• Advances in materials Research
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• v.11 no.2
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• pp.111-120
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• 2022

A novel nonlocal model with one thermal relaxation time is presented to investigates the thermal damages and the temperature in biological tissues generated by laser irradiations. To obtain these models, we used the theory of the non-local continuum proposed by Eringen. The thermal damages to the tissues are assessed completely by the denatured protein ranges using the formulations of Arrhenius. Numerical results for temperature and the thermal damage are graphically presented. The effects nonlocal parameters and the relaxation time on the distributions of physical fields for biological tissues are shown graphically and discussed.

• Horticultural Science & Technology
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• v.30 no.4
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• pp.371-377
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• 2012

This study was conducted to investigate the physiological and structural damages to cadmium (Cd) in Acorus calamus var. angustatus as a native aquatic species in Korea. In addition to the physiological responses such as plant growth, photosynthesis, and root activity, the structural damages in leaf and root tissues were observed through light and scanning electronic microscopy. The five-leaf plants were treated with different Cd concentrations 0, 10, 25, and 50 ${\mu}M$ for 15 days. The plant damages to Cd were significant at 10-25 ${\mu}M$ Cd physiologically and at 25-50 ${\mu}M$ Cd structurally. The physiological damages in the shoot part (photosynthesis) started at 10 ${\mu}M$ Cd whereas those in root part (root activity) were serious above 25 ${\mu}M$ Cd. On the other hand, the structural damages began at 25 ${\mu}M$ Cd in the leaf and root tissues similarly, but the plant tissue destruction was more serious in the roots than in leaves. Based on the plant physiological and structural damages, 10 ${\mu}M$ was assumed to be the limited concentration for sustainable growth and landscaping ability in Acorus calamus var. angustatus to Cd.

• Advances in materials Research
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• v.12 no.1
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• pp.31-42
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• 2023

In the present article, the effects of three thermal relaxation times in living tissue under the three-phaselag (TPL) bioheat model are introduced. Using the Laplace transforms, the analyticalsolution of the temperature and the resulting thermal damagesin living tissues are obtained. The experimental data are used to validate the analytical solutions. By the formulations of Arrhenius, the thermal damage of tissue is estimated. Numerical outcomes for the temperature and the resulting of thermal damages are presented graphically. The effects of parameters, such as thermalrelaxation times, blood perfusion rate on tissue temperature are also discussed in detail.

• Journal of Life Science
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• v.17 no.11
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• pp.1571-1575
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• 2007

This research was carried out to investigate the effects of Hambag mushroom on the oxidative stress in diabetic rats, Sprague-Dawley. The diabetic rats induced by streptozotocin were fed with hambag mushroom-powder(G. frondosa) for 6 weeks. For the level of oxidative stress in liver and pancreas tissues, it was studied by measuring LPO (lipid oxide) level as an indicator of lipid peroxidation, XOD(xanthine oxidase) as one of important sources for free radicals and the levels of GSH and GST as anti-oxidant systems. Also, as an indicator of liver damaged by oxidative stress, the activities of serum ALT and AST were measured. It was observed that the levels of ALT, AST, LPO and XOD were higher by about two times in both tissues from diabetic rats than in those from control rats. This indicates that the oxidative stress induced by diabetes caused the tissues damages. However, these levels were decreased in the tissues from rats with hambag mushroom-powder. Futhermore, the activity of GST were higher in both tissues from diabetic rats fed with hambag mushroom-powder than in those from diabetic rats. Thus, it is considered that the hambag mushroom-powder decreases the level of oxidative stress by increasing activity of anti-oxidant system such as GSH and GST. It is suggested that the hambag mushroom-powder can be useful for preventing the tissues damaged by diabetes-induced oxidative stress.

• Food Science and Biotechnology
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• v.15 no.4
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• pp.612-616
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• 2006

The protective effect of water extract of ash tree leaves (ALE) against oxidative damages was investigated in paracetamol-induced BALB/c mice. Biochemical analysis of anti-oxidative enzymes, immunoblot analyses of hepatic cytochrome P450 2El (CYP2E1), and the gene expression of tumor necrosis factor (TNF-${\alpha}$) were examined to determine the extract's protective effect and its possible mechanisms. BALB/c mice were divided into three groups: normal, paracetamol-administered, and ALE-pretreated groups. A single dose of paracetamol led to a marked increase in lipid peroxidation as measured by malondialdehyde (MDA). This was associated with a significant reduction in the hepatic antioxidant system, e.g., glutathione (GSH). Paracetamol administration also significantly elevated the expression of CYP2E1, according to immunoblot analysis, and of TNF-${\alpha}$ mRNA in liver. However, ALE pretreatment prior to the administration of paracetamol significantly decreased hepatic MDA levels. ALE restored hepatic glutathione and catalase levels and suppressed the expression of CYP2E1 and TNF-${\alpha}$ observed in inflammatory tissues. Moreover, ALE restored mitochondrial ATP content depleted by the drug administration. These results show that the extract of ash tree leaves protects against paracetamol-induced oxidative damages by blocking oxidative stress and CYP2E1-mediated paracetamol bioactivation.

• Journal of information and communication convergence engineering
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• v.12 no.2
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• pp.104-108
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• 2014

The field of body sensor networks has attracted interest of many researchers due to its potential to revolutionize medicine. These sensors are usually implanted inside the human body and communicate among themselves. In the process of receiving, processing, or transmitting data, these devices produce heat. This heat damages the tissues surrounding the devices in the case of prolonged exposure. In this paper, to reduce this damages, we have improved and evaluated two protocols-the least temperature routing protocol and adaptive least temperature routing protocol-by implementing clustering as well as a leadership rotation algorithm. We used Castalia to simulate a basic body area network cluster composed of 6 nodes. A throughput application was used to simulate all the nodes sending data to one sink node. Simulations results shows that improved communication protocol with leadership rotation algorithm significantly reduce the energy consumption as compared to a scheme without leadership rotation algorithm.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.3
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• pp.710-718
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• 2006

The present study was carried out to investigate the effect of Chihyo-san (CHS) administration on asthma induced by Alum/OVA treatment in the mice. In CHS-treated animal group, lung weight, which was increased after asthma induction, was significantly decreased, and total number of cells in the lung, peripheral lymph node (PLN) and spleen tissue was significantly decreased in CHS-treated group compared to the asthma control group. The number of immune cells including natural killer (NK) cells in asthmatic animals was largely regulated by CHS treatment, showing a similar pattern as that of CsA-treated positive control group. Levels of mRNAs encoding inflammatory cytokines IL-5, IL-13, $TNF-{\alpha}$, and eotaxin were determined by RT-PCR in the lung tissue and showed decreases in CHS-treated group to the similar levels of CsA-treated control group, Histamine level in the serum was significantly lower in CHS-treated group than asthma-induced control group. Both haematoxylin and eosin staining and Masson's trichrome staining results showed decreased number of inflammatory cells, reduced immune cell infiltration, and normalized epithelial cell layering in the bronchial tissue of CHS-treated mouse group. Thus, the present findings suggest that CHS may be useful for protecting bronchial tissues from consistent inflammatory damages that occur in asthma patients.

• BMB Reports
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• v.40 no.6
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• pp.1039-1049
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• 2007

Overdoses of acetaminophen cause hepato-renal oxidative stress. The present study was undertaken to investigate the protective effect of a 43 kDa protein isolated from the herb Cajanus indicus, against acetaminophen-induced hepatic and renal toxicity. Male albino mice were treated with the protein for 4 days (intraperitoneally, 2 mg/kg body wt) prior or post to oral administration of acetaminophen (300 mg/kg body wt) for 2 days. Levels of different marker enzymes (namely, glutamate pyruvate transaminase and alkaline phosphatase), creatinine and blood urea nitrogen were measured in the experimental sera. Intracellular reactive oxygen species production and total antioxidant activity were also determined from acetaminophen and protein treated hepatocytes. Indices of different antioxidant enzymes (namely, superoxide dismutase, catalase, glutathione-S-transferase) as well as lipid peroxidation end-products and glutathione were determined in both liver and kidney homogenates. In addition, Cytochrome P450 activity was also measured from liver microsomes. Finally, histopathological studies were performed from liver sections of control, acetaminophen-treated and protein pre- and post-treated (along with acetaminophen) mice. Administration of acetaminophen increased all the serum markers and creatinine levels in mice sera along with the enhancement of hepatic and renal lipid peroxidation. Besides, application of acetaminophen to hepatocytes increased reactive oxygen species production and reduced the total antioxidant activity of the treated hepatocytes. It also reduced the levels of antioxidant enzymes and cellular reserves of glutathione in liver and kidney. In addition, acetaminophen enhanced the cytochrome P450 activity of liver microsomes. Treatment with the protein significantly reversed these changes to almost normal. Apart from these, histopathological changes also revealed the protective nature of the protein against acetaminophen induced necrotic damage of the liver tissues. Results suggest that the protein protects hepatic and renal tissues against oxidative damages and could be used as an effective protector against acetaminophen induced hepato-nephrotoxicity.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.2
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• pp.147-155
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• 1999

Antioxidant effects of serotonin and L-DOPA on neuronal tissues were examined by studying the oxidative damages of brain synaptosomal components. The study further explored the mechanism by which they exert protective actions. Serotonin and L-DOPA (1 ${\mu}M$ to 1 mM) significantly inhibited lipid peroxidation of brain tissues by either $Fe^{2+}$ and ascorbate or t-butyl hydroperoxide in a dose dependent fashion. Protective effect of serotonin on the peroxidative actions of both systems was greater than that of L-DOPA. Protein oxidation of synaptosomes caused by $Fe^{2+}$ and ascorbate was attenuated by serotonin and L-DOPA. Protein oxidation more sensitively responded to L-DOPA rather than serotonin. Serotonin and L-DOPA (100 ${\mu}M$) decreased effectively the oxidation of synaptosomal sulfhydryl groups caused by $Fe^{2+}$ and ascorbate. The production of hydroxyl radical caused by either $Fe^{3+},$ EDTA, H_2O_2$ and ascorbate or xanthine and xanthine oxidase was significantly decreased by serotonin and L-DOPA (1 mM). Equal concentrations of serotonin and L-DOPA restored synaptosomal $Ca^{2+}$ uptake decreased by $Fe^{2+}$ and ascorbate, which is responsible for SOD and catalase. Protective effects of serotonin and L-DOPA on brain synaptosomes may be attributed to their removing action on reactive oxidants, hydroxyl radicals and probably iron-oxygen complex, without chelating action on iron.

• Journal of the Korean Society of Food Science and Nutrition
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• v.38 no.12
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• pp.1815-1819
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• 2009

Based on the soft and rigid extents, tissues are mainly divided into two groups in mammals, soft tissues including heart, lung, kidney and brain, and hard tissues including tendon, cartilage, teeth and bone. Among various tissues, bone, a dynamic rigid organ, is continuously remodeled by the opposing functional activity between bone formation by osteoblasts and bone destruction by osteoclasts. Bone protects the soft tissues and provides mineral reservoirs, which can supply the mineral needs of other soft tissues to normally maintain cellular function. While calcification in bone is an important action to fundamentally support the body and protect the soft tissues, calcification in soft tissues, including the heart, aorta, kidney, lung and spleen, results in severe organ damages, eventually causing sudden death. A growing body of evidence indicates that the osteoporotic patient who are aging, post-menopausal, diabetes and chronic kidney disease simultaneously represent a high clinical incidence of soft tissue calcification, illustrating a link between soft tissue calcification and bone decalcification (osteoporosis). This study will review what is currently known about the connection between bone decalcification and soft tissue calcification.