The increasing demand for ultrasonic flow meter (UFM) is due to the absence of moving, protruding parts projecting into the measured flow, transient response, high accuracy and wide range, so that it becomes important in flow measurement. By analyzing the error sources and magnitude of measurements in water, considering the uncertainty caused by sound speed profile and standard length, comprehensively. This research proposes a method to trace the transit time to standard length. Firstly, based on the servo driving and automatic displacement control, a facility which can provide displacement with a minimum displacement step of 10μm, is designed, and has been precisely calibration by laser interferometer. The error function of water temperature uniformity on transit time measurement is evaluated by theoretical model. A high-precision constant system is developed to control the temperature gradient in water better than 5mK, and the Anton Paar MKT50 platinum wire resistance thermometer is being used as the temperature standard. Assuming that the ultrasonic waveform does not change during propagation in water. The transit time for multiple reflections between fixed stainless steel protective layer and movable reflector is measured. The time difference between two different reflections of same wave can be obtained by high-precision cross-correlation algorithm, and the center frequency of the first five cycles are calculated through Hilbert transform. Through the linear increasing experiments, the effects of reflection times, path length and test temperature to the measurement of transit time are compared.

Background: Activating transcription factor 3 (ATF3) is an early response gene that is activated in response to atherosclerotic stimulation and may be an important factor in inhibiting the progression of atherosclerosis. In this study, we directly measured the expression of ATF3 and inflammatory factors in human coronary atherosclerotic plaques to examine the relationship between ATF3 expression, inflammation and structural stability in human coronary atherosclerotic plaques. Methods: A total of 68 coronary artery specimens were collected from the autopsy group, including 36 cases of sudden death from coronary heart disease (SCD group) and 32 cases of acute death caused by mechanical injury with coronary atherosclerosis (CHD group). Twenty-two patients who had no coronary heart disease were collected as the control group (CON group). Haematoxylin-eosin staining was used to observe changes in arterial structure. Western blotting and immunohistochemistry were used to measure the expression and distribution of ATF3, Full list of author information is available at the end of the article-2-inflammatory factors and matrix metalloproteinase-9 (MMP-9) and vascular cell adhesion molecule 1 (VCAM1) in the coronary artery. The Pearson correlation coefficient was used to analyse the correlation between ATF3 protein expression and inflammatory factors and between ATF3 protein expression and structure-related indexes in the lesion group. Results: Compared with those in the control group, the intima and necrotic core in the coronary artery were thickened, the fibrous cap became thin and the degree of vascular stenosis was increased in the lesion group, while the intima and necrotic core became thicker and the fibrous cap became thinner in the SCD group than in the CHD group (P < 0.05). There was no or low expression of ATF3, inflammatory factors, VCAM1 and MMP-9 in the control group, and the expression of inflammatory factors, VCAM1 and MMP-9 in the SCD group was higher than that in CHD group, while the expression of ATF3 in the SCD group was significantly lower than that in CHD group (P < 0.05). In the lesion group, the expression of ATF3 was negatively correlated with intimal and necrotic focus thickness, positively correlated with fibrous cap thickness (P < 0.01), and negatively correlated with inflammatory factors, VCAM1 and MMP-9 (P < 0.01). Conclusions: The expression of ATF3 may be related to the progression and stability of atherosclerotic plaques, and may affect the structural stability of atherosclerotic plaques by regulating the inflammatory response, thus participating in the regulation of atherosclerotic progression.