A 56‐year‐old woman came to the hospital with fever and skin eruptions. A rise in myogenic enzyme and the presence of antileucocyte antibody were noticed, along with the gradual appearance of myalgia in both lower extremities, and muscle weakness. Steroid therapy was started under the diagnosis of polymyositis. The steroid was reduced because of mental disturbance but immediately the patient developed high fever. Various forms of treatment were carried out but there was no improvement, and the patient died. At autopsy there were scattered purpura on the skin, and the muscles were atrophic and yellowish‐grey in color. Histopathologically, there was inflammatory cell infiltration and muscle fiber degeneration visible in many of the muscles, and the findings showed evidence of polymyositis. There were intranuclear inclusions in the lungs, ovaries, and adrenal glands, and this was diagnosed as generalized cytomegalic inclusion disease. Fibrin thrombi were found in the kidneys, lungs, and adrenal glands and this was pathologically diagnosed as disseminated intravascular coagulation. Endothelial cell damage caused by cytomegalovirus was assumed to be involved to a large extent in triggering the disseminated intravascular coagulation. ACTA PATHOL. JPN. 35: 723–730, 1985.
In the field of Dermatology, one of the representatives of oxidative stresses is ultraviolet irradiation. Repetitive ultraviolet exposure results in cutaneous photoaging. Otherwise, polychlorinated biphenyls (PCB) give rise to superoxide, which means Yusho patients have been affected by oxidative stress for more than thirty years. In order to examine the influence of oxidative stress by PCB to the skin, we measured the "areas cutanea" in the inner aspect of upper arm in Yusho patients and in age-matched controls. "Areas cutanea" were significantly smaller in Yusho patients than in controls. Although PCB can give an oxidative stress, the influence seemed to be little to the skin. There might be another mechanisms involved in this result except the oxidative stress by PCB. Further examination should be conducted in the future.
High-performance bottom-gate thin-film transistors (TFTs) have been realized with excimer-laser-crystallized polysilicon films, for the first time. TFT characteristics were greatly dependent on the silicon film thickness as well as the pulsed-laser energy density. It was found also that posthydrogenation based on hydrogen-radical annealing improves the TFT characteristics drastically. The field-effect mobilities exceeded 220 cm 2 /Vs for electrons and 140 cm 2 /Vs for holes, respectively.
In order to model and understand complex dynamics such as automotive engines, it is meaningful to find a low dimensional structure embedded in a large number of physical variables. In this paper, we utilize several types of autoencoders for feature extraction of internal dynamics data of an engine air path system. In particular, the practical usefulness is examined through its application to dimensionality reduction, state estimation, and data replication. In addition, a unified framework of feature extraction and dynamics identification is also discussed.
In the recent article by Spronck et al.[1], the authors concluded that β and cardio-ankle vascular index (CAVI) are inherently blood pressure (BP)-dependent, potentially leading to erroneous conclusions in arterial stiffness trials. There are some useful insights in the article, and these might contribute to a deeper understanding of the concept of measuring arterial stiffness, but the title of the article and the conclusions reached are ultimately inaccurate and misrepresent the concept of the CAVI. We would like to explain our reasoning behind why we reached this conclusion. First, as the authors point out, there is a difference between Hayashi's beta (described as βo in this article) [2] and Kawasaki's beta (β) [3]. Hayashi's beta is based on a reference BP at 100 mmHg, whereas Kawasaki's beta is based on DBP. It is not possible to measure the diameter change around a reference value of 100 mmHg clinically in each patient. Therefore, for practical reasons, Kawasaki's method has been employed. The difference between β and βo has already been referred to by Kawasaki et al.[3]. He reported that this difference is not clinically significant. Kawasaki's β arterial mathematical model has been generally accepted and has prevailed. This is one reason why CAVI was developed based upon Kawasaki's β. Even though there are differences between βo and β, both are mathematical models reflecting proper arterial stiffness independently from BP at measurement time. However, in their article, the authors assumed βo as a 'ground truth' and only demonstrated that β changed with BP in comparison with βo. They provided no evidence or logical arguments to assess which method is superior to the other. Therefore, the statement that 'Arterial stiffness index beta inherently depends on blood pressure' is incorrect. Second, the authors presented the equation cardio-ankle vascular index o (CAVIo) = 2ρPWV2/Pd − ln(Pd/Pref) [Eq. (9)] and compared it with CAVI using simulation data. They demonstrated that CAVIo is not dependent on BP, whereas CAVI does change with BP. CAVI and CAVIo are based on stiffness index β and a wave equation derived from Newton's second law (Bramwell–Hill's equation in the case of the artery). The difference between CAVI and CAVIo is that CAVI employs β over a range of diastolic to systolic pressures and CAVIo employs β at diastolic pressure. Bramwell–Hill's equation is then applied to the β or βo equation. We employed SBP and DBP in the measurement of CAVI [4]. CAVIo uses diastolic pressure as the standard reference value. If the length of the arterial pathway being measured is short enough, diastolic pressure would not significantly change. However, it is known that diastolic pressure decreases, and systolic pressure increases from the origin of the aorta to the peripheral arteries [5]. Therefore, in case of the long arterial pathway, adoption of one point of DBP only becomes less accurate as a reference value representing the entire length of the pathway. In this way, there is a concern that CAVIo along a long pathway becomes less accurate. In the case of CAVI, both SBP and DBP are used. Although both methods are mathematically different and each have rational basis, both also have their limitations. The clinical utilities of both equations will be important, and those are presented later. Third, the authors compiled Table 1 based upon a virtual calculation. At a glance, it seems that the authors tested both arterial stiffness indexes when BP changed, and that CAVIo did not change, whereas CAVI did change. However, upon closer scrutiny, it seems that the simulation was designed not to change the CAVIo value between baseline and follow-up, and clinical data were generated using normally distributed random numbers simulating biological variation. As there is a mathematical difference between CAVI and CAVIo, it is natural that CAVI would change in relation to CAVIo, when BP changed. Therefore, the results of the simulation only showed that there are some differences between CAVI and CAVIo when BP changes, but no evidence or logic was presented to show which method is more accurate than the other. No clinical data of any kind were included in this simulation, though the terms 'young subject' and 'older subject' are included in the text, which may cause some misunderstanding. As for the relationship between CAVI and BP at the time of measurement, the independency of CAVI from BP was confirmed experimentally in man in vivo in Shirai et al. [6]. In this article, we demonstrated that by administration of metoprolol, β1 selective blocker, BP decreased, but CAVI did not significantly change, indicating that CAVI is independent from BP at measuring time. Fourth, we tried to find out the actual difference between both CAVI and CAVIo in two clinical studies. At first, we reanalyzed part of the data of the article in Shirai et al. [6] as shown in Fig. 1. When metoprolol was administered, BP decreased, and both CAVI and CAVIo did not change significantly. When doxazosin was administered, BP decreased. At this time, CAVI and CAVIo decreased in the same way. The tendency of both values was parallel and essentially the same. The significance in statistical analysis was almost the same.FIGURE 1: The comparison between cardio-ankle vascular index and cardio-ankle vascular index o during administration of metoprolol and doxazosin. Data are presented as the mean ± standard error. Paired t test was used to compare preadministration and postadministration value. * P < 0.05, ** P < 0.01, *** P < 0.001. BP, blood pressure; CAVI, cardio-ankle vascular index; CAVIo, cardio-ankle vascular index o; HR, heart rate.Next, we reanalyzed the epidemiologic data reported by Suzuki et al.[7]. The number of patients was 3665 in the healthy group and 4988 in the hypertensive group. Patients were also divided by sex and age (elderly or working age). CAVI and CAVIo values of the hypertensive group were significantly higher than those in the healthy group in all sex and age categories (Fig. 2). The significance in statistical analysis of both indexes was the same.FIGURE 2: The comparison between cardio-ankle vascular index and cardio-ankle vascular index o in a hypertensive group and a healthy group. Data are presented as the mean ± SD. Unpaired Student's t test was used in comparisons with two groups. * P < 0.001. CAVI, cardio-ankle vascular index; CAVIo, cardio-ankle vascular index o.These results suggested that the claim that the existing implementation of CAVI could lead to erroneous conclusions in arterial stiffness trials is not at all the case. In summary, the beta theory-derived index, which the authors presented in Eq. (9), is elegantly presented and has some merit in mathematical terms. However, the equation used by CAVI is perfectly valid as a tool for measuring arterial stiffness in a real-world setting. The difference between the two arterial mathematical methods has been shown not to be significant. Even though there is some difference between the two methods, both are mathematical models that represent actual arterial stiffness, and as such, both can be considered valid for use. In practice, there is no possibility that CAVI could lead to erroneous conclusions in arterial stiffness trials. These results suggest that the title of this article and its conclusions should be amended as they misrepresent the essence and effectiveness of CAVI. ACKNOWLEDGEMENTS Conflicts of interest There are no conflicts of interest.
Male Wistar rats weighing 280g were subjected to the stress condition in which the rats were thrusted unceasingly and harassingly with a bamboo stick by the reseacher, for twenty minutes a day for a period of three and twelve months. The blood pressure reached a high mean value (191±3 S. E.) in twelve months. Mean organweight to body-weight ratios of heart, kidney and adrenal gland when compared to nonstressed controls were increased, and that of thymus was decreased. One of the animals subjected to the stress developed significant vascular pathology in the form of panarteritis like arteriopathy and simple fibrous intimal thickening, and others disclosed nothing of vascular changes. The analysis of relative thickness of media to radius in the branches of coronary arteries resulted in no change between subjected rats and controls in thickness of media, compared to that of spontaneously hypertensive reats (SHR) which disclosed medial hypertrophy.
