasively measured using ultrasound-based motion estimation techniques. In conclusion, our novel methodology can assess the stress-strain relationship of the aortic wall locally in vivo and quantify informative parameters which are related to vascular disease.