• Advances in materials Research
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• 제11권2호
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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.

• 원예과학기술지
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• 제30권4호
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• pp.371-377
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• 2012

국내 자생 수생식물인 창포의 중금속 카드뮴(Cd)에 대한 생리적 구조적 장해를 알아보고자 본 연구를 실시하였다. Cd 농도에 따른 생장률, 광합성, 뿌리활력의 생리적 반응과 잎과 뿌리 조직의 해부학적 상해 반응을 조사하였다. 잎이 5매 전개된 식물체를 대상으로 Cd 농도를 반치사농도 범위이하 조건에서 0(control), 10, 25, $50{\mu}M$로 15일간 처리하였다. Cd에 대한 생리적 장해는 $10-25{\mu}M$, 구조적 상해는 $25-50{\mu}M$ 범위에서 나타났다. 생리적 장해의 경우 지상부(광합성)는 $10{\mu}M$, 지하부(뿌리활력)는 $25{\mu}M$에서 발생하였다. 구조적 상해의 경우 지상부(엽육조직)와 지하부(뿌리조직) 모두 $25{\mu}M$에서 시작되었으나, Cd 농도가 증가할수록 엽육조직보다는 뿌리조직의 상해 정도가 현저하였다. Cd에 대한 창포의 생리적, 구조적 장해 반응을 고려할 때, Cd 오염지역에서 창포의 경관적 가치와 지속적인 생장을 유지할 수 있는 Cd 한계농도는 $10{\mu}M$ 정도인 것으로 확인되었다.

• Advances in materials Research
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• 제12권1호
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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.

• 생명과학회지
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• 제17권11호
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• pp.1571-1575
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• 2007

본 연구는 당뇨병으로 인한 산화적 스트레스에 대한 함박잎새버섯분말의 효과를 밝히기 위하여 SD계 흰쥐를 STZ로 당뇨를 유발하여 간 및 신장 조직에서 조사하였다. 또한 당뇨흰쥐에 함박잎새버섯분말 1-2% 첨가하여 6주간 식이하였다. 산화적 스트레스의 지표물질인 LPO를 비롯하여 유발원 XOD 활성도를 측정하였다. 또한 이에 따른 간조직 손상 확인을 위해 혈청 ALT와 AST 활성도를 측정하였다. 특히 함박잎새버섯분말의 항산화적 효능을 위해 이들 지표물질들과 더불어 항산화체계의 중요 요소인 GSH 농도와 GST 활성도를 당뇨군, 당뇨-잎새버섯분말투여군 그리고 정상군에서 측정하였다. 당뇨군은 정상군과 비교하여 LPO 농도를 비롯하여 XOD 활성도가 유의하게 높았다. 특히 이러한 결과로 추정되는 간 조직 손상이 정상군보다 유의하게 높은 ALT 및 AST 활성도가 혈청에서 확인되었다. 그러나 당뇨-잎새버섯분말투여군에서는 LPO 농도, XOD 활성도를 비롯하여 조직손상의 지표인 ALT 및 AST 활성도가 당뇨군보다 유의하게 감소하였다. 항산화물질인 GSH 농도는 당뇨군 및 당뇨-잎새버섯분말투여군 비교에서 유의한 차이가 없었으나 GST 활성도는 당뇨-잎새버섯분말투여군이 당뇨군보다 유의하게 높았다. 따라서 당뇨유발성 산화적 스트레스에 대한 잎새버섯분말의 효능은 GSH 농도 변화보다 GST 활성도를 증가시키고 또한 산화적 스트레스의 유발원인 XOD 활성도 감소의 유도를 통해 이루어지는 것으로 추정된다. 결론적으로 당뇨는 산화적 스트레스를 증가시키며 조직손상을 유발한다. 그러나 함박잎새버섯분말은 항산화물질 및 효소계의 활성도를 증가시켜 당뇨유발-산화적 스트레스 감소를 유도하여 조직 손상을 감소시키는 것이 확인되었다.

• Food Science and Biotechnology
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• 제15권4호
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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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• 제12권2호
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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.

• 동의생리병리학회지
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• 제20권3호
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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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• 제40권6호
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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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• 제3권2호
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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.

• 한국식품영양과학회지
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• 제38권12호
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• pp.1815-1819
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• 2009

여러 단백질과 다양한 무기질(칼슘 등)을 함유한 단단한 기관인 골은 정상적으로 다른 연조직 세포로 무기질을 공급하는 역할을 수행하지만, 비타민 결핍, 노화, 폐경기 및 대사성 질환 등으로 인해서 골다공증이 유발되고 동시에 다양한 연조직(심장, 대동맥, 신장, 허파, 췌장 등)의 석회화가 빈번히 유도된다. 같은 중간엽 줄기세포로부터 유래되는 연조직을 구성하는 세포와 조골세포 사이에서는 상호 횡간의 분화가 될 수 있는 여지가 있어, 연조직 세포는 칼슘 축적으로 골을 형성하는 조골세포와 유사한 세포로 분화될 수 있다. 연조직을 이루는 다양한 연조직 장기의 칼슘 축적으로 인한 석회화는 치명적인 장기손상으로 생명을 위협할 수 있으므로 적극적인 예방과 치료가 중요할 것이다. 골다공증과 연조직 석회화는 상호 밀접한 연계성이 있어 한 가지의 질병이 진행되면 다른 질병이 연속적으로 발병할 우려가 있으므로 초기 질병에 대한 적극적인 치료가 필요하다. 향후 초고속고령화 사회 진입으로 이의 두 질환의 급격한 증가가 예상되므로, vitamin K와 D를 비롯한 다양한 무기질을 균형적으로 조절할 수 있는 식습관과 다량의 항산화제를 함유한 음식물 섭취로 이의 질환을 예방할 수 있을 것이다.