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국가지정 음압격리 입원치료병상의 슬라이딩 도어의 개폐속도 및 의료진의 이동속도에 따른 오염공기 유출에 관한 해석적 연구
이두루나(Du Ru Na Lee),홍진관(Jin Kwan Hong) 대한설비공학회 2018 설비공학 논문집 Vol.30 No.5
To prevent secondary infections in national inpatient isolation units, this study conducted flow analysis for opening/closing speeds of sliding doors of negative pressure isolation rooms and medical workers’ moving speeds among various factors that might cause outflow of contaminated air from negative pressure isolation rooms to the outside. Subject situations were divided into cases where medical workers’ moving speed remained the same while opening/closing speed of doors changed and cases where opening/closing speed of doors changed while medical workers’ moving speed remained the same to figure out internal flow characteristics of negative pressure isolation rooms and anteroom. Three speeds were designated for each of sliding door opening/closing speeds and medical workers’ moving speeds. Results showed that the outflow of contaminated air decreased as sliding door opening/closing speeds increased and as medical workers’ moving speeds decreased. Results of this study can be used as evidentiary material to set standard operation procedures to minimize diffusion of contaminated air where national inpatient isolation units are designed and operated.
Deficiency of iNOS Does Not Prevent Isoproterenol-induced Cardiac Hypertrophy in Mice
Hye-Na Cha,Geu-Ru Hong,Yong-Woon Kim,Jong-Yeon Kim,Jin-Myoung Dan,So-Young Park 대한생리학회-대한약리학회 2009 The Korean Journal of Physiology & Pharmacology Vol.13 No.3
We investigated whether deficiency of inducible nitric oxide synthase (iNOS) could prevent isoproterenol-induced cardiac hypertrophy in iNOS knockout (KO) mice. Isoproterenol was continuously infused subcutaneously (15 mg/kg/day) using an osmotic minipump. Isoproterenol reduced body weight and fat mass in both iNOS KO and wild-type mice compared with saline-infused wild-type mice. Isoproterenol increased the heart weight in both iNOS KO and wild-type mice but there was no difference between iNOS KO and wild-type mice. Posterior wall thickness of left ventricle showed the same tendency with heart weight. Protein level of iNOS in the left ventricle was increased in isoproterenol-infused wild-type mice. The gene expression of interleukin-6 (IL-6) and transforming growth factor-Ղ (TGF-Ղ) in isoproterenol-infused wild-type was measured at 2, 4, 24, and 48-hour and isoproterenol increased both IL-6 (2, 4, 24, and 48-hour) and TGF-Ղ (4 and 24-hour). Isoproterenol infusion for 7 days increased the mRNA level of IL-6 and TGF-Ղ in iNOS KO mice, whereas the gene expression in wild-type mice was not increased. Phosphorylated form of extracellular signal-regulated kinases (pERK) was also increased by isoproterenol at 2 and 4-hour but was not increased at 7 days after infusion in wild-type mice. However, the increased pERK level in iNOS KO mice was maintained even at 7 days after isoproterenol infusion. These results suggest that deficiency of iNOS does not prevent isoproterenol- induced cardiac hypertrophy and may have potentially harmful effects on cardiac hypertrophy.
Effects of moderate pressure on premeability and viability of Saccharomyces cerevisiae cells
Shi-Ru Jia,Na-Chen,Yu-Jie Dai,Chang-Sheng Qiao,Jian-Dong Cui,Bo-Ning Liu 한국화학공학회 2009 Korean Journal of Chemical Engineering Vol.26 No.3
With CO2 and N2 as the pressure media, the effects of the moderate pressure (0.1-1.0MPa) and the holding time on the conductivities of the cell suspension of Saccharomyces cerevisiae CICC1447 and Saccharomyces cerevisiae CICC1339, as well as the absorbances of the supernatant (after centrifuged) at 280 nm (A280) and 260 nm (A260) were determined. The membrane permeability of Saccharomyces cerevisiae CICC1447 increased significantly and the cell leakage was aggravated with the pressure increase. For Saccharomyces cerevisiae CICC1339, the conductivity of the cell suspension, A280 and A260 of the supernatant fluctuated with the pressure increase; as a whole, they increased with pressure. Different from high pressure, a moderate pressure not only remarkably improved the permeability of the yeast cell membrane, but also kept yeast cell viability; moreover, the integrity of the yeast cell membrane could be maintained.
Deficiency of iNOS Does Not Prevent Isoproterenol-induced Cardiac Hypertrophy in Mice
Cha, Hye-Na,Hong, Geu-Ru,Kim, Yong-Woon,Kim, Jong-Yeon,Dan, Jin-Myoung,Park, So-Young The Korean Society of Pharmacology 2009 The Korean Journal of Physiology & Pharmacology Vol.13 No.3
We investigated whether deficiency of inducible nitric oxide synthase (iNOS) could prevent isoproterenol-induced cardiac hypertrophy in iNOS knockout (KO) mice. Isoproterenol was continuously infused subcutaneously (15 mg/kg/day) using an osmotic minipump. Isoproterenol reduced body weight and fat mass in both iNOS KO and wild-type mice compared with saline-infused wild-type mice. Isoproterenol increased the heart weight in both iNOS KO and wild-type mice but there was no difference between iNOS KO and wild-type mice. Posterior wall thickness of left ventricle showed the same tendency with heart weight. Protein level of iNOS in the left ventricle was increased in isoproterenol-infused wild-type mice. The gene expression of interleukin-6 (IL-6) and transforming growth factor-${\beta}$ (TGF-${\beta}$) in isoproterenol-infused wild-type was measured at 2, 4, 24, and 48-hour and isoproterenol increased both IL-6 (2, 4, 24, and 48-hour) and TGF-${\beta}$ (4 and 24-hour). Isoproterenol infusion for 7 days increased the mRNA level of IL-6 and TGF-${\beta}$ in iNOS KO mice, whereas the gene expression in wild-type mice was not increased. Phosphorylated form of extracellular signal-regulated kinases (pERK) was also increased by isoproterenol at 2 and 4-hour but was not increased at 7 days after infusion in wild-type mice. However, the increased pERK level in iNOS KO mice was maintained even at 7 days after isoproterenol infusion. These results suggest that deficiency of iNOS does not prevent isoproterenol-induced cardiac hypertrophy and may have potentially harmful effects on cardiac hypertrophy.