• 대한기계학회논문집B
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• 제26권9호
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• pp.1284-1291
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• 2002

Combustion instabilities are an important concern associated with lean premixed combustion. Laboratory-scale dump combustor was used to understand the underlying mechanisms causing combustion instabilities. Experiments were conducted at atmospheric pressure and sound level meter was used to track the pressure fluctuations inside the combustor. Instability maps and phase-resolved OH chemiluminescence images were obtained at several conditions to investigate the mechanism of combustion instability and relations between pressure wave and heat release rate. It showed that combustion instability was susceptible to occur at higher value of equivalence ratio (>0.6) as the mean velocity was decreased. Instabilities exhibited a longitudinal mode with a dominant frequency of ∼341.8 Hz, which corresponded to a quarter wave mode of combustor. Heat release and pressure waves were in-phase when instabilities occurred. Rayleigh index distribution gave a hint about the location where the strong coherence of pressure and heat release existed. These results also give an insight to the control scheme of combustion instabilities. Emission test revealed that NOx emissions were affected by not only equivalence ratio but also combustion instability.

• Journal of Chest Surgery
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• 제19권2호
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• pp.197-208
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• 1986

Propranolol is one of clinically useful antiarrhythmic agents and electrophysiologically classified as group II. And the negative inotropic effect which is not related to adrenolytic effect has been demonstrated with high concentration of propranolol. On the other hand, it has been well known that the calcium plays a central role in excitation-contraction coupling process of myocardium and also in electrophysiological changes of cell membrane. Author studies the effect of propranolol on calcium uptake and release in sarcoplasmic reticulum and mitochondria prepared from porcine myocardium to investigate the mechanism of action of propranolol on myocardium. The results are summarized as follow: 1] The maximum Ca++-uptake of sarcoplasmic reticulum is inhibited by propranolol in a dose dependent manner. 2] The release of calcium from sarcoplasmic reticulum is not affected by propranolol but with higher than 1x10-3 M of propranolol, rate of calcium release from sarcoplasmic reticulum is decreased. 3] Propranolol inhibits the maximum uptake and uptake rate of calcium in mitochondria non-competitively. [Ki = 6.21 x 10-4 M] 4] The rate of Na+ induced calcium release from mitochondrion shows a function of [Na+]2 and is inhibited by propranolol with the concentration significantly lower than that affect the calcium uptake in sarcoplasmic reticulum and in mitochondria [Ki = 2.91 x 10-5 M]. These results suggest that propranolol affects the intracellular calcium homeostasis which may considered to be one of the mechanism of action of propranolol on myocardium.

• Nuclear Engineering and Technology
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• 제47권5호
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• pp.608-616
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• 2015

The migration of silver (Ag) in silicon carbide (SiC) and $^{110m}Ag$ through SiC of irradiated tristructural isotropic (TRISO) fuel has been studied for the past three to four decades. However, there is no satisfactory explanation for the transport mechanism of Ag in SiC. In this work, the diffusion coefficients of Ag measured and/or estimated in previous studies were reviewed, and then pre-exponential factors and activation energies from the previous experiments were evaluated using Arrhenius equation. The activation energy is $247.4kJ{\cdot}mol^{-1}$ from Ag paste experiments between two SiC layers produced using fluidized-bed chemical vapor deposition (FBCVD), $125.3kJ{\cdot}mol^{-1}$ from integral release experiments (annealing of irradiated TRISO fuel), $121.8kJ{\cdot}mol^{-1}$ from fractional Ag release during irradiation of TRISO fuel in high flux reactor (HFR), and $274.8kJ{\cdot}mol^{-1}$ from Ag ion implantation experiments, respectively. The activation energy from ion implantation experiments is greater than that from Ag paste, fractional release and integral release, and the activation energy from Ag paste experiments is approximately two times greater than that from integral release experiments and fractional Ag release during the irradiation of TRISO fuel in HFR. The pre-exponential factors are also very different depending on the experimental methods and estimation. From a comparison of the pre-exponential factors and activation energies, it can be analogized that the diffusion mechanism of Ag using ion implantation experiment is different from other experiments, such as a Ag paste experiment, integral release experiments, and heating experiments after irradiating TRISO fuel in HFR. However, the results of this work do not support the long held assumption that Ag release from FBCVD-SiC, used for the coating layer in TRISO fuel, is dominated by grain boundary diffusion. In order to understand in detail the transport mechanism of Ag through the coating layer, FBCVD-SiC in TRISO fuel, a microstructural change caused by neutron irradiation during operation has to be fully considered.

• The Korean Journal of Physiology
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• 제22권2호
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• pp.259-272
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• 1988

Type I allergic reaction and it's related clinical manifestations are known to occur by the effects of various chemical mediators. These chemical mediators are released from circulating basophils and tissue mast cells, which become 'sensitized' through the binding of antigens and antibodies of the IgE type to their cell surface receptors. Efforts to elucidate the mechanism of the release of these mediators, especially that of histamine, have been persued for years. The mechanism is not yet clarified at the present time. Recent reports of hyaluronidase, an enzyme known to be involved in the tissue inflammatory process, as possible participant in type I allergic reaction, initiated this study. Relationships between the hyaluronidase activity and histamine release from the sensitized rat peritoneal mast cells were investigated. Also anti-allergic agents, tranilast and disodium cromoglycate, along with known histamine releasers, morphine and compound 48/80, were used to observe the inhibitory and stimulatory effects of these substances on the hyaluronidase activity as well as histamine release from the rat mast cells. The results obtained are summarized as follows: 1) Hyaluronidase activity and histamine release from sensitiaed rat peritoneal mast cells started to increase on the 4th day of postsensitization. Hyaluronidase activity reached it's peak value on the 7th day of postsensitization and that of histamine release on the 14th day of postsensitization. 2) Hyaluronidase activity and histamine release from sensitized rat peritoneal mast cells, pre-treated with tranilast revealed significant decrease in comparison with those of non-treated cells. 3) Hyaluronidase activity and histamine release from sensitized rat peritoneal mast cells, pre-treated with tranilast, followed by morphine injection, revealed significant increase in comparison with those of tranilast treated cells. 4) In vitro study of hyaluronidase activity and histamine release from un-sensitized rat peritoneal mast cells, using morphine and compound 48/80 as activators, revealed significant increase compared to those of non-activator used cells. 5) In vitro study of hyaluronidase activity and histamine release from un-sensitized rat peritoneal mast cells, pre-treated with tranilast and disodium cromoglycate, using confound 48/80 and morphine as activators revealed significant decrease in comparison with those of tranilast and disodium cromoglycate treated cells. From above results, participation of enzyme hyaluronidase in the process of histamine release from sensitized rat pertioneal mast cells, could be suggested. It was also quite evident that the clinically used anti-allergic agents, tranilast and disodium cromoglycate, have significant inhibitory function on the hyaluronidase activity and histamine release from sensitized rat peritoneal mast cells, while morphine significantly increased the hyaluronidase activity and histamine release from sensitized rat peritoneal mast cells.

• BMB Reports
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• 제28권4호
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• pp.301-305
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• 1995

Considering the stimulatory effects of ginsenosides from Panax ginseng C. A. Meyer on the release of nitric oxide from bovine aortic endothelial cells in vitro and vasodilatation of rabbit pulmonary artery in vivo, the present study is designed to investigate the mechanism of nitric oxide release by ginsenosides in calf pulmonary artery endothelial cells, Nitric oxide release was determined in endothelial cells treated with ginsenosides and compared with those of the receptor-dependent agonists, bradykinin and ADP and the receptor-independent calcium ionophore $A_{23187}$. The results showed that total saponin and ginsenoside $Rg_1$, not $Rb_1$, stimulated nitric oxide release measured as conversion to L-citrulline. The nitric oxide releasing properties of total saponin and ginsenoside $Rg_1$ were different; total saponin stimulated only conversion to L-citrulline, like $A_{23187}$, while ginsenoside $Rg_1$ stimulated both L-arginine transport and conversion to L-citrulline, as bradykinin or ADP did.

• KSBB Journal
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• 제6권1호
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• pp.79-83
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• 1991

생물고분자인 PHB로 고분자 matrix를 제조하여 대상약물인 silver sulfadiazine의 방출기전을 연구하였다. 고분자 matrix내의 PHB의 함유량 증가와 matrix의 두께비가 증가할수록 방출속도는 늦어졌다. 그러나 가소제량이 증가함에 따라 방출 기전은 각각 18, 17, 16, 12 및 10시간으로 감소하였다. 이 제형은 약물방출기전은 Higuchi model에 따른 확산으로 생각되었다. 결론적으로 PHB의 함유량과 가소제의 함유량 및 matrix 두께의 상관관계를 조절하므로써 특정한 약물의 방출기전을 얻을 수 있는 maxtrx형태의 개발 가능성을 보였다.

• Bulletin of the Korean Chemical Society
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• 제22권5호
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• pp.467-475
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• 2001

A triblock copolymer based on $poly(\varepsilon-caprolactone)$ (PCL) as the hydrophobic part and poly(ethylene glycol) (PEG) as the hydrophilic portion was synthesized by a ring-opening mechanism of ${\varepsilon}-caprolactone$ with PEG containing a hydroxyl group at bot h ends as an initiator. The synthesized block copolymers of PCL/PEG/PCL (CEC) were confirmed and characterized using various analysis equipment such as 1H NMR, DSC, FT-IR, and WAXD. Core-shell type nanoparticles of CEC triblock copolymers were prepared using a dialysis technique to estimate their potential as a colloidal drug carrier using a hydrophobic drug. From the results of particle size analysis and transmission electron microscopy, the particle size of CEC core-shell type nanoparticles was determined to be about 20-60 nm with a spherical shape. Since CEC block copolymer nanoparticles have a core-shell type micellar structure and small particle size similar to polymeric micelles, CEC block copolymer can self-associate at certain concentrations and the critical association concentration (CAC) was able to be determined by fluorescence probe techniques. The CAC values of the CEC block copolymers were dependent on the PCL block length. In addition, drug loading contents were dependent on the PCL block length: the larger the PCL block length, the higher the drug loading content. Drug release from CEC core-shell type nanoparticles showed an initial burst release for the first 12 hrs followed by pseudo-zero order release kinetics for 2 or 3 days. CEC-2 block copolymer core-shell type nanoparticles were degraded very slowly, suggesting that the drug release kinetics were governed by a diffusion mechanism rather than a degradation mechanism irrelevant to the CEC block copolymer composition.

• Bulletin of the Korean Chemical Society
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• 제23권11호
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• pp.1579-1584
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• 2002

Since surfactant or emulsifiers remained on the nanoparticle surface significantly affect the physicochemical properties, the biodegradation rate, the biodistribution, and the biocompatibility of nanoparticles, surfactant-free nanoparticles should be good candidate. surfactant-free PLGA nanoparticles were successfully prepared by both the dialysis method and the solvent diffusion method. The PLGA nanoparticles prepared using the solvent diffusion method has a smaller particle size than the dialysis method. The solvent diffusion method was better for a higher loading efficiency than the dialysis method but the nanoparticle yield was lower. Testosterone (TST) release from the PLGA nanoparticles was dependent on the particle size rather than the drug contents. Testosterone release from the PLGA nanoparticles prepared by the solvent diffusion method using acetone was faster than those prepared by the dialysis method. TST release from the PLGA nanoparticles prepared by the solvent diffusion method using acetone and the dialysis method using dimethylformamide (DMF) was completed for 4 days while the PLGA nanoparticles prepared by the dialysis method using acetone showed approximately 80% TST release after 4 days. Since the PLGA nanoparticle degradation ratio was below 20% within 5 days at all samples while TST release completed within 4 days, TST release was dependent on the diffusion mechanism rather than degradation.

• KSBB Journal
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• 제10권4호
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• pp.461-467
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• 1995

본 연구에서는 약물 전달체(키토산, 키토산.엽, 술폰화키토산)에 prednisolone을 분산시켜 제조한 고분자 매트릭스를 poly (DL-lactide)로 피막을 형성시킨 후 pH 1.2와 pH 7.4 인산염 완충용액에서 약물 방출실험을 하였다. 약물 방출시간은 pH 1.2에서 보다 pH 7.4에서 더 지연되였으며 약물 전달체의 함유량이 증가함에 따라 약물의 방출시간도 지연되었다. 피막된 고분자 매트릭스의 종류에 따라 지연된 약물의 방출시간은 키토산의 경우가 가장 길었으 며, 술폰화키토산, 키토산.염의 순셔였다. Monolith IC 고분자 매트릭스에 비해 2배 정도의 약물의 방출 지연성을 보인 피막된 monolithic 고분자 매트럭스 가 방출조절형 제제로서 더 바람직한 것으로 관찰되었다. 이러한 제형들은 초기 급격한 약물 방출속도의 변화를 억 제 하는 sustained release pattern 제 제 임을 확인할 수 있었다.

• 대한의생명과학회지
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• 제27권3호
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• pp.170-176
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• 2021

Thapsigargin (TG), a sarco/endoplasmic reticulum (ER) Ca²⁺-ATPase (SERCA) inhibitor, has been widely used as an agonist for platelet aggregation for decades. In this study, we investigated the effect of TG on the release of lactate dehydrogenase (LDH) for platelets and elucidated its mechanism. Platelet LDH release and platelet aggregation were increased by TG treatment; 1,000 nM of TG induced the complete lysis of platelets. Other agonists such as collagen (2.5 ㎍/mL), thrombin (0.1 U/mL), and ADP (10 mM) did not induce significant platelet LDH release despite platelet aggregation. Finally, we investigated the effects of pharmacological inhibitors on TG-induced platelet aggregation and LDH release. SP600125, a JNK inhibitor, and LY294002, a PI-3K inhibitor, inhibited TG-induced platelet LDH release but not platelet aggregation. Forskolin, an adenylyl cyclase activator, also inhibited LDH release without affecting platelet aggregation by TG. These results suggest that the TG-induced platelet aggregation was accompanied by LDH release but regulated by a different signaling pathway.