• Title/Summary/Keyword: biomedical

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Differences of Blood Oxygen Saturation between 20s and 60s due to Amount of Highly Concentrated Oxygen Administration (고농도 산소 공급량에 따른 20대와 60대의 혈중 산소 포화도의 차이)

  • Choi, Mi-Hyun;Kim, Ji-Hye;Lee, Su-Jeong;Yang, Jae-Woong;Yi, Jeong-Han;Jun, Jae-Hoon;Kim, Hyun-Jun;Lee, Tae-Soo;Chung, Soon-Cheol
    • Science of Emotion and Sensibility
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    • v.13 no.1
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    • pp.41-46
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    • 2010

  • The purpose of this study was to examine differences between 20s and 60s in blood oxygen saturation due to 93% oxygen administration of the three levels(1L/min, 3L/min, 5L/min). Ten 20s male($25.0{\pm}1.8$ years), ten 20s female($23.7{\pm}1.9$ years), ten 60s male($68.0{\pm}2.6$ years), and ten 60s female($65.5{\pm}3.1$ years) were selected as the subjects for this study. The oxygen supply equipment(OXUS Co.) provided oxygen by supply rate(i.e., 1L/min, 3L/min, and 5L/min) at a constant rate of 93% oxygen. The experiment consisted of three phases, i.e., Prehyperoxia(5min), Hyperoxia(10min), and Post-hyperoxia(5min). Blood oxygen saturation were measured throughoutthe three phases. By increasing the amount of highly concentrated oxygen administration, blood oxygen saturation was increased. Blood oxygen saturation of 20s was higher than 60s. Blood oxygen saturation was greater during Hyperoxia than during Pre- and Post-hyperoxia. However, rising rate of blood oxygen saturation of 60s by oxygen administration was higher than 20s.

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Protective effects of Tat-NQO1 against oxidative stress-induced HT-22 cell damage, and ischemic injury in animals

  • Jo, Hyo Sang;Kim, Duk-Soo;Ahn, Eun Hee;Kim, Dae Won;Shin, Min Jea;Cho, Su Bin;Park, Jung Hwan;Lee, Chi Hern;Yeo, Eun Ji;Choi, Yeon Joo;Yeo, Hyeon Ji;Chung, Christine Seok Young;Cho, Sung-Woo;Han, Kyu Hyung;Park, Jinseu;Eum, Won Sik;Choi, Soo Young
    • BMB Reports
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    • v.49 no.11
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    • pp.617-622
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    • 2016

  • Oxidative stress is closely associated with various diseases and is considered to be a major factor in ischemia. NAD(P)H: quinone oxidoreductase 1 (NQO1) protein is a known antioxidant protein that plays a protective role in various cells against oxidative stress. We therefore investigated the effects of cell permeable Tat-NQO1 protein on hippocampal HT-22 cells, and in an animal ischemia model. The Tat-NQO1 protein transduced into HT-22 cells, and significantly inhibited against hydrogen peroxide ($H_2O_2$)-induced cell death and cellular toxicities. Tat-NQO1 protein inhibited the Akt and mitogen activated protein kinases (MAPK) activation as well as caspase-3 expression levels, in $H_2O_2$ exposed HT-22 cells. Moreover, Tat-NQO1 protein transduced into the CA1 region of the hippocampus of the animal brain and drastically protected against ischemic injury. Our results indicate that Tat-NQO1 protein exerts protection against neuronal cell death induced by oxidative stress, suggesting that Tat-NQO1 protein may potentially provide a therapeutic agent for neuronal diseases.

  • https://doi.org/10.5483/BMBRep.2016.49.11.117 인용 PDF KSCI

Inhibitory Effect of Cordycepin on Human Platelet Aggregation

  • Cho, Hyun-Jeong;Ham, Hye-Seon;Lee, Tae-Kyung;Jung, Young-Jin;Park, Sun-A;Kang, Hyo-Chan;Park, Hwa-Jin
    • Biomedical Science Letters
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    • v.10 no.1
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    • pp.1-8
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    • 2004

  • Cordycepin separated from Cordyceps militaris is a major physiologic active component in Cordyceps militaris. The platelet aggregation is stimulated by $Ca^{2+}$, which is either mobilized from intracellular endoplasmic reticulum or transported from extracellular space. cGMP antagonizes the actions of $Ca^{2+}$. Based on these facts, we have investigated the effects of cordycepin on the mobilization of $Ca^{2+}$ and the production of cGMP on collagen ($10\mu$g/ml)-induced human platelet aggregation. Cordycepin potently stimulated the human platelet aggregation induced by collagen ($10\mu$g/ml) in a dose-dependent manner. Cordycepin (500 $\mu$M) inhibited also the collagen-induced human platelet aggregation in the presence both 1 mM and 2 mM of $CaCl_2$. These are in accord with the results that cordycepin inhibited the $Ca^{2+}$- influx on collagen-induced human platelet aggregation. These results suggest that cordycepin decrease the intracellular $Ca^{2+}$ concentration to inhibit collagen-induced human platelet aggregation. Besides, cordycepin increased the level of cGMP on collagen-induced human platelet aggregation. This result is related with the decrease of intracellular $Ca^{2+}$ concentration, because cGMP inhibits the mobilization of $Ca^{2+}$. In addition, cordycepin inhibited the human platelet aggregation induced by LY -83583, inhibitor of guanylate cyclase. This result suggested that cordycepin inhibit the platelet aggregation by stimulating the activity of guanylate cyclase. In conclusion, we demonstrated that cordycepin might have the antiplatelet function by inhibiting $Ca^{2+}$-mobilization via the stimulation of the production of cGMP.

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