• YAKHAK HOEJI
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• v.45 no.1
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• pp.85-92
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• 2001

Nitric oxide is a tonically produced vasodilator that maintains blood pressure in the normal animal. The chronic inhibition of nitric oxide synthase (NOS) elicits the hypertension in rats. However, the mechanism of hypertension induced by chronic inhibition of NOS is not clear. Thus, to clarify the mechanism of the occurance of hypertension, the changes in $\alpha$-adrenergic systems in rats treated with NOS inhibitors for 21 days were examined. Chronic administration of L-NAME significantly increased in the basal blood pressure, but chronic administration of 7-nitroindazole did not. Phenylephrine and G-protein stimulator elicited the more potent contraction in the aorta of the L-NAME-induced hypertensive rats. However when the contractile responses by phenylephrine and G-protein stimulator were calculated the proportion to the contraction by 25 mM KCL, there was no difference between the vehicle-treated rats and the L-NAME-treated rats. The density of $\alpha$-adrenergic receptors in aortic tissue was not changed by the chronic inhibition of NOS. These results suggest that hypertension induced by chronic inhibition of NOS is due to the inhibition of eNOS and the increased responses to the adrenergic drugs are due to the changes of the intracellular contactile mechanism of aortic tissue rather than the changes of receptor density.

• Journal of Electrochemical Science and Technology
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• v.10 no.1
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• pp.69-81
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• 2019

The corrosion inhibiting mechanism of Vietnam orange peel essential oil (OPEO) for mild steel in 1 N HCl solution was investigated elaborately. Corrosion inhibition ability of OPEO was characterized by electrochemical polarization, electrochemical impedance spectroscopy (EIS), and weight loss method. In the corrosive solution, OPEO worked as a mixed inhibitor and the inhibition efficiency of OPEO increased with the increase of its concentration. High inhibition efficiencies over 90% were achieved for the concentration of 3 - 4 g/L OPEO, comparable to that of 3.5 g/L urotropine (URO), a commercial corrosion inhibitor for acid media used in industry. By using adsorption isotherm models (Langmuir, Temkin and Frumkin), thermodynamic parameters of adsorption were calculated. The obtained results indicated physical adsorption mechanism of OPEO on the steel surface. The components responsible for the corrosion inhibition activity of OPEO were not only D-limonene, but also other compounds, which contain C=O, C=C, O-H, C-O-C, -C=CH and C-H bonding groups in the molecules.

• YAKHAK HOEJI
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• v.27 no.4
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• pp.321-329
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• 1983

The review characterized active site(s) of MAO with respect to metal ions, hydrophobic and polar region, sulfhydryl group and flavin moiety. The mechanism of inhibition was dealt with three representative types of inhibitors; phenylcyclopropylamines, acetylenic amines, and hydrazines. Multiple forms of MAO was shortly described in relation to their selective inhibition. 84 reference were cited.

• Environmental Engineering Research
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• v.10 no.1
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• pp.22-30
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• 2005

Nitrite accumulation is not unusual in batch processes such as sequencing batch reactor (SBR) with high-strength of ammonium or nitrate wastewaters. A possible mechanism of nitrite inhibition on Acinetobacter was depicted in a biochemical model, which the protonated species, nitrous acid form of nitrite, affects proton relating transport at the proton-pumping site crossing the cell membrane under unlimited carbon and phosphorus conditions. This effect exerts inhibition of phosphorylation under aerobic condition and yields low APT/ADP ratio, consequently decrease poly-P synthesis and phosphorus uptake from outside the cell in the model.

• Molecules and Cells
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• v.42 no.3
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• pp.210-217
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• 2019

The maintenance of mitochondrial function is closely linked to the control of senescence. In our previous study, we uncovered a novel mechanism in which senescence amelioration in normal aging cells is mediated by the recovered mitochondrial function upon Ataxia telangiectasia mutated (ATM) inhibition. However, it remains elusive whether this mechanism is also applicable to senescence amelioration in accelerated aging cells. In this study, we examined the role of ATM inhibition on mitochondrial function in Hutchinson-Gilford progeria syndrome (HGPS) and Werner syndrome (WS) cells. We found that ATM inhibition induced mitochondrial functional recovery accompanied by metabolic reprogramming, which has been known to be a prerequisite for senescence alleviation in normal aging cells. Indeed, the induced mitochondrial metabolic reprogramming was coupled with senescence amelioration in accelerated aging cells. Furthermore, the therapeutic effect via ATM inhibition was observed in HGPS as evidenced by reduced progerin accumulation with concomitant decrease of abnormal nuclear morphology. Taken together, our data indicate that the mitochondrial functional recovery by ATM inhibition might represent a promising strategy to ameliorate the accelerated aging phenotypes and to treat age-related disease.

• Corrosion Science and Technology
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• v.23 no.1
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• pp.20-32
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• 2024

Metal corrosion in acidic environments is a major issue in various industrial applications. This study evaluates the 4-piperonylideneaminoantipyrine (PPDAA) corrosion inhibition efficiency for mild steel in a hydrochloric acid (HCl) solution. The weight loss method was used to determine the corrosion inhibition efficiency at different concentrations and immersion time periods. Results revealed that the highest inhibition efficiency (94.3%) was achieved at 5 mM concentration after 5 hours of immersion time. To inspect the surface morphology of the inhibitor film on the mild steel surface, scanning electron microscopy (SEM) was used before and after immersion in 1.0 M HCl. Density functional theory (DFT) calculations were performed to investigate the molecular structure and electronic properties of the inhibitor molecule to understand the corrosion inhibition mechanism. Theoretical results showed that the inhibitor molecule can adsorb onto the mild steel surface through its nitrogen and oxygen atoms, forming a protective layer that prevents HCl corrosive attack. These findings highlight the potential of PPDAA as an effective corrosion inhibitor for mild steel in HCl solution. Moreover, combining experimental and theoretical approaches provides insights into the mechanism of corrosion inhibition, which is essential for developing effective strategies to prevent metal corrosion in acidic environments.

• Journal of Microbiology and Biotechnology
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• v.24 no.12
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• pp.1673-1678
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• 2014

The interactive inhibitory effects of pH and chloride on the catalysis of laccase from Trametes versicolor were investigated by studying the alteration of inhibition characteristics of sodium chloride at different pHs for the oxidation of 2,2'-azino-bis (3-ethylbenzthiazoline-6-sulfonic acid). At pH 3.0, the addition of sodium chloride (50 mM) brought about a 40-fold increase in $K{_m}^{app}$ and a 4-fold decrease in $V_{max}{^{app}}$. As the pH increased to 7.0, the inhibitory effects of sodium chloride became significantly weakened. The mixed-inhibition mechanism was successfully used to quantitatively estimate the competitive and uncompetitive inhibition strengths by chloride at two different pHs (pH 3.0 and 6.0). At pH 3.0, the competitive inhibition constant, $K_i$, was 0.35 mM, whereas the uncompetitive inhibition constant, $K{_i}^{\prime}$, was 18.1 mM, indicating that the major cause of the laccase inhibition by chloride is due to the competitive inhibition step. At a higher pH of 6.0, where the inhibition of the laccase by hydroxide ions takes effect, the inhibition of the laccase by chloride diminished to a great extent, showing increased values of both the competitive inhibition constant ($K_i=23.7mM$) and uncompetitive inhibition constant ($K{_i}^{\prime}=324mM$). These kinetic results evidenced that the hydroxide anion and chloride share a common mechanism to inhibit the laccase activity.

• Physical Therapy Korea
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• v.8 no.4
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• pp.81-89
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• 2001

There are two independent mechanisms to control the segmental reflex gain in humans during gait. They are presynaptic inhibition and homosynaptic depression. Through the mechanism of the presynaptic inhibition, the muscle spindle afferent feedback can be properly gated during eccentric phase of gait. The modulation of the presynaptic inhibition is reflected in the level of H-reflex at a constant EMG level. During the eccentric muscle activation presynaptic inhibition should increase to account for the lower amplitude level of H-reflex at a constant level of EMG. Homosynaptic depression is another mechanism responsible for regulating the effectiveness of the muscle spindle afferent feedback. Both the presynaptic inhibition and the monosynaptic depression are responsible for modulating reflex gain during gait initiation. Reflex modulation is influenced not only as a passive consequence of the alpha motor neuron excitation level, but also through supraspinal mechanisms. Spastic paretic patients show the impaired soleus H-reflex modulation either during the initial stance phase, or during the swing phase. This abnormal modulatory mechanism can partially and artificially be restored by the application of peripheral stimulus to the sole of the foot, provided that the segmental circuitry remains functional.

• YAKHAK HOEJI
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• v.39 no.5
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• pp.565-568
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• 1995

A new antiplatelett agent, aspalatone ([3-(2-methyl-4-pyronyl)]-2-acetyloxybenzoate) was demonstrated to inhibit MDA generation from arachidonic acid catalyzed by partially purified bovine seminal vesicle cyclooxygenase. This inhibition was also observed with acetylsalicylic acid. The results suggest that the mechanism for the antiplatelet effect of aspalatone is, like acetylsalicylic acid, due to its inhibition of cyclooxygenase.

• YAKHAK HOEJI
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• v.58 no.4
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• pp.223-228
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• 2014

The present study was undertaken to investigate the influence of sulforaphane on vascular smooth muscle contractility and to determine the mechanism involved. We hypothesized that sulforaphane, the primary ingredient of broccoli of cruciferous vegetables, plays a role in vascular relaxation through inhibition of Rho-kinase in rat aortae. Intact of denuded arterial rings from male Sprague-Dawley rats were used and isometric tensions were recorded using a computerized data acquisition system. Interestingly, sulforaphane significantly inhibited fluoride, phorbol ester or thromboxane $A_2$ mimetic-induced contraction in denuded muscles suggesting that additional pathways different from endothelial nitric oxide synthesis such as inhibition of Rho-kinase or MEK might be involved in the vasorelaxation. Furthermore, sulforaphane inhibited thromboxane $A_2$-induced increases in pERK1/2 levels suggesting the mechanism including inhibition of thromboxane $A_2$-induced increases in ERK1/2 phosphorylation. This study provides evidence that sulforaphane induces vascular relaxation through inhibition of Rho-kinase or MEK in rat aortae.