• Title/Summary/Keyword: Lethal Shock Factor

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Study for Characteristics of DDAM using MIL-S-901D Shock Test and Transient Response Analysis (MIL-S-901D 충격시험과 과도응답해석을 이용한 DDAM 특성에 관한 연구)

  • Song, Oh-Seop;Kim, Yong
    • Transactions of the Korean Society for Noise and Vibration Engineering
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    • v.16 no.11 s.116
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    • pp.1132-1139
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    • 2006
  • Non-contact underwater explosions against surface ship could cause extensive equipment damage during wartime service. Thus, the need to develop methods for the design of shock resistant equipment structures and systems was strongly established. In analytical methods, DDAM(Dynamic Design and Analysis Method) and transient repsonse method are used for ship shock design. In this paper, to analyze the characteristics of DDAM, medium weight shock test, DDAM and transient response analysis for missile system equipment are performed.

Heat Shock Responses for Understanding Diseases of Protein Denaturation

  • Kim, Hee-Jung;Hwang, Na Rae;Lee, Kong-Joo
    • Molecules and Cells
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    • v.23 no.2
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    • pp.123-131
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    • 2007
  • Extracellular stresses induce heat shock response and render cells resistant to lethal stresses. Heat shock response involves induction of heat shock proteins (Hsps). Recently the roles of Hsps in neurodegenerative diseases and cancer are attracting increasing attention and have accelerated the study of heat shock response mechanism. This review focuses on the stress sensing steps, molecules involved in Hsps production, diseases related to Hsp malfunctions, and the potential of proteomics as a tool for understanding the complex signaling pathways relevant to these events.

Compound K Rich Fractions Regulate NF-κB-dependent Inflammatory Responses and Protect Mice from Endotoxin-induced Lethal Shock

  • Yang, Chul-Su;Yuk, Jae-Min;Ko, Sung-Ryong;Cho, Byung-Goo;Sohn, Hyun-Joo;Kim, Young-Sook;Wee, Jae-Joon;Do, Jae-Ho;Jo, Eun-Kyeong
    • Journal of Ginseng Research
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    • v.32 no.4
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    • pp.315-323
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    • 2008
  • In the previous studies, we isolated the compound K rich fractions (CKRF) and showed that CKRF inhibited Toll-like receptor (TLR) 4- or TLR9-induced inflammatory signaling. To extend our previous studies,1) we investigated the molecular mechanisms of CKRF in the TLR4-associated signaling via nuclear factor (NF)-${\kappa}B$, and in vivo role of CKRF for induction of tolerance in lipopolysaccharide (LPS)-induced septic shock. In murine bone marrow-dervied macrophages, CKRF significantly inhibited the induction of mRNA expression of proinflammatory mediators such as tumor necrosis factor-${\alpha}$, interleukin-6, cyclooxygenase-2, and inducible nitric oxide synthase. In addition, CKRF significantly attenuated the transcriptional activities of TLR4/LPS-induced NF-${\kappa}B$. Nuclear translocation of NF-${\kappa}B$ in response to LPS stimulation was significantly abrogated by pre-treatment with CKRF. Furthermore, CKRF inhibited the recruitment of p65 to the interferon-sensitive response element flanking region in response to LPS. Finally, oral administration of CKRF significantly protected mice from Gram-negative bacterial LPS-induced lethal shock and inhibited systemic inflammatory cytokine levels. Together, these results demonstrate that CKRF modulates the TLR4-dependent NF-${\kappa}B$ activation, and suggest a therapeutic role for Gram-negative septic shock.

Differential Induction of Septic Shock by Lipopolysacchrides from E. coli and S. abortus (S. abortus 유래 LPS와 E. coli 유래 LPS에 의한 패혈증성 쇽 유도 작용 비교)

  • Cho, Jae-Youl;Yoo, Eun-Sook
    • YAKHAK HOEJI
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    • v.51 no.1
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    • pp.44-50
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    • 2007
  • Acute septic shock is one of inflammatory diseases mediated by pro-inflammatory cytokines such as tumor necrosis factor (TNF)-${\alpha}$. In this study, we examined the pathological difference and mechanism of lipopolysaccharides isolated from E. coli (E-LPS) or S. abortus (S-LPS) on inducing acute septic shock in ICR mouse. All mice were died by intraperitoneal treatment of S-LPS with 0.75 mg/kg, whereas E-LPS treated with even 3 mg/kg only showed 30% of mice lethal, indicating that S-LPS may be more feasible in triggering a strong septic shock condition. The secretion pattern of TNF-${\alpha}$, a critical pro-inflammatory cytokine in septic shock condition, was also distinct between E-LPS- and S-LPS-treated groups. Thus, S-LPS strikingly increased serum level of TNF-${\alpha}$ (6 ng/ml) at 1 h, while E-LPS just displayed at 2 ng/ml level. However the interaction of S-LPS with LPS receptor toll like receptor (TLR)-4, was not stronger than that of E-LPS, according to experiments with macrophage cell line RAW264.7 cells. Thus, E-LPS rather than S-LPS strongly enhanced the production of TNF-${\alpha}$. Interestingly, S-LPS more strongly up-regulated splenocyte proliferation, compared to E-LPS group, whereas there was no difference between S- or E-LPS treated groups in proliferation of Balb/c- or C57BL/6-originated splenic lymphocytes. Therefore, our data suggest that S-LPS is a more active endotoxin and that the strong septic shock-inducing effect of S-LPS seems due to the enhancement of early TNF-${\alpha}$ production and S-LPS-sensitive lymphocyte proliferation.

Safety Evaluation of Recombinant Human Factor VIII(GC-γ AHF) (유전자 재조합 Human Factor VIII(GC-γ AHF)의 안전성에 관한 연구)

  • 김민영;손장원;신민기;배미옥;김현우;최진혁;김준성;문서현;김정현
    • Toxicological Research
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    • v.18 no.1
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    • pp.87-98
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    • 2002
  • This study was conducted to evaluate the safety of a recombinant human Factor VIII(GC-$\gamma$ AHF) manufactured by Korea Green Cross Company with different technology according to the Regulation of Korean Food and Drug Administration (l 998. 12. 3). In acute toxicity test, both genders of Sprague-Dawley rats and Beagle dogs were administered intravenously with GC-$\gamma$ AHF of three doses (3,125, 625 and 125 IU/kg), and single dose of 3,125 IU/kg, respectively. No dead animal and abnormal autopsy findings were found in Control and GC-$\gamma$ AHF treated group. Therefore, the 50% lethal dose ($LD_{50}$) of GC-$\gamma$ AHF was conidered to be higher than 3,125 IU/kg in rats and dogs. In the four weeks repeated intravenous toxicity study, GC-$\gamma$ AHF was administrated intravenosly to both genders of rats and dogs with 3 doses (500, 150, 50 IU/kg). There were neither dead animals nor significant changes of body weights during the experimental Period. In addition, no significant GC-$\gamma$ AHF related changes were found in clinical sign, urinalysis and other finding. Statistically changes were observed in hematological, biochemical and organ weight parameters of treated groups: however these changes were not dose dependent. No histopathological lesion were observed in both control and treated animals. Above data suggest that no observed adverse effect level of test materials in rats and dogs might be over 500 IU/kg/day in this study. In ocular irritation test, any injury on iris, conjunctiva and cornea in rabbits were not observed. The acute ocular irritation index (A.O.I.), mean ocular irritation index (M.O.I.) and Day-7 individual ocular irritation Index (I.O.I.) of GC-$\gamma$ AHF were 0. In the primary skin Irritation test, the primary irritation index (P.I.I.) oj GC-$\gamma$ AHF were 0. Therefore, the GC-$\gamma$ AHF is considered not to have the primary skin and eye toxicity in rabbits. In active systemic anaphylaxis (ASA) test, GC-$\gamma$ AHF and GC-$\gamma$ AHF emulsified with Freund's complete adjuvant (FCA) did not induce any symptom of anaphylactic shock in guinea pigs. In passive cutaneous anaphylxis (PCA) test, after sensitization with antisera of GC-$\gamma$ AHF sensitized mice, blue spots were observed on the hypodermis of back of rats, but diameter of each spot was smaller than 5 mm in each test groups except the positive control group. Based on the results of this study, GC-$\gamma$ AHF is not conidered to have any antigenic potential. In conclusion, at levels of up to 500 IU/kg, GC-$\gamma$ AHF did not produce treatment-related toxicity under the conditions of these acute-, four week repeated-toxicity, primary skin and eye toxicity, and antigenicity test.

Anti-Inflammatory Effect of Hot Water Extract of Aronia Fruits in LPS-Stimulated RAW 264.7 Macrophages (LPS 자극 RAW 264.7 대식세포에 있어서 아로니아 열매 열수 추출물의 항염증 효과)

  • Yang, Hui;Oh, Kwang-Hoon;Yoo, Yung Choon
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.44 no.1
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    • pp.7-13
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    • 2015
  • In this study, anti-inflammatory activity of hot water extract of Aronia fruits (AF-H) was examined. Pre-treatment with AF-H significantly inhibited production of nitric oxide (NO) and prostaglandin E-2 in a dose-dependent manner in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. The inhibitory effect of AF-H on LPS-induced inflammation was also confirmed by down-regulation of inducible NO synthase as well as cyclooxygenase-2 protein expression. Furthermore, treatment with AF-H significantly inhibited secretion of inflammatory cytokines such as tumor-necrosis $factor-{\alpha}$ and interleukin-6. Signal transduction pathway studies further indicated that AF-H inhibited LPS-induced activation of nuclear $factor-{\kappa}B$, but not mitogen-activated protein kinase. Treatment with AF-H also partially protected against LPS-induced lethal shock in C57BL/6 mice, although its effect was not statistically significant. These results suggest that AF-H is a more promising nutraceutical or medicinal agent for inhibition of LPS-induced inflammation or inflammation-related diseases.