• Journal of International Academy of Physical Therapy Research
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• v.11 no.4
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• pp.2237-2243
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• 2020

Background: The myofascial release technique is known to be an effective technique for increasing posterior fascia flexibility in short hamstring syndrome (SHS) subjects. But therapeutic mechanism of myofascial relaxation remains unclear. Recently, the theory of autonomic nervous system domination has been raised, however, a proper study to test the theory has not been conducted. Objectives: To investigate whether the application of the myofascial release technique can induce changes in the autonomic nervous system and affect the secretion of stress hormones and myofascial relaxation. Design: Quasi-experimental study. Methods: Twenty-four subjects with SHS were randomly divided into two groups. In the experimental group, the suboccipital muscle inhibition (SMI) technique was applied to the subjects for 4 min in supine position, and in the control group, the subjects were lying in the supine position only. A forward flexion distance (FFD) was conducted, blood pressure, heart rate, and cortisol levels were measured before and after the intervention and 30 min after intervention to determine myofascial relaxation and stress hormone levels. The evaluation was conducted separately in blind by an evaluator. Results: A FFD decreased in the experimental group, no change in cortisol was observed. On the contrary, a decrease in cortisol appeared in the control group after 30 minutes. Conclusion: The myofascial release technique is an effective treatment to increase the range of motion through posterior superior myofascial chain, but there is no evidence that myofascial release technique can control the autonomic nervous system.

• The Korean Journal of Pharmacology
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• v.30 no.3
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• pp.263-272
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• 1994

Since it was been reported that the depolarization-induced ACh release is inhibited by activation of presynaptic $A_1-adenosine$ heteroreceptor in hippocampus, a large body of experimental data on the post-receptor mechanism of this process has been accumulated. But, the post-receptor mechanism of presynaptic $A_1-adenosine$ receptor on the ACh release has not been clearly elucidated yet. Therefore, it was attempted to clarify the post-receptor mechanisms of the $A_1-adenosine$ receptor-mediated control of ACh release in this study. Slices from rat hippocampus were equilibrated with $^3H-choline$ and the release of the labelled products was evoked by electrical stimulation (3 Hz, 5 $VCm^{-1}$, 2ms, rectangular pulses), and the influence of various agents on the evoked tritium-outflow was investigated. Adenosine, in concentrations ranging from $0.3{\sim}300\;{\mu}M$, decreased the ACh release in a dose-dependent manner, without affecting the basal rate of release. The adenosine effects were significantly inhibited by $DPCPX\;(2\;{\mu}M)$, a selective $A_1-receptor$ antagonist. The responses to N-ethylmaleimide $(10&30{\mu}M)$, a SH-alkylating agent of G-protein, were characterized by increments of the evoked ACh-release and the basal release, and the adenosine effects were completely abolished by NEM pretreatment. PDB $(1{\sim}10\;{\mu}M)$, a specific protein kinase C (PKC) activator, increased, whereas PMB $(0.03{\sim}1\;mg)$, a PKC inhibitor, decreased the evoked ACh-release, and the adenosine effects were not affected by these agents. Nifedipine $(1\;{\mu}M)$, a $Ca^{2+}\;-channel$ blocker of dihydropyridine analogue, significantly inhibited the adenosine effect, but glibenclamide, a $K^+-channel$ blocker, did not. Finally, 8-bromo cyclic AMP $(100\;&\;300{\mu}M)$, a membrane-permeable analogue of cAMP, did not alter the ACh release, but adenosine effects were inhibited by pretreatment with large dose of 8-br-cAMP $(300\;{\mu}M)$. These results indicate that the decrement of the evoked ACh-release by $A_1-adenosine$ receptor is mediated by the G-protein, and nifedipine-sensitive $Ca^{2+}-channel$ and adenylate cyclase system are coupled partly to this effect, and that protein kinase C and glibenclamide-sensitive $K{^+}-channel$ are not involved in this process.

• Journal of Industrial Technology
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• v.26 no.A
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• pp.47-54
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• 2006

To improve passenger safety, seat belt systems with pre-tensioner that tightens seat belt webbing using explosive just before collision are widely used these days. Even though seatbelt must not unlatched without passengers' operation. explosive power of pre-tensioner can cause unlocking of a buckle. To prevent the unlocking, an anti-g mass that blocks displacement of the release button has been attached to the buckle. In this study, the dynamics and statics of locking mechanism associated with operation of anti-g buckle has been theoretically investigated, and important design variables that affect the operation of anti-g buckle have been identified. Through the total seat belt system's dynamic simulation using force and displacement inputs obtained from seat belt sled test, design of the proposed anti-g buckle has been validated.

• The Korean Journal of Physiology
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• v.10 no.1
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• pp.55-59
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• 1976

Most investigators have come to stress two different concepts of mechanism controlling renin release; intrarenal baroreceptor theory and the macula densa theory(Vander 1967, Thurau and Masson 1974). In the macula densa theory, the specific macula densa parameter, most commonly suggested as a possible signal, is either the osmolality or the concentration of sodium in the tubular fluid (Thurau 1964, Vander and Miller 1964, Reeves and Sommers 1965). It has been shown that sodium plays an important role in the release of renin either in vivo (Thurau 1964, Vander and Miller 1964, Thurau et al 1972) or in vitro experiments(Oelkers et al 1970, Hammerson et al 1971, Michelakis 1971). On the other hand the osmolality appears to have no effect on the release of renin in vivo (Vander 1967, Thurau and Masson 1974). However, there has been little attempt to study the effect of osmolality on in vitro renin release. We therefore undertook the present investigation to elucidate the effect of osmolality on renin release and to further test the sodium influence upon the release of renin from isolated kidney slice preparations. Isolated renal cortical slices were washed with normal Krebs-Hensenleit bicarbonate buffer solution and incubated for 30 minutes in a medium containing an appropriate concentration of sodium and osmolality. The renin released into the medium was measured by the method of radioimmunoassay(Haber et al 1969). The results obtained are as follows; 1. The release of renin from renal cortical slices was progressively inhibited as the sodium concentration in the medium increased. 2. No significant alteration in renin release was observed when osmolality of the medium was changed. These results suggest that the release of renin from the renal cortical slices is directly affected by the changes in sodium concentration in the medium, but is not influenced by the alterations in osmolality.

• The Korean Journal of Pharmacology
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• v.31 no.2
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• pp.145-152
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• 1995

The effects and interactions of $4{\beta}-phorbol$ 12,13-dibutyrate(PDB) and polymyxin B(PMB) with adenosine on the electrically-evoked norepinephrine (NE) release were studied in the rat hippocampus. Slices from the rat hippocampus were equilibrated with $^3H-noradrenaline$ and the release of the labelled product, $^3H-NE$, which evoked by electrical stimulation$(3\;Hz,\;2\;ms,\;5\;VCm^{-1},\;rectangular\;pulses)$ was measured. PDB$(0.3{\sim}10\;{\mu}M)$, a selective protein kinase C(PKC) activator, increased the evoked NE release in a dose related fashion while increasing the basal rate of release. And the effects of $1\;{\mu}M$ PDB were significantly inhibited by $0.3\;{\mu}M$ tetrodotoxin(TTX) pretreatment or $Ca^{++}-free$ medium. $PMB(0.03{\sim}1\;mg)$, a specific PKC inhibitor, decreased the NE release in a dose dependent manner while increasing the basal rate of release. Adenosine $(1{\sim}10\;{\mu}M)$ decreased the NE release without changing the basal rate of release, and this effect was significantly inhibited by 8-cyclopentyl-1,3-dipropylxanthine$(2\;{\mu}M)$, a selective $A_1-receptor$ antagonist, treatment. Also, adenosine effects were significantly inhibited by PDB-and PMB-pretreatment. These results suggest that the PKC plays a role in the NE release in the rat hippocampus and might be participated in a post-receptor mechanism of the $A_1-adenosine$ receptor.

• Biomolecules & Therapeutics
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• v.29 no.6
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• pp.630-636
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• 2021

Eupafolin, a constituent of the aerial parts of Phyla nodiflora, has neuroprotective property. Because reducing the synaptic release of glutamate is crucial to achieving pharmacotherapeutic effects of neuroprotectants, we investigated the effect of eupafolin on glutamate release in rat cerebrocortical synaptosomes and explored the possible mechanism. We discovered that eupafolin depressed 4-aminopyridine (4-AP)-induced glutamate release, and this phenomenon was prevented in the absence of extracellular calcium. Eupafolin inhibition of glutamate release from synaptic vesicles was confirmed through measurement of the release of the fluorescent dye FM 1-43. Eupafolin decreased 4-AP-induced [Ca²⁺]_i elevation and had no effect on synaptosomal membrane potential. The inhibition of P/Q-type Ca²⁺ channels reduced the decrease in glutamate release that was caused by eupafolin, and docking data revealed that eupafolin interacted with P/Q-type Ca²⁺ channels. Additionally, the inhibition of calcium/calmodulin-dependent protein kinase II (CaMKII) prevented the effect of eupafolin on evoked glutamate release. Eupafolin also reduced the 4-AP-induced activation of CaMK II and the subsequent phosphorylation of synapsin I, which is the main presynaptic target of CaMKII. Therefore, eupafolin suppresses P/Q-type Ca²⁺ channels and thereby inhibits CaMKII/synapsin I pathways and the release of glutamate from rat cerebrocortical synaptosomes.

• 한국연소학회:학술대회논문집
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• 2012.11a
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• pp.309-310
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• 2012

Modeling of biodiesel combustion on compression ignition engine was conducted by using the KIVA3v-Release 2 code coupled with Chemkin chemistry solver2. In order to calculate the chemical kinetics of combustion of biodiesel, a reduced mechanism of methyl decanoate and methyl 9-decanoate was used. It is composed of 123 species and 394 reactions. Also, the experiments were performed on a single-cylinder engine. The simulation results agreed well with experiments results. And soot concentrations of biodiesel were lower than those of diesel.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.87.2-88
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• 2003

The present study was conducted to investigate the effects of pinacidil, a potassium channel opener, on arterial blood pressure, catecholamine release and vascular contractile responses in the normotensve rats and to establish the mechanism of action. Phenylephrine (an adrenergi $_1$-receptor agonist) and high potassium (a membrane- depolarizing agent) caused greatly contractile responses in the isolated aortic strips, respectively. These phenylephrine (10$\^$-5/ M)-induced contractile responses were dose-dependently depressed in the presence of pinacidil (25 ∼ 100 ${\mu}$M). (omitted)

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.319.2-319.2
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• 2002

Chitin is a major component of the shells of crustacea such as crab. shrimp and crawfish. Renal dipeptidase (RDPase. EC 3.4.13.19), an ectoenzyme of renal proximal tubules. is covalently bound to outer leaflet of lipid bilayer via glycosylphosphatidylinositol (GPI)-anchor. The biological role of RDPase was suggested as the hydrolysis of dipeptide into free-amino acids before renal reabsorption. The underlying biochemical mechanism of decreased RDPase release was suggested as nitric oxide (NO) production. (omitted)

• Archives of Pharmacal Research
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• v.24 no.2
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• pp.126-135
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• 2001

Quinacrine (QU), a phospholipase-A2 (PLA-2) inhibitor has been used clinically as a chemotherapeutic adjuvant. To understand the mechanisms leading to its chemotherapeutic effect, we have investigated QU-induced apoptotic signaling pathways in human cervical squamous carcinoma HeLa cells. In this study, we found that QU induced cytochrome c-dependent apoptotic signaling. The release of pro-apoptotic cytochrome c was QU concentration- and time-dependent, and preceded activation of caspase-9 and -3. Flow cytometric FACScan analysis using fluorescence intensities of $DiOC_6$/ demonstrated that QU-induced cytochrome c release was independent of mitochondrial permeability transition (MPT), since the concentrations of QU that induced cytochrome c release did not alter mitochondrial membrane potential (${\blacktriangle}{\Psi}_m$). Moreover, kinetic analysis of caspase activities showed that cytochrome c release led to the activation of caspase-9 and downstream death effector caspase-3, Caspase-3 inhibitor (Ac-DEVD-CHO) partially blocked QU-induced apoptosis, suggesting the importance of caspase-3 in this apoptotic signaling mechanism. Supplementation with arachidonic acid (AA) sustained caspase-3 activation induced by QU. Using inhibitors against cellular arachidonate metabolism of lipooxygenase (Nordihydroxyguaiaretic Acid, NDGA) and cyclooxygenase (5,8,11,14-Eicosatetraynoic Acid, ETYA) demonstrated that QU-induced apoptotic signaling may be dependent on its role as a PLA-2 inhibitor. Interestingly, NDCA attenuated QU-induced cytochrome c release, caspase activity as well as apoptotic cell death. The blockade of cytochrome c release by NDCA was much more effective than that attained with cyclosporin A (CsA), a MPT inhibitor. ETYA was not effective in blocking cytochrome c release, except under very high concentrations. Caspase inhibitor z-VAD blocked the release of cytochrome c suggesting that this signaling event is caspase dependent, and caspase-8 activation may be upstream of the mitochondrial events. In summary, we report that QU induced cytochrome c-dependent apoptotic signaling cascade, which may be dependent on its role as a PLA-2 inhibitor. This apoptotic mechanism induced by QU may contribute to its known chemotherapeutic effects.