Electrochemical Quartz Crystal microbalance is a tool that is capable of measuring nanogram-scale mass change on electrode surface. When applying alternating voltage to the quartz crystal with metal electrode formed on both sides, a resonant frequency by inverse piezoelectric effect depends on its thickness. The resonant frequency changes sensitively by mass change on its electrode surface; frequency increase with metal dissolution and decrease with metal deposition on the electrode surface. The relationship between resonant frequency and mass change is shown by Sauerbrey equation so that the mass change during metal dissolution can be measured in real time. Especially, it is effective in the case of reaction mechanism and rate studies accompanied by precipitation, volatilization, compound formation, etc. resulting in difficulties on ex-situ AA or ICP analysis. However, it should be carefully considered during EQCM experiments that temperature, viscosity, and hydraulic pressure of solution, and stress and surface roughness can affect on the resonant frequency. Application of EQCM was shown as a case study on leaching of platinum using aqueous chlorine for obtaining activation energy. A platinum electrode of quartz crystal oscillator with 1000 Å thickness exposed to solution was used as leaching sample. Electrogenerated chlorine as oxidant was purged and its concentration was controlled in hydrochloric acid solution. From the experimental results, platinum dissolution by chlorine is chemical reaction control with activation energy of 83.5 kJ/mol.
This study was carried out to investigate abiotic and biotic environmental factors affecting homoharringtonine (HHT) contents of Cephalotaxus koreana, whereby, to provide basic information of high value-added industry production of HHT as a promising anti-cancer agent. For correlation between abiotic environmental factors (soil moisture, soil pH, habitat density and temperature) and HHT contents, the contents were highly correlated with soil moisture (0.77) and soil pH (-0.68). For multiple regression analysis of relationship between abiotic environmental factors (soil moisture and soil pH) and HHT contents, soil moisture appeared to be strongly affecting the contents relatively due to being significant at only its regression coefficient ($26.48^{***}$). For the effect of biotic environmental factors (damage index) affecting HHT contents, the contents was quadratic with equation of $H=278.23+1242D-398.87D^2$, also, damage index had strong effect on the contents. Finally, for the result of the most influencing an environmental factor on HHT contents, both damage index and soil moisture were suitable in second polynomial regression, also, damage index ($R^2=0.73^{***}$) was turned out to be more influencing factor than soil moisture ($R^2=0.67^{**}$) on HHT contents relatively. Therefore, we predict that HHT contents in the trees of Cephalotaxus koreana is produced as a chemical defense mechanism triggered by a stress-related damage of fungi or insects.
Ji, Seon Yeong;Hwangbo, Hyun;Kim, Min Yeong;Kim, Da Hye;Park, Beom Su;Park, Joung-Hyun;Lee, Bae-Jin;Lee, Hyesook;Choi, Yung Hyun
Journal of Marine Bioscience and Biotechnology
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v.13
no.2
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pp.86-93
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2021
A high salt diet contributes to kidney damage by causing hypoxia and oxidative stress. Recently, an increase in dietary salt has been reported to induce an inflammatory phenotype in immune cells, further contributing to kidney damage. However, studies on the exact mechanism and role of a high salt diet on the inflammatory response in the kidneys are still insufficient. In this study, a cisplatin-induced acute kidney injury model using C57BL/6 mice was used to analyze the effect of salt intake on kidney injury. Results showed that high salt administration aggravated kidney edema in mice induced by treatment with cisplatin. Moreover, the indicators of kidney and liver function impairment were significantly increased in the group cotreated with high salt compared with that treated with cisplatin alone. Furthermore, the exacerbation of kidney damage by high salt administration was also associated with a decrease in the number of cells in the immune regulatory system. Additionally, high salt administration further decreased renal perfusion functions along with increased cisplatin-induced damage to proximal tubules. This was accompanied by increased expression of T cell immunoglobulin, mucin domain 1 (a biomarker of kidney injury), and Bax (a pro-apoptotic factor). Moreover, cisplatin-induced expression of proinflammatory mediators and cytokines, including cyclooxygenase-2 and tumor necrosis factor-α in kidney tissue, was further increased by high salt intake. Therefore, these results indicate that the kidney's inflammatory response by high salt treatment can further promote kidney damage caused by various pathological factors.
Park, Jung-Wook;Guglielmi, Yves;Graupner, Bastian;Rutqvist, Jonny;Park, Eui-Seob
Tunnel and Underground Space
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v.29
no.3
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pp.197-213
/
2019
We simulated the fault reactivation experiment conducted at 'Main Fault' intersecting the low permeability clay formations of Mont Terri Underground Research Laboratory in Switzerland using TOUGH-FLAC simulator. The fluid flow along a fault was modelled with solid elements and governed by Darcy's law with the cubic law in TOUGH2, whereas the mechanical behavior of a single fault was represented by creating interface elements between two separating rock blocks in FLAC3D. We formulate the hydro-mechanical coupling relation of hydraulic aperture to consider the elastic fracture opening and failure-induced dilation for reproducing the abrupt changes in injection flow rate and monitoring pressure at fracture opening pressure. A parametric study was conducted to examine the effects of in-situ stress condition and fault deformation and strength parameters and to find the optimal parameter set to reproduce the field observations. In the best matching simulation, the fracture opening pressure and variations of injection flow rate and monitoring pressure showed good agreement with field experiment results, which suggests the capability of the numerical model to reasonably capture the fracture opening and propagation process. The model overestimated the fault displacement in shear direction and the range of reactivated zone, which was attributed to the progressive shear failures along the fault at high injection pressure. In the field experiment results, however, fracture tensile opening seems the dominant mechanism affecting the hydraulic aperture increase.
In the engineering barriers of high-level radioactive waste disposal, gases could be generated through a number of processes. If the gas production rate exceeds the gas diffusion rate, the pressure of the gas increases and gases could migrate through the bentonite buffer. Because people and the environment can be exposed to radioactivity, it is very important to clarify gas migration in terms of long-term integrity of the engineered barrier system. In particular, it is necessary to identify the hydro-mechanical mechanism for the dilation flow, which is a very important gas flow phenomenon only in medium containing large amounts of clay materials such as bentonite buffer, and to develop and validate new numerical approach for the quantitative evaluation of the gas migration phenomenon. Therefore, in this study, we developed a two-phase flow model considering the mechanical damage model in order to simulate the gas migration in the engineered barrier system, and validated with 1D gas flow modelling through saturated bentonite under constant volume boundary conditions. As a result of numerical analysis, the rapid increase in pore water pressure, stress, and gas outflow could be simulated when the dilation flow was occurred.
The existence of different thermodynamic properties results in various undesirable effects, such as thermal deformation and residual stress, in heat-welding processes. The solid-state junction, by using explosive or electromagnetic forces, i.e., high-velocity impact welding without employing heat is advantageous in joining materials with different thermodynamic properties. In the solid-state junction, the joining is performed within a short time, a high velocity and large deformations are accompanied by interfacial surfaces. The numerical analysis models play an important role in the understanding of the mechanism of high-velocity impact welding. However, in the analysis of high velocity and large deformations, the conventional Lagrangian method has low reliability due to the occurrence of entanglements. In this study, high-velocity impact welding between Cu and CP-Ti with different thermodynamic properties was performed using a un-gridded numerical method, SPH (Smoothed Particle Hydrodynamics), and interfacial morphology occurred. As a result of the analysis, the interfacial morphology was confirmed and the compared degree of shape (straight, vortex), period, length, and so on appeared differently depending on the relationship between the parameters (impact angle and speed).
Park, Jung-Hyun;Yang, Doo-Hwa;Woo, Chang-Hoon;An, Hee-Duk
Journal of Korean Medicine Rehabilitation
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v.31
no.1
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pp.17-32
/
2021
Objectives The present study was designed to find out the therapeutic effects and possible underlying mechanism of Buja-tang, a herbal complex formula on experimental monosodium iodoacetate (MIA)-induced osteoarthritis. Methods Osteoarthritis models were created via intra-joint injection of MIA (50 μL with 80 mg/mL) in rats. Rats were divided into five groups and each group consisted of seven. Normal group was not injected MIA and did a normal diet. Control group injected MIA and received distilled water. Indo injected MIA and oral administration of 5 mg/kg of indomethacin. BJTL injected MIA and oral administration of 100 mg/kg of Buja-tang. BJTH injected MIA and oral administration of 200 mg/kg of Buja-tang. We analyzed weight-bearing ability of hind paws, oxidative stress related factor, antioxidant protein, inflammatory protein, inflammatory messenger and cytokine in joint tissue. Pathological observation of knee cartilage tissue structures was also performed with hematoxylin & eosin and safranin-O chromosomes. Results Weight-bearing ability of hind paws showed a tendency to reduce pain. The incidence of nicotinamide adenine dinucleotide phosphate oxidase and p22phox in articular tissue was significantly reduced, and the incidence of nuclear factor-erythroid 2-related factor 2 and heme oxygenase-1 and superoxide dismutases was significantly increased. The incidence of phosphorylated inhibitor of κBα, nuclear factor-kappa B p65, inducible nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor alpha, interleukin (IL)-6, and IL-1β decreased significantly. In pathological observation, cartilage tissue damaged by MIAs in biopsy has significantly recovered from Buja-tang administration. Conclusions Buja-tang has anti-inflammation, antioxidation and pain relief effects. So this is thought to inhibit the progress of osteoarthritis in rat caused by the MIA.
Background: The incidence of ischemic cerebrovascular disease is increasing in recent years and has been one of the leading causes of neurological dysfunction and death. Ginsenoside Rg1 has been found to protect against neuronal damage in many neurodegenerative diseases. However, the effect and mechanism by which Rg1 protects against cerebral ischemia-reperfusion injury (CIRI) are not fully understood. Here, we report the neuroprotective effects of Rg1 treatment on CIRI and its possible mechanisms in mice. Methods: A bilateral common carotid artery ligation was used to establish a chronic CIRI model in mice. HT22 cells were treated with Rg1 after OGD/R to study its effect on [Ca2+]i. The open-field test and poleclimbing experiment were used to detect behavioral injury. The laser speckle blood flowmeter was used to measure brain blood flow. The Nissl and H&E staining were used to examine the neuronal damage. The Western blotting was used to examine MAP2, PSD95, Tau, p-Tau, NOX2, PLC, p-PLC, CN, NFAT1, and NLRP1 expression. Calcium imaging was used to test the level of [Ca2+]i. Results: Rg1 treatment significantly improved cerebral blood flow, locomotion, and limb coordination, reduced ROS production, increased MAP2 and PSD95 expression, and decreased p-Tau, NOX2, p-PLC, CN, NFAT1, and NLRP1 expression. Calcium imaging results showed that Rg1 could inhibit calcium overload and resist the imbalance of calcium homeostasis after OGD/R in HT22 cells. Conclusion: Rg1 plays a neuroprotective role in attenuating CIRI by inhibiting oxidative stress, calcium overload, and neuroinflammation.
The thioredoxin reductase (TrxR) system is essential for cell survival and function by playing a pivotal role in maintaining homeostasis of cellular redox and regulating signal transduction pathways. The TrxR system comprises thioredoxin (Trx), TrxR, and nicotinamide adenine dinucleotide phosphate. Trx reduced by the catalytic reaction of the TrxR enzyme reduces downstream proteins, resulting in protection against oxidative stress and regulation of cell differentiation, growth, and death. Cancer cells survive by improving their intracellular antioxidant capacity to eliminate excessively generated reactive oxygen species (ROS) due to infinite cell proliferation and a high metabolic rate. Therefore, cancer cells have high dependence and sensitivity to antioxidant systems, suggesting that focusing on TrxR, a representative antioxidant system, is a potential strategy for cancer therapy. Several studies have revealed that TrxR is expressed at high levels in various types of cancers, and research on anticancer activity targeting the TrxR system is increasing. In this review, we discuss the feasibility and value of the TrxR system as a strategy for anticancer activity research by examining the relationship between the function of the intracellular TrxR system and the development and progression of cancer, considering the anticancer activity and mechanism of TrxR inhibitors.
Zhengxuan, Wang;Mingcai, Liang;Hui, Li;Bingxiao, Liu;Lin, Yang
Nutrition Research and Practice
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v.16
no.6
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pp.729-744
/
2022
BACKGROUND/OBJECTIVES: 4-Hydroxy-2-nonenal (HNE) is a biomarker for oxidative stress to induce inflammation. Methionine is an essential sulfur-containing amino acid with antioxidative activity. On the other hand, the evidence on whether and how methionine can depress HNE-derived inflammation is lacking. In particular, the link between the regulation of the nuclear factor-κB (NF-κB) signaling pathway and methionine intake is unclear. This study examined the link between depression from HNE accumulation and the anti-inflammatory function of ⳑ-methionine in rats. MATERIALS/METHODS: Male Wistar rats (3-week-old, weighing 70-80 g) were administered different levels of ⳑ-methionine orally at 215.0, 268.8, 322.5, and 430.0 mg/kg body weight for two weeks. The control group was fed commercial pellets. The hepatic HNE contents and the protein expression and mRNA levels of the inflammatory mediators were measured. The interleukin-10 (IL-10) and glutathione S-transferase (GST) levels were also estimated. RESULTS: Compared to the control group, hepatic HNE levels were reduced significantly in all groups fed ⳑ-methionine, which were attributed to the stimulation of GST by ⳑ-methionine. With decreasing HNE levels, ⳑ-methionine inhibited the activation of NF-κB by up-regulating inhibitory κBα and depressing phosphoinositide 3 kinase/protein kinase B. The mRNA levels of the inflammatory mediators (cyclooxygenase-2, interleukin-1β, interleukin-6, inducible nitric oxide synthase, tumor necrotic factor alpha) were decreased significantly by ⳑ-methionine. In contrast, the protein expression of these inflammatory mediators was effectively down regulated by ⳑ-methionine. The anti-inflammatory action of ⳑ-methionine was also reflected by the up-regulation of IL-10. CONCLUSIONS: This study revealed a link between the inhibition of HNE accumulation and the depression of inflammation in growing rats, which was attributed to ⳑ-methionine availability. The anti-inflammatory mechanism exerted by ⳑ-methionine was to inhibit NF-κB activation and to up-regulate GST.
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