• Journal of Chest Surgery
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• 제24권7호
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• pp.637-646
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• 1991

Effect of noradrenaline and endothelium on the high K+ or Ach-induced contraction were investigated in the pig myocardial coronary artery. The helical strip of isolated pig myocardial coronary artery was immersed in the Tris-buffered Tyrode`s solution equilibrated with 100% O2 at 37oC and its isometric tension was measured. High K+ and Ach-induced contraction were dose-dependent. By denuding the endothelium, dose-contraction curve of K+ was not shifted significantly to the left and upward, but that of Ach was shifted significantly to same direction 25 mM K+ - and Ach-induced contraction were relaxed by norepinephrine[NE]. NE-induced relaxation was blocked by the pretreatment of propranolol, which was known as b-adrenoceptor blocker. And, phenylephrine known as a-adrenoceptor agonist, and clonidine known as a-adrenoceptor agonist increased the 25mM K+ - induced contraction respectively. Denuding of endothelium did not show any significant effects on NE-induced relaxation and contraction increased by phenylephrine and clonidine. Tyramine increased 25mM K+ - induced contraction further. The contractile response by tyramine on the 25mM K+ - induced contraction was not blocked by the pretreatment of phentolamine, but was partially blocked by the pretreatment of atropine. From the above results, it is suggested that activation of a1-and a2-adrenoceptors induce the contraction, activation of b-adrenoceptors induce the relaxation, and NE-induced relaxation is mainly due to activation of b-adrenoceptors. Also it is suggested that denudation of endothelium did not influence NE-induced relaxation, but influence Ach-induced contraction in the pig myocardial coronary artery.

• International Journal of Oral Biology
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• 제42권1호
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• pp.1-8
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• 2017

In the present study, we investigated the role of peripheral ionotropic receptors in artemin-induced thermal hyperalgesia in the orofacial area. Male Sprague-Dawley rats weighting 230 to 280 g were used in the study. Under anesthesia, a polyethylene tube was implanted in the subcutaneous area of the vibrissa pad, which enabled drug-injection. After subcutaneous injection of artemin, changes in air-puff thresholds and head withdrawal latency time were evaluated. Subcutaneous injection of artemin (0.5 or $1{\mu}g$) produced significant thermal hyperalgesia in a dose-dependent manner. However, subcutaneous injection of artemin showed no effect on air-puff thresholds. IRTX ($4{\mu}g$), a TRPV1 receptor antagonist, D-AP5 (40 or $80{\mu}g$), an NMDA receptor antagonist, or NBQX (20 or $40{\mu}g$), an AMPA receptor antagonist, was injected subcutaneously 10 min prior to the artemin injection. Pretreatment with IRTX and D-AP5 significantly inhibited the artemin-induced thermal hyperalgesia. In contrast, pretreatment with both doses of NBQX showed no effect on artemin-induced thermal hyperalgesia. Moreover, pretreatment with H-89, a PKA inhibitor, and chelerythrine, a PKC inhibitor, decreased the artemin-induced thermal hyperalgesia. These results suggested that artemin-induced thermal hyperalgesia is mediated by the sensitized peripheral TRPV1 and NMDA receptor via activation of protein kinases.

• 대한약침학회지
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• 제16권4호
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• pp.30-35
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• 2013

Objectives: This study was designed to investigate the effects of Calculus Bovis-Fel Uris-Moschus pharmacopuncture (BUM) on the regional cerebral blood flow (rCBF) and the mean arterial blood pressure (MABP) in normal and cerebral ischemic rats and to investigate a possible pathway involved in the effects of BUM. Methods: The changes in the rCBF and the MABP following BUM into Fengfu (GV16) were determined by using a laser-Doppler flow meter and a pressure transducer, respectively. Results: BUM significantly increased the rCBF and decreased the MABP in normal rats in a dose-dependent manner. The effect on the rCBF was significantly inhibited by pretreatment with methylene blue (0.01 mg/kg, intraperitoneal), an inhibitor of guanylate cyclase, but was not affected by pretreatment with indomethacin (1 mg/kg, intraperitoneal), an inhibitor of cyclooxygenase. The BUM-induced decrease of the MABP was changed neither by methylene blue nor by indomethacin pretreatment. In the cerebral ischemic rats, the rCBF was stably increased upon cerebral reperfusion in the BUM group in contrast to the rapid and marked increase in the control group. Conclusion: This study demonstrated that BUM into Fengbu (GV16) increased the rCBF in a dose-dependent manner in the normal state; furthermore, it improved the stability of the rCBF in the ischemic state upon reperfusion. Also, the effects of BUM on the rCBF were attenuated by inhibition of guanylate cyclase, suggesting that the effects involved the guanylate cyclase pathway.

• Restorative Dentistry and Endodontics
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• 제43권2호
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• pp.14.1-14.16
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• 2018

Objectives: The aim of this systematic review was to critically analyze previously published studies of the effects of dentin surface pretreatment with deproteinizing agents on the bonding of self-etch (SE) adhesives to dentin. Additionally, a meta-analysis was conducted to quantify the effects of the above-mentioned surface pretreatment methods on the bonding of SE adhesives to dentin. Materials and Methods: An electronic search was performed using the following databases: Scopus, PubMed and ScienceDirect. The online search was performed using the following keywords: 'dentin' or 'hypochlorous acid' or 'sodium hypochlorite' and 'self-etch adhesive.' The following categories were excluded during the assessment process: non-English articles, randomized clinical trials, case reports, animal studies, and review articles. The reviewed studies were subjected to meta-analysis to quantify the effect of the application time and concentration of sodium hypochlorite (NaOCl) and hypochlorous acid (HOCl) deproteinizing agents on bonding to dentin. Results: Only 9 laboratory studies fit the inclusion criteria of this systematic review. The results of the meta-analysis revealed that the pooled average microtensile bond strength values to dentin pre-treated with deproteinizing agents (15.71 MPa) was significantly lower than those of the non-treated control group (20.94 MPa). Conclusions: In light of the currently available scientific evidence, dentin surface pretreatment with deproteinizing agents does not enhance the bonding of SE adhesives to dentin. The HOCl deproteinizing agent exhibited minimal adverse effects on bonding to dentin in comparison with NaOCl solutions.

• Restorative Dentistry and Endodontics
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• 제28권5호
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• pp.363-368
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• 2003

The purpose of this study is to evaluate the effect of additional enamel etching with phosphoric acid on the microleakage of the adhesion of self-etching primer system. Class V cavity($4mm{\times}3mm{\times}1.5mm$) preparations with all margins in enamel were prepared on buccal surface of 42 extracted human upper central incisor teeth. Prepared teeth were randomly divided into 3 groups. Group 1：no additional pretreatment with 37% phosphoric acid (NE). Group 2：additional pretreatment with 37% phosphoric acid for 10 seconds (E10s). Group 3：additional pretreatment with 37% phosphoric acid for 20 seconds (E20s). The adhesives(Clearfil SE $Bond^{\circledR}$, Kuraray, Osaka, Japan) and composite resins(Clearfil $AP-X^{\circledR}$, Osaka, Kuraray, Japan) were applied following the manufacturer's instructions. All the specimens were finished with the polishing disc(3M dental product, St Paul, MN, USA), thermocycled for 500 cycles between $5^{\circ}C$ and $55^{\circ}C$ and resected apical 3-mm root. 0.028 stainless steel wire was inserted apically into the pulp chamber of each tooth and sealed into position with sticky wax. Surrounding tooth surface was covered with a nail varnish 2 times except areas 1mm far from all the margins. After drying for one day, soaked the samples in the distilled water. Microleakage was assessed by electrochemical method(System 6514, $Electrometer^{\circledR}$), Keithley, USA) in the distilled water. In this study, the microleakage was the lowest in group 1 (NE) and the highest in group 3(E20s)(NE

• The Korean Journal of Physiology and Pharmacology
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• 제20권5호
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• pp.467-476
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• 2016

In the present study, we examined the effect of pertussis toxin (PTX) administered centrally in a variety of stress-induced blood glucose level. Mice were exposed to stress after the pretreatment of PTX (0.05 or 0.1 mg) i.c.v. or i.t. once for 6 days. Blood glucose level was measured at 0, 30, 60 and 120 min after stress stimulation. The blood glucose level was increased in all stress groups. The blood glucose level reached at maximum level after 30 min of stress stimulation and returned to a normal level after 2 h of stress stimulation in restraint stress, physical, and emotional stress groups. The blood glucose level induced by cold-water swimming stress was gradually increased up to 1 h and returned to the normal level. The intracerebroventricular (i.c.v.) or intrathecal (i.t.) pretreatment with PTX, a $G_i$ inhibitor, alone produced a hypoglycemia and almost abolished the elevation of the blood level induced by stress stimulation. The central pretreatment with PTX caused a reduction of plasma insulin level, whereas plasma corticosterone level was further up-regulated in all stress models. Our results suggest that the hyperglycemia produced by physical stress, emotional stress, restraint stress, and the cold-water swimming stress appear to be mediated by activation of centrally located PTX-sensitive G proteins. The reduction of blood glucose level by PTX appears to due to the reduction of plasma insulin level. The reduction of blood glucose level by PTX was accompanied by the reduction of plasma insulin level. Plasma corticosterone level up-regulation by PTX in stress models may be due to a blood glucose homeostatic mechanism.

• The Korean Journal of Physiology and Pharmacology
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• 제24권5호
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• pp.423-431
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• 2020

This study aimed to evaluate the effect of curcumin on brain hypoxic-ischemic (HI) damage in neonatal rats and whether the phosphoinositide 3-kinase (PI3K)/Akt/vascular endothelial growth factor (VEGF) signaling pathway is involved. Brain HI damage models were established in neonatal rats, which received the following treatments: curcumin by intraperitoneal injection before injury, insulin-like growth factor 1 (IGF-1) by subcutaneous injection after injury, and VEGF by intracerebroventricular injection after injury. This was followed by neurological evaluation, hemodynamic measurements, histopathological assessment, TUNEL assay, flow cytometry, and western blotting to assess the expression of p-PI3K, PI3K, p-Akt, Akt, and VEGF. Compared with rats that underwent sham operation, rats with brain HI damage showed remarkably increased neurological deficits, reduced right blood flow volume, elevated blood viscosity and haematocrit, and aggravated cell damage and apoptosis; these injuries were significantly improved by curcumin pretreatment. Meanwhile, brain HI damage induced the overexpression of p-PI3K, p-Akt, and VEGF, while curcumin pretreatment inhibited the expression of these proteins. In addition, IGF-1 treatment rescued the curcumin-induced down-regulated expression of p-PI3K, p-Akt, and VEGF, and VEGF overexpression counteracted the inhibitory effect of curcumin on brain HI damage. Overall, pretreatment with curcumin protected against brain HI damage by targeting VEGF via the PI3K/Akt signaling pathway in neonatal rats.

• Korean Journal of Chemical Engineering
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• 제35권12호
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• pp.2403-2412
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• 2018

The present study was aimed at evaluating the effect of variable sodium carbonate ($Na_2CO_3$) loading during wet air oxidation (WAO) pretreatment of rice straw in reducing biomass recalcitrance. The research study was intended to increase the cellulose recovery, hemicellulose solubilization, lignin removal in the solid fraction and limiting the generation of inhibitors in the liquid fraction while reducing the chemical input. The operating condition of $169^{\circ}C$, 4 bar, 18 min and 6.5 g/L $Na_2CO_3$ loading resulted in maximum cellulose recovery of 82.07% and hemicellulose solubilization and lignin removal of 85.43% and 65.42%, respectively, with a total phenolic content of 0.36 g/L in the liquid fraction. The crystallinity index increased from 47.69 to 51.25 along with enzymatic digestibility with an increase in $Na_2CO_3$ loading from 0 to 6.5 g/L as a result of removal of barriers for saccharification via effective cleavage of ether and ester bonds cross-linking the carbohydrates and lignin as indicated by FT-IR spectroscopy. A further increase in the $Na_2CO_3$ loading to 9.5 g/L did not significantly increase the sugar release. Thus, it was concluded that 6.5 g/L $Na_2CO_3$ during WAO is sufficient to increase the delignification and deacetylation, leading to significant changes in apparent cellulose crystallinity inter alia improvement in cellulose accessibility and digestibility of rice straw.

• Biomolecules & Therapeutics
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• 제29권5호
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• pp.498-505
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• 2021

Amyotrophic lateral sclerosis (ALS) is a lethal neurological disorder characterized by the deterioration of motor neurons. The aim of this study was to investigate alteration of cationic amino acid transporter (CAT-1) activity in the transport of lysine and the pretreatment effect of lysine on pro-inflammatory states in an amyotrophic lateral sclerosis cell line. The mRNA expression of cationic amino acid transporter 1 was lower in NSC-34/hSOD1^G93A (MT) than the control cell line (WT), lysine transport is mediated by CAT-1 in NSC-34 cell lines. The uptake of [³H]L-lysine was Na⁺-independent, voltage-sensitive, and strongly inhibited by inhibitors and substrates of cationic amino acid transporter 1 (system y⁺). The transport process involved two saturable processes in both cell lines. In the MT cell line, at a high-affinity site, the affinity was 9.4-fold higher and capacity 24-fold lower than that in the WT; at a low-affinity site, the capacity was 2.3-fold lower than that in the WT cell line. Donepezil and verapamil competitively inhibited [³H]L-lysine uptake in the NSC-34 cell lines. Pretreatment with pro-inflammatory cytokines decreased the uptake of [³H]L-lysine and mRNA expression levels in both cell lines; however, the addition of L-lysine restored the transport activity in the MT cell lines. L-Lysine exhibited neuroprotective effects against pro-inflammatory states in the ALS disease model cell lines. In conclusion, studying the alteration in the expression of transporters and characteristics of lysine transport in ALS can lead to the development of new therapies for neurodegenerative diseases.

• 약학회지
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• 제24권1호
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• pp.15-25
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• 1980

The investigation is concerned with the action of ginseng saponin on the contractile force in the rat heart and with the elucidation of the mechanism of the action. The effect of total ginseng saponin, ginsenoside Rb$_{1}$ of protopanaxadiol derivatives and ginsenoside Re of protopanaxatriol derivatives on the contractile force in isolated spontaneously beating normal rat heart was investigated. Total ginseng saponin was obtained from white ginseng by the method of Shibata and Namba. Ginsenoside Rb$_{1}$ and ginsenoside Re were isolated by the method of and Han, respectively. Total ginseng saponin exhibited a slight increase of the contractile force. Ginsenoside Rb$_{1}$ increased markedly the contractile force and dose dependent increase in contractile force was observed. However, ginsenoside Re did not increase the contractile force, but it prevented spontaneous decrease of the contractility of the heart. The mixture of the same dose of ginsenoside Rb$_{1}$ and Re showed a slight increase in the contractile force and its effect was similar to that obtained by total ginseng saponin. Pretreatment with propranolol abolished the positive inotropic effect of ginsenoside Rb$_{1}$ and the positive inotropic effect of ginsenoside Rb$_{1}$ was not observed in a reserpinized rat heart. Pretreatment with ginsenoside Re decreased or abolished the positive inotropic effect of epinephrine. Activities of Na+, K+ -ATPase were inhibited by ginsenoside Rb$_{1}$, total ginseng saponin and ginsenoside Re and these inhibitory effects were dose dependent. The results suggest that catecholamine release or inhibition of Na+, K+ -ATPase activities may be involved in the positive inotropic effect of gindenoside Rb$_{1}$. Ginsenoside Re counteracted the positive inotropic effect of ginsenoside Rb$_{1}$.