Journal of the Society of Naval Architects of Korea
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v.57
no.5
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pp.305-311
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2020
This study presents a probabilistic time series forecast of ship structural response using Bayesian inference combined with Volterra linear model. The structural response of a ship exposed to irregular wave excitation was represented by a linear Volterra model and unknown uncertainties were taken care by probability distribution of time series. To achieve the goal, Volterra series of first order was expanded to a linear combination of Laguerre functions and the probability distribution of Laguerre coefficients is estimated using the prepared data by treating Laguerre coefficients as random variables. In order to check the validity of the proposed methodology, it was applied to a linear oscillator model containing damping uncertainties, and also applied to model test data obtained by segmented hull model of 400,000 DWT VLOC as a practical problem.
Although the core mechanisms of Attention Deficit/Hyperactivity Disorder (ADHD) are unknown, several ADHD-associated proteins have been studied. G-protein - coupled receptor kinase interacting protein-1 (GIT1) is a multifunctional adapter protein that affects neuron growth and dendrite formation. GIT1-deficient mice have shown ADHD-like behavior and also recovered through amphetamine treatment. In this study, gliotransmitters were investigated in both intracellular and extracellular space from GIT1-deficient mice. To measure the amount of gliotransmitters, primary astrocyte cultures were taken from the cerebral and cerebellar cortices of wild (WT), hetero (HE), and knock-out (KO) mice. Major gliotransmitters were analyzed using high-performance liquid chromatography. It was observed that the amount of excitatory and inhibitory gliotransmitters were dependent on genotype and showed a change in excitation/inhibition ratios. Interestingly, the major excitatory gliotransmitter, glutamate, existed at the lowest level in WT mice, but the amount of inhibitory gliotransmitters, gamma-aminobutyric acid (GABA) and glycine, varied depending on brain region. Remarkably, an increased amount of GABA was measured at the intracellular cerebrum in WT mice compared with KO mice. It was presumed that KO mice would secrete more inhibitory gliotransmitters to compensate for GIT1 depletion or else acquire a defect to reuptake-secreted GABA. This may be a possible mechanism for ADHD pathology.
Since its detection in 1980, the $8-{\mu}m$ north-polar brightening of $CH_4$ on Juptier has not moved from $180^{\circ}$ (SysIII) longitude. The $8-{\mu}m$$CH_4$ brightening is mostly thermal and very similar to that of $13-{\mu}m$$C_2H_2$ emissions, but the morphology of these hydrocarbon north-polar brightenings are very different from that of the $3-{\mu}m$$H_3{^+}$ auroral oval suggesting a significantly different excitation process yet unknown heating mechanism. Recently, Kim et al. (submitted to Icarus, 2015) found that that the center of the $3-{\mu}m$$CH_4$ northern bright spot is located at ${\sim}200^{\circ}$ (SysIII) longitude, which is ${\sim}20^{\circ}$ west from the center of the $8-{\mu}m$ north-polar bright spot, and it does not coincide with the $3-{\mu}m$$H_3{^+}$ bright spot. They found significantly high temperatures (500 ~ 850K) from $CH_4$ rotational lines on the $3-{\mu}m$ bright spot above the $1-{\mu}bar$ pressure level, while we find cooler temperatures (<350K) over the the $8-{\mu}m$ spot. They also found that the upper states of the $3-{\mu}m$$CH_4$ bands are mostly populated by non-thermal excitations, such as auroral particle precipitations and/or Joule heatings in contrast to the $8-{\mu}m$ thermal emission. This finding indicates that the $10-{\mu}m$ hydrocarbon brightening is confined to low altitudes below the $1-{\mu}bar$ level eliminating the long-suggested possibility of direct auroral bombardments while opening a new possibility of dynamical origin for the $10-{\mu}m$ brightening.
This paper reports the structural health monitoring benchmark study results for the Canton Tower using Bayesian methods. In this study, output-only modal identification and finite element model updating are considered using a given set of structural acceleration measurements and the corresponding ambient conditions of 24 hours. In the first stage, the Bayesian spectral density approach is used for output-only modal identification with the acceleration time histories as the excitation to the tower is unknown. The modal parameters and the associated uncertainty can be estimated through Bayesian inference. Uncertainty quantification is important for determination of statistically significant change of the modal parameters and for weighting assignment in the subsequent stage of model updating. In the second stage, a Bayesian model updating approach is utilized to update the finite element model of the tower. The uncertain stiffness parameters can be obtained by minimizing an objective function that is a weighted sum of the square of the differences (residuals) between the identified modal parameters and the corresponding values of the model. The weightings distinguish the contribution of different residuals with different uncertain levels. They are obtained using the Bayesian spectral density approach in the first stage. Again, uncertainty of the stiffness parameters can be quantified with Bayesian inference. Finally, this Bayesian framework is applied to the 24-hour field measurements to investigate the variation of the modal and stiffness parameters under changing ambient conditions. Results show that the Bayesian framework successfully achieves the goal of the first task of this benchmark study.
Xiang, Ziru;Chan, Tommy H.T.;Thambiratnam, David P.;Nguyen, Theanh
Smart Structures and Systems
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v.17
no.6
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pp.917-933
/
2016
In a prestressed concrete bridge, the magnitude of the prestress force (PF) decreases with time. This unexpected loss can cause failure of a bridge which makes prestress force identification (PFI) critical to evaluate bridge safety. However, it has been difficult to identify the PF non-destructively. Although some research has shown the feasibility of vibration based methods in PFI, the requirement of having a determinate exciting force in these methods hinders applications onto in-service bridges. Ideally, it will be efficient if the normal traffic could be treated as an excitation, but the load caused by vehicles is difficult to measure. Hence it prompts the need to investigate whether PF and moving load could be identified together. This paper presents a synergic identification method to determine PF and moving load applied on a simply supported prestressed concrete beam via the dynamic responses caused by this unknown moving load. This method consists of three parts: (i) the PF is transformed into an external pseudo-load localized in each beam element via virtual distortion method (VDM); (ii) then these pseudo-loads are identified simultaneously with the moving load via Duhamel Integral; (iii) the time consuming problem during the inversion of Duhamel Integral is overcome by the load-shape function (LSF). The method is examined against different cases of PFs, vehicle speeds and noise levels by means of simulations. Results show that this method attains a good degree of accuracy and efficiency, as well as robustness to noise.
Ultrapure ferritic stainless steel provides a new generation of long-span metal roof systems with continuous welding technology, which exhibits many unknown behaviors during wind excitation. This study focuses on the wind-resistant capacity of a new continuous welding stainless steel roof (CWSSR) system. Full-scale testing on the welding joints and the CWSSR system is performed under uniaxial tension and static ultimate wind uplift loadings, respectively. A finite element model is developed with mesh refinement optimization and is further validated with the testing results, which provides a reliable way of investigating the parameter effect on the wind-induced structural responses, namely, the width and thickness of the roof sheeting and welding height. Research results show that the CWSSR system has predominant wind-resistant performance and can bear an ultimate wind uplift loading of 10.4 kPa without observable failures. The welding joints achieve equivalent mechanical behaviors as those of base material is produced with the current of 65 A. Independent structural responses can be found for the roof sheeting of the CWSSR system, and the maximum displacement appears at the middle of the roof sheeting, while the maximum stress appears at the connection supports between the roof sheeting with a significant stress concentration effect. The responses of the CWSSR system are greatly influenced by the width and thickness of the roof sheeting but are less influenced by the welding height.
The power loss analysis was carried out for Ni-Cu-Zn ferrite sample with different content of NiO and ZnO. The power loss, Pcv decreases monotonically with increasing temperature and attains to a certain value at around 100~120 degrees Celsius. The frequency dependence of Pcv can be explained by Pcv~f$^n$, and n is independent of the frequency, f up to 1 MHz. The Pcv decreases with an increase in ZnO/NiO. The Pcv was separated to hysteresis loss(Ph) and residual loss(Pcv-Ph). The temperature characteristics and compositional dependence of Pcv can be attributed to the Ph, while Pcv-Ph is not affected by both temperature and ZnO/NiO. By analyzing temperature and composition dependence of Ph and initial permeability, ${\mu}_i$ like following equations could be formularized. ${\mu}_i{\mu}_0=I_s^2/(K_I+b{\sigma}_0{\lambda}_s)$ Wh=13.5(I$_s^2/{\mu}_i{\mu}_0)$ Where ${\mu}_0$ is permeability of vacuum, I$_s$ is saturation magnetization, K$_I$ is anisotropy constant, $s_0$ is internal heterogeneous stress, ${\lambda}_s$ is magnetostriction constant, b is unknown constant, and Wh is hysteresis loss per one cycle of excitation (Ph=Wh${\times}$f). Steinmetz constant of Ni-Cu-Zn ferrite, m=1.64~2.2 is smaller than that of Mn-Zn ferrites, which suggests the difference of loss mechanisms between these materials.
Proceedings of the Korean Institute of Resources Recycling Conference
/
2004.12a
/
pp.3-11
/
2004
The power loss analysis was carried out for Ni-Cu-Zn ferrite samples with different content of NiO and ZnO. The power loss, Pcv decreases monotonically wi increasing temperature and attains to a certain value at around $100\~120$ degrees Celsius. The frequency dependence of Pcv can be explained by $Pcv\~f^n$', and n is independent of the frequency, f up to 1MHz. The Pcv decreases with an increase in ZnO/NiO. The Pcv was separated to hysteresis loss, Ph and residual loss, (Pcv-Ph). The temperature characteristics and compositional dependence of Pcv can be attributed to the Ph, while (Pcv-Ph) is not affected by both temperature and ZnO/NiO. By analyzing temperature and composition dependence of Ph and initial permeability, ${\mu}^i$ following equations could be formularized. $${\mu}_i{\mu}o=I_x\;^2/(K_1+bs_ol_s)\;\;\;\;(1)$$$Wh=13.5(I_s\;^2/{\mu}_i{\mu}_o)\;\;\;\;(2)$$ Were ${\mu}_o$ is permeability of vacuum, $I_s$ saturation magnetization, $K_1$ anisotropy constant, $S_o$ internal heterogeneous stress, $I_s$, magnetostriction constant, b unknown constant. Wh hysteresis loss per one cycle of excitation (Ph: Wh*f). Steinmetz constant of Ni-Cu-Zn ferrites, $m=1.64\~2.2$ is smaller than the one of Mn-Zn ferrites, which suggests the difference of loss mechanism between these materials.
The ryanodine receptor, a $Ca^{2+}$ release channel of the sarcoplasmic reticulum (SR), is responsible for the rapid release of $Ca^{2+}$ that activates cardiac muscle contraction. In the excitation-contraction coupling cascade, activation of SR $Ca^{2+}$ release channel is initiated by the activity of sarcolemmal $Ca^{2+}$ channels, the dihydropyridine receptors. Previous study showed that the relaxation defect of diabetic heart was due to the changes of the expressional levels of SR $Ca^{2+}$ATPase and phospholamban. In the diabetic heart contractile abnormalities were also observed, and one of the mechanisms for these changes could include alterations in the expression and/or activity levels of various $Ca^{2+}$ regulatory proteins involving cardiac contraction. In the present study, underlying mechanisms for the functional derangement of the diabetic cardiomyopathy were investigated with respect to ryanodine receptor, and dihydropyridine receptor at the transcriptional and translational levels. Quantitative changes of ryanodine receptors and the dihydropyridine receptors, and the functional consequences of those changes in diabetic heart were investigated. The levels of protein and mRNA of the ryanodine receptor in diabetic rats were comparable to these of the control. However, the binding capacity of ryanodine was significantly decreased in diabetic rat hearts. Furthermore, the reduction in the binding capacity of ryanodine receptor was completely restored by insulin. This result suggests that there were no transcriptional and translational changes but functional changes, such as conformational changes of the $Ca^{2+}$ release channel, which might be regulated by insulin. The protein level of the dihydropyridine receptor and the binding capacity of nitrendipine in the sarcolemmal membranes of diabetic rats were not different as compared to these of the control. In conclusion, in diabetic hearts, $Ca^{2+}$ release processes are impaired, which are likely to lead to functional derangement of contraction of heart. This dysregulation of intracellular $Ca^{2+}$ concentration could explain for clinical findings of diabetic cardiomyopathy and provide the scientific basis for more effective treatments of diabetic patients. In view of these results, insulin may be involved in the control of intracellular $Ca^{2+}$ in the cardiomyocyte via unknown mechanism, which needs further study.
It is well known that extracellular Calcium plays a very important role in several steps of smooth muscle excitability and contractility, and there have been many concerns about factors influencing the distribution of extracellular Ca++ and the Ca++ flux through the cell membrane of the smooth muscle. Based on the assumption that Mg++ may also play an important role in the excitation and contraction processes of the smooth muscle by taking part in affecting Ca++ distribution and flux, many researches are being performed about the exact role of Mg++, especially in the vascular smooth muscle. But yet the effect of Mg++ in the smooth muscle activity is not clarified, and moreover the mechanism of Mg++ action is almost completely unknown. Present study attempted to clarify the effect of Mg++ on the excitability and contractility in the multiunit and unitary smooth muscle, and the mechanism concerned in it. The preparations used were the guinea-pig aortic strip as the experimental material of the multiunit smooth muscle and the rat uterine strip as the one of the unitary smooth muscle. The tissues were isolated from the sacrificed animal and were prepared for recording the isometric contraction. The effects of Mg++ and Ca++ were examined on the electrically driven or spontaneous contraction of the preparations. And the effects of these ions were also studied on the K+ or norepinephrine contracture. All experiments were performed in tris-buffered Tyrode solution which was aerated with 100% 02 and kept at 35oC. The results obtained were as follows: 1] Mg++ suppressed the phasic contraction induced by electrical field stimulation dose-dependently in the guinea-pig aortic strip, while the high concentration of Ca++ never recovered the decreased tension. These phenomena were not changed by the a - or b - adrenergic blocker. 2]Mg++ played the suppressing effect on the low concentration [20 and 40 mM] of K+-contracture in the aortic muscle, but the effect was not shown in the case of 100mM K+-contracture. 3] Mg++ also suppressed the contracture induced by norepinephrine in the aortic preparation. And the effect of Mg++ was most prominent in the contracture by the lowest [10 mM] concentration of norepinephrine. 4] In both the spontaneous and electrically driven contractions of the uterine strip, Mg++ decreased the amplitude of peak tension, and by the high concentration of Ca++ the amplitude of tension was recovered unlike the aortic muscle. 5] The frequency of the uterine spontaneous contraction increased as the [Ca++] / [Mg++] ratio increased up to 2, but the frequency decreased above this level. 6] Mg++ decreased the tension of the low[20 and 40mM] K+-contracture in the uterine smooth muscle, but the effect did not appear in the 100mM K+-contracture. From the above results, the following conclusion could be made. 1] Mg++ seems to suppress the contractility directly by acting on the smooth muscle itself, besides through the indirect action on the nerve terminal, in both the aortic and uterine smooth muscles. 2] The fact that the depressant effect of Mg++ on the K+-contracture is in inverse proportion to an increase of K+ concentration appears resulted from the extent of the opening state of the Ca++ channel. 3] Mg++ may play a depressant role on both the potential dependent and the receptor-operated Ca++ channels. 4] The relationship between the actions of Mg++ and Ca++ seems to be competitive in uterine muscle and non-competitive in aortic strip.
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