• Title/Summary/Keyword: Contributory

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Arachidonate-induced Oxygen Radical Production and Cellular Damage in Ischemic-Reperfused Heart of Rat (허혈-재관류 적출심장에서 Arachidonic Acid에 의한 산소라디칼 생성 및 심근손상)

  • Lee, Yun-Song;Kim, Yong-Sik;Park, Seong-Ho;Myung, Ho-Jin;Kim, Myung-Suk
    • The Korean Journal of Pharmacology
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    • v.27 no.2
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    • pp.109-118
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    • 1991
  • The present study was conducted to assess the possible contribution of arachidonic acid to generation of reactive oxygen metabolites and myocardial damage in ischemic-reperfused heart. Langendorff preparations of isolated rat heart were made ischemic by hypoperfusion (0.5 ml/min) for 45 min, and then followed by normal oxygenated reperfusion (7 ml/min). The generation of superoxide anion was estimated by measuring the SOD-inhibitable ferricytochrome C reduction. The myocardial cellular damage was observed by measuring LDH released into the coronary effluent. Oxygenated reperfusion following a period of ischemia produced superoxide anion, which was inhibited by both indomethacin (60 nmole/ml) and ibuprofen $(30\;{\mu}g/ml)$. Sodium arachidonate $(10^{-7}-10^{-2}{\mu}g/ml)$ administered during the period of oxygenated reperfusion stimulated superoxide anion production dose-dependently. The rate of arachidonate-induced superoxide generation was markedly inhibited by indomethacin, a cyclooxygenase inhibitor; nordihydroguaiaretic acid (NDGA), a lipoxygenase inhibitor, and by eicosatetraynoic acid (ETYA), a substrate inhibitor of arachidonic acid metabolism. The release of LDH was increased by Na arachidonate and was inhibited by superoxide dismutase. The release of LDH induced by arachidonic acid was also inhibited by indomethacin, NDGA and ETYA. In conclusion, the present result suggests that arachidonic acid metabolism is involved in the production of reactive oxygen metabolite and plays a contributory role in the genesis of reperfusion injuy of myocardium.

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p16INK4a Promoter Hypermethylation in Sputum, Blood, and Tissue from Non-Small Cell Lung Cancer and Pulmonary Inflammation (비소세포폐암과 염증성 폐질환에서 가래와 혈액 및 조직에서 p16INK4a Promoter 과메틸화)

  • Kim, Jeong Pyo;Kim, Kyong Mee;Kwon, Soon Seog;Kim, Young Kyoon;Kim, Kwan Hyoung;Moon, Hwa Sik;Song, Jeong Sup;Park, Sung Hak;Ahn, Joong Hyun
    • Tuberculosis and Respiratory Diseases
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    • v.60 no.2
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    • pp.160-170
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    • 2006
  • Background : The aberrant promoter hypermethylation of p16INK4a, as a tumor suppressor gene, is contributory factor to non-small cell lung cancer(NSCLC). However, its potential diagnostic impact of lung cancer is unclear. This study measured the level of $p16^{INK4a}$ promoter hypermethylation in the sputum and blood, and compared this with the level measured in the tissue obtained from NSCLC and pulmonary inflammation. Methods : Of the patients who visited the Our Lady of Mercy Hospital in Incheon, Korea for an evaluation of a lung mass and underwent blood, sputum, and tissue tests, 23patients (18 NSCLC, 5 pulmonary inflammation) were enrolled in this study. DNA was extracted from each sample and the level of p16INK4amethylation was determined using methylation-specific polymerase chain reaction. Results : $p16^{INK4a}$ methylation of the blood was observed in 88.9% (16 of 18) and 20.0% (1 of 5) of NSCLC and from pulmonary inflammation samples, respectively (P=0.008). Methylation of the sputum was observed in 83.3% (10 of 12) 80.0% (4 of 5) of NSCLC and pulmonary inflammation samples, respectively (P=1.00). Among the 8 NSCLC tissue samples, methylation changes were detected in 75.0% of samples (6 cases). Four out of seven tissue samples (57.1%) showed concordance, being methylated in both the blood and sputum. Conclusions : There was a higher level of $p16^{INK4a}$ methylation of the blood from NSCLC patients than from pulmonary inflammation. The tissue showed a high concordance with the blood in the NSCLC samples. These findings suggest that $p16^{INK4a}$ promoter hypermethylation of the blood can used to discriminate between NSCLC and pulmonary inflammation.

Effect of Cervi Pantotrichum Cornu Herbal acupuncture on protease activities, antioxidant in Rheumatoid arthritis rats (류마티스 관절염 실험용쥐의 활액에서 단백분해효소의 활성 및 항산화에 대한 녹용약침의 효과)

  • Park, Sang-Dong;Kim, Min-Jeong;Lee, A-Ram;Jang, Jun-Hyouk;Kim, Kyung-Ho
    • Journal of Acupuncture Research
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    • v.19 no.2
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    • pp.51-64
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    • 2002
  • We have compared(using the same series of experimental tissue samples) the levels of proteolytic enzyme activities and free radical-induced protein damage in synovial fluid from RA and CPH cases. Many protease types showed significantly increased (typically by a factor of approximately 2-3-fold) activity in RA, compared to normal rats. However, CPH significantly reduced the cytoplasmic enzyme activities of arginyl aminopeptidase, leucyl aminopeptidase, pyroglutamyl aminopeptidase, tripeptidyl aminopeptidase, and proline endopeptidase to almost about 1/10 each. For the Iysosomal proteases, synovial fluid samples from RA rats, CPH significantly reduced the enzyme activities of cathepsin B, dipeptidyl aminopeptidase I and dipeptidyl aminopeptidase II. In extracellular matrix degrading(collagenase, tissue elastase) and leukocyte as sociated proteases (leukocyte elastase, cathepsin G), CPH decreased these enzyme activities of collagenase, tissue elastase and leukocyte associated elastase in RA. In cytoplasmic and lysosomal protease activities in plasma from RA. CPH and normal plasma samples were not significantly different, suggesting that altered activity of plasma proteases (particularly those enzymes putatively involved in the immune response) is not a contributory factor in the pathogenesis of RA. In addition, the level of free radical induced damage to synovial fluid proteins was approximately twice that in RA, compared with CPH. CPH significantly decreased the level of ROS induced oxidative damage to synovial fluid proteins (quantified as protein carbonyl derivative). Therefore we conclude that both proteolytic enzymes and free radicals are likely to be of equal potential importance as damaging agents in the pathogenesis of inflammatory joint disease, and that the design of novel therapeutic strategies for patients with the latter disorder should include both protease inhibitory and free radical scavenging elements. In addition, the protease inhibitory element should be designed to inhibit the action of a broad range of protease mechanistic types (i.e. cysteine-, metallo- and serine- proteinases and peptidases). However, increased protein damage induced by ROS could not be rationalised in terms of compromised antioxidant total capacity, since the latter was not significantly altered in RA synovial fluid or plasma compared with CPH.

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Influence of Obstructive Sleep Apnea on Soluble Intercellular Adhesion Molecule-1 and Vascular Endothelial Growth Factor (폐쇄성 수면 무호흡이 Soluble Intercellular Adhesion Molecule-1과 Vascular Endothelial Growth Factor에 미치는 영향)

  • Kim, Jeong Pyo;Lee, Sang Haak;Kwon, Soon Seog;Kim, Young Kyun;Kim, Kwan Hyoung;Song, Jeong Sup;Park, Sung Hak;Moon, Hwa Sik
    • Tuberculosis and Respiratory Diseases
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    • v.56 no.4
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    • pp.364-373
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    • 2004
  • Background : Obstructive sleep apnea is a contributory factor of hypertension, arrhythmia, ischemic heart disease and other cardiovascular diseases. However, the pathophysiology underlying this relationship is unclear. Recent reports have shown that the soluble intercellular adhesion molecule-1(sICAM-1) and vascular endothelial growth factor(VEGF) are involved in the initiation and progression of atherosclerosis, and some reports state that increased levels of these cytokines are found in patients with obstructive sleep apnea. In this study, the levels of sICAM-1 and VEGF were measured in patients with obstructive sleep apnea in order to determine if obstructive sleep apnea is involved in the pathophysiology of cardiovascular diseases. Methods : Thirty-seven patients were chosen amongst a population who visited the Sleep Disorders Clinic of St. Paul's Hospital in Seoul, Korea for a diagnosis of obstructive sleep apnea and who had subsequently undergone an overnight polysomnography at the clinic. The sera from these patients were retrieved after an overnight polysomnography session and the samples were kept at $-70^{\circ}C$. The cytokine levels were determined with ELISA and the relationships between the serum levels of sICAM-1 and VEGF along with polysomnography parameters were analyzed. Results : No statistically significant correlation was observed between the sICAM-1 levels and the apnea-hypopnea index(r=0.27, P>0.05). Positive correlations were found between the apnea-hypopnea index and serum VEGF levels (r=0.50, P<0.01), the apnea index and the serum sICAM-1 levels (r=0.31, P<0.01), and the apnea index and the serum VEGF levels (r=0.45, P<0.01). Conclusions : Obstructive apnea or hypopnea leads to an increase in the sICAM-1 and VEGF levels. Such an increase in the cytokine levels most likely leads to the higher incidence of cardiovascular diseases observed in patients with obstructive sleep apnea.

The Limitation of Air Carriers' Cargo and Baggage Liability in International Aviation Law: With Reference to the U.S. Courts' Decisions (국제항공법상 화물.수하물에 대한 운송인의 책임상한제도 - 미국의 판례 분석을 중심으로 -)

  • Moon, Joon-Jo
    • The Korean Journal of Air & Space Law and Policy
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    • v.22 no.2
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    • pp.109-133
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    • 2007
  • The legal labyrinth through which we have just walked is one in which even a highly proficient lawyer could easily become lost. Warsaw Convention's original objective of uniformity of private international aviation liability law has been eroded as the world community ha attempted again to address perceived problems. Efforts to create simplicity and certainty of recovery actually may have created less of both. In any particular case, the issue of which international convention, intercarrier agreement or national law to apply will likely be inconsistent with other decisions. The law has evolved faster for some nations, and slower for others. Under the Warsaw Convention of 1929, strict liability is imposed on the air carrier for damage, loss, or destruction of cargo, luggage, or goods sustained either: (1) during carriage in air, which is comprised of the period during which cargo is 'in charge of the carrier (a) within an aerodrome, (b) on board the aircraft, or (c) in any place if the aircraft lands outside an aerodrome; or (2) as a result of delay. By 2007, 151 nations had ratified the original Warsaw Convention, 136 nations had ratified the Hague Protocol, 84 had ratified the Guadalajara Protocol, and 53 nations had ratified Montreal Protocol No.4, all of which have entered into force. In November 2003, the Montreal Convention of 1999 entered into force. Several airlines have embraced the Montreal Agreement or the IATA Intercarrier Agreements. Only seven nations had ratified the moribund Guatemala City Protocol. Meanwhile, the highly influential U.S. Second Circuit has rendered an opinion that no treaty on the subject was in force at all unless both affected nations had ratified the identical convention, leaving some cases to fall between the cracks into the arena of common law. Moreover, in the United States, a surface transportation movement prior or subsequent to the air movement may, depending upon the facts, be subject to Warsaw, or to common law. At present, International private air law regime can be described as a "situation of utter chaos" in which "even legal advisers and judges are confused." The net result of this barnacle-like layering of international and domestic rules, standards, agreements, and criteria in the elimination of legal simplicity and the substitution in its stead of complexity and commercial uncertainty, which manifestly can not inure to the efficient and economical flow of world trade. All this makes a strong case for universal ratification of the Montreal Convention, which will supersede the Warsaw Convention and its various reformulations. Now that the Montreal Convention has entered into force, the insurance community may press the airlines to embrace it, which in turn may encourage the world's governments to ratify it. Under the Montreal Convention, the common law defence is available to the carrier even when it was not the sole cause of the loss or damage, again making way for the application of comparative fault principle. Hopefully, the recent entry into force of the Montreal Convention of 1999 will re-establish the international legal uniformity the Warsaw Convention of 1929 sought to achieve, though far a transitional period at least, the courts of different nations will be applying different legal regimes.

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Expressions of Matrix Metalloproteinase-9 and Tissue Inhibitor of Metalloproteinase-2 with Changes of Interleukin-6 and Interleukin-18 in Atherosclerotic Lesions of Hypercholesterolemic Rabbits (고콜레스테롤혈증 가토의 죽상경화성 병변에서 Interleukin-6와 Interleukin-18의 변화 및 Matrix Metalloproteinase-9과 Tissue Inhibitor of Metalloproteinase-2의 발현)

  • 권영무;김성숙;장봉현
    • Journal of Chest Surgery
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    • v.35 no.6
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    • pp.407-419
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    • 2002
  • Atherosclerosis is a chronic inflammatory disease of the arterial wall characterized by progressive accumulation of lipids, cells, and extracellular matrix. Matrix metalloproteinases(MMPs) and tissue inhibitor of metalloproteinases(TIMPS) contribute to vascular matrix remodeling in atherosclerosis, and some cytokines may play role in the synthesis or activation of MMPs or TIMPs. Material and Method: We produced experimental atherosclerotic plaques in 9 rabbits by atherogenic hypercholesterol diet for 12 weeks, and 10 other rabbits were used as control group with standard laboratory chow, At that time, 19 rabbits were sacrificed and aorta, coronary arteries and blood specimens were prepared. The expressions of MMP-9, TIMP-2 and interleukin(IL)-18, and the bioactivity of IL-6 were investigated with H&E stain, immunohistochemical stain, immunoblotting(Western blot analysis), and bioassay. Result: Serum cholesterol in the experimental group increased up to 1258$\pm$262 mg/dL(control group: 41$\pm$7 mg/dL). All experimental group showed well-developed atherosclerotic plaques in aorta and coronary artery. The expression of MMP-9 in aorta and coronary artery of the experimental group showed significant increase than that of the control group by immunohistochemistry. Among the experimental group, complicated lesions with intimal rupture or complete luminal occlusion, demonstrated stronger expression of MMP-9. Interestingly, there was no difference in expression of TIMP-2 between the experimental and the control group. These findings were confirmed by Western blot analysis. The bioassay revealed significant up-regulation of serum bioactivity of IL-6 in the experimental group(4819.60$\pm$2021.25 IU/$m\ell$) compared to that of IL-6 in the control group(27.20 $\pm$ 12.19 IU/$m\ell$). IL-18 was expressed in all atherosclerotic plaques, whereas little or no expression was detected in the control group. Conclusion: The increased MMP-9 expression along with the unchanged TIMP-2 expression seem to be contributory factors in extracellular matrix degradation in atherosclerosis. Focal overexpression of MMP-9 may promote plaque destabilization and cause complications of atherosclerotic plaques such as thrombosis with/without acute coronary syndrome. Elevation of IL-6 and IL-18 may be more than just markers of atherosclerosis but actual participants in lesion development. Identification of critical regulatory pathway is important to improve the understanding of the cellular and molecular basis of atherosclerosis and may open the way for novel therapeutic strategies.

Impact of Weather on Prevalence of Febrile Seizures in Children (소아의 열성경련에 날씨가 미치는 영향)

  • Woo, Jung Hee;Oh, Seok Bin;Yim, Chung Hyuk;Byeon, Jung Hye;Eun, Baik-Lin
    • Journal of the Korean Child Neurology Society
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    • v.26 no.4
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    • pp.227-232
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    • 2018
  • Purpose: Febrile seizure (FS) is the most common type of seizure in children between 6 months to 5 years of age. A family history of febrile seizures can increase the risk a child will have a FS. Yet, prevalence of FS regarding external environment has not been clearly proved. This study attempts to determine the association between prevalence of FS and weather. Methods: This study included medical records from the Korea National Health Insurance Review and Assessment Service. Data were collected from 29,240 children, born after 2004, diagnosed with FS who were admitted to one of the hospitals in Seoul, Korea, between January 2009 and December 2013. During the corresponding time period, data from the Korea Meteorological Administration on daily monitoring of four meteorological factors (sea-level pressure, amount of precipitation, humidity and temperature) were collected. The relationships of FS prevalence and each meteorological factor will be designed using Poisson generalized additive model (GAM). Also, the contributory effect of viral infections on FS prevalence and weather will be discussed. Results: The amount of precipitation was divided into two groups for comparison: one with less than 5 mm and the other with equal to or more than 5 mm. As a result of Poisson GAM, higher prevalence of FS showed a correlation with smaller amount of precipitation. Smoothing function was used to classify the relationships between three variables (sea-level pressure, humidity, and temperature) and prevalence of FS. FS prevalence was correlated with lower sea-level pressure and lower humidity. FS prevalence was high in two temperature ranges (-7 to $-1^{\circ}C$ and $18-21^{\circ}C$). Conclusion: Low sea-level pressure, small amount of precipitation, and low relative air humidity may increase FS prevalence risk.