• Korean Journal of Agricultural Science
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• v.10 no.2
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• pp.345-353
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• 1983

The polyurethane foam impregnated with 5, 7-dibromo-8-hydroxyquinoline (DBHQ) has been studied to be applied to the quantitative adsorption and recovery of Hg(II) from the aqueous solutions. The adsorption of Hg(II) by DBHQ-OPP foam is due to the chelation between DBHQ-OPP foam and Hg(II) on the foam, forming each colored insoluble chelate with 1:2 mole ratio. The optimum experimental conditions for the adsorption of Hg(II) has been determined. The quantitative recovery of Hg(II) adsorption by the OPP foam and reuse of DBHQ-OPP foam were investigated. Hypothesis on the adsorption and separation mechanism of Hg(II) and DBHQ to the polyurethane foam was proposed.

• BMB Reports
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• v.55 no.11
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• pp.528-534
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• 2022

Mitochondria are cellular organelles that perform various functions within cells. They are responsible for ATP production, cell-signal regulation, autophagy, and cell apoptosis. Because the mitochondrial proteins that perform these functions need Ca²⁺ ions for their activity, mitochondria have ion channels to selectively uptake Ca²⁺ ions from the cytoplasm. The ion channel known to play the most important role in the Ca²⁺ uptake in mitochondria is the mitochondrial calcium uniporter (MCU) holo-complex located in the inner mitochondrial membrane (IMM). This ion channel complex exists in the form of a complex consisting of the pore-forming protein through which the Ca²⁺ ions are transported into the mitochondrial matrix, and the auxiliary protein involved in regulating the activity of the Ca²⁺ uptake by the MCU holo-complex. Studies of this MCU holo-complex have long been conducted, but we didn't know in detail how mitochondria uptake Ca²⁺ ions through this ion channel complex or how the activity of this ion channel complex is regulated. Recently, the protein structure of the MCU holo-complex was identified, enabling the mechanism of Ca²⁺ uptake and its regulation by the MCU holo-complex to be confirmed. In this review, I will introduce the mechanism of action of the MCU holo-complex at the molecular level based on the Cryo-EM structure of the MCU holo-complex to help understand how mitochondria uptake the necessary Ca²⁺ ions through the MCU holo-complex and how these Ca²⁺ uptake mechanisms are regulated.

• Journal of the Korean institute of surface engineering
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• v.47 no.3
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• pp.128-136
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• 2014

In the present study, we successfully developed an eco-friendly chemical etching solution and proper condition for plating on ABS material. The mechanism of forming Ni plating layer on ABS substrate is known as following. In general, the etching solution used for the etching process is a solution of chromic acid and sulfuric acid. The etching solution is given to the surface resulting in elution of butadiene group, so-called anchor effect. Such a rough surface can easily adsorb catalyst resulting in the increase of adhesion between ABS substrate and Ni plating layer. However a use of chromic acid is harmful to environment. It is, therefore, essential to develop a new alternative solution. In the present study, we proposed an eco-friendly etching solution composed of potassium permanganate, sulfuric acid and phosphoric acid. This solution was testified to observe the surface microstructure and the pore size of electrical Ni plating layer, and the adhesive correlation between deposited layers fabricated by electro Ni plating was confirmed. The result of the present study, the newly developed, eco-friendly etching solution, which is a mixture of potassium permanganate 25 g/L, sulfuric acid 650ml/L and phosphoric acid 250ml/L, has a similar etching effect and adhesion property, compared with the commercially used chromium acid solution in the condition at $70^{\circ}C$ for 5 min.

• International Journal of Oral Biology
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• v.43 no.1
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• pp.43-51
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• 2018

$K^+$ channels are key components of the primary and secondary basolateral $Cl^-$ pump systems, which are important for secretion from the salivary glands. Paroxetine is a selective serotonin reuptake inhibitor (SSRI) for psychiatric disorders that can induce QT prolongation, which may lead to torsades de pointes. We studied the effects of paroxetine on a human $K^+$ channel, human ether-a-go-go-related gene (hERG), expressed in Xenopus oocytes and on action potential in guinea pig ventricular myocytes. The hERG encodes the pore-forming subunits of the rapidly-activating delayed rectifier $K^+$ channel ($I_{Kr}$) in the heart. Mutations in hERG reduce $I_{Kr}$ and cause type 2 long QT syndrome (LQT2), a disorder that predisposes individuals to life-threatening arrhythmias. Paroxetine induced concentration-dependent decreases in the current amplitude at the end of the voltage steps and hERG tail currents. The inhibition was concentration-dependent and time-dependent, but voltage-independent during each voltage pulse. In guinea pig ventricular myocytes held at $36^{\circ}C$, treatment with $0.4{\mu}M$ paroxetine for 5 min decreased the action potential duration at 90% of repolarization ($APD_{90}$) by 4.3%. Our results suggest that paroxetine is a blocker of the hERG channels, providing a molecular mechanism for the arrhythmogenic side effects of clinical administration of paroxetine.

• Journal of Veterinary Science
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• v.22 no.5
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• pp.59.1-59.13
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• 2021

Background: Antimicrobial peptides (AMPs) have been identified as promising compounds for consideration as novel antimicrobial agents. Objectives: This study analyzed the efficacy of cecropin B against Haemophilus parasuis isolates through scanning electron microscopy (SEM) and atomic force microscopy (AFM) experiments. Results: Cecropin B exhibited broad inhibition activity against 15 standard Haemophilus parasuis (HPS) strains and 5 of the clinical isolates had minimum inhibition concentrations (MICs) ranging from 2 to 16 ㎍/mL. Microelectrophoresis and hexadecane adsorption assays indicated that the more hydrophobic and the higher the isoelectric point (IEP) of the strain, the more sensitive it was to cecropin B. Through SEM, multiple blisters of various shapes and dents on the cell surface were observed. Protrusions and leakage were detected by AFM. Conclusions: Based on the results, cecropin B could inhibit HPS via a pore-forming mechanism by interacting with the cytoplasmic membrane of bacteria. Moreover, as cecropin B concentration increased, the bacteria membrane was more seriously damaged. Thus, cecropin B could be developed as an effective anti-HPS agent for use in clinical applications.