Background: Statins can regulate the production of pro-inflammatory cytokines and inhibit MMP production or activation in a variety of types of cells. This study evaluated whether statins would inhibit MMP release from human lung fibroblasts, which play a major role in remodeling processes. Methods: This study, using an in-vitro model (three-dimensional collagen gel contraction system), evaluated the effect of cytokines (tumor necrosis factor-${\alpha}$, TNF-a and interleukin-$1{\beta}$, IL-1b) on the MMP release and MMP activation from human lung fibroblasts. Collagen degradation induced by cytokines and neutrophil elastase (NE) was evaluated by quantifying hydroxyproline. Results: In three-dimensional collagen gel cultures (3D cultures) where cytokines (TNF-a and IL-1b) can induce the production of MMPs by fibroblasts, it was found that simvastatin inhibited MMP release. In 3D cultures, cytokines together with NE induced collagen degradation and can lead to activation of the MMP, which was inhibited by simvastatin. Conclusion: Simvastatin may play a role in regulating human lung fibroblast functions in repair and remodeling processes by inhibiting MMP release and the conversion from the latent to the active form of MMP.
The Transactions of the Korean Institute of Electrical Engineers D
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v.49
no.11
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pp.599-609
/
2000
The new design methodology of a hybrid fuzzy controller by means of the genetic algorithms is presented. First, a hybrid fuzzy controller(HFC) related to the optimal estimation of control parameters is proposed. The control input for the system in the HFC combined PID controller with fuzzy controller is a convex combination of the FLC's output and PID's output by a fuzzy variable, namely, membership function of weighting coefficient. Second, an auto-tuning algorithms utilizing the simplified reasoning method and genetic algorithms is presented to automatically improve the performance of hybrid fuzzy controller. Especially, in order to auto-tune scaling factors and PID parameters of HFC using GA, three kinds of estimation modes such as basic, contraction, and expansion mode are effectively utilized. The proposed HFC is evaluated and discussed to show applicability and superiority with the and of three representative processes.
The present study was undertaken to investigate the effects of age on angiotensin II (AII) response and antagonistic activity of losartan using aortic rings and liver homogenates from rats ranging in age from 0.7 to 20 months. Whether the endothelium was present or not, the maximum contractile response to AII decreased with age. Removal of the endothelium enhanced AII-induced maximum contraction and these endothelial effects seemed to be due to endothelium-derived relaxing factor (EDRF) in all ages. Equilibrium binding studies demonstrated an age-related decrease in maximum binding $(B_{max})$ with little change in binding affinity $(K_d)$. In rat aorta, the extent of losartan-induced parallel shifts $(K_B)$ in AII concentration-response curves was not significantly different between ages. In addition, $IC_{50}$ value of losartan in competition binding was not changed with age in rat liver homogenates. These results suggest that the potency of losartan is not altered with age in rat aorta and liver, although AII-induced contractile response and the maximum AII binding decreased significantly with age.
Kim, Won-Ho;Kim, Jong-Man;Park, Hyung-Ki;Park, Eun-Young
Physical Therapy Korea
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v.14
no.3
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pp.9-15
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2007
The purpose of this study was to investigate electromyographic activities of the flexor digitorum superficialis (FDS) and the flexor carpi ulnaris (FCU) by the shape of the ultrasound head. Twelve healthy subjects participated and performed ultrasound therapy with a round head and a long handled head during each 5-minute application. Electromyographic activities of the FDS and FCU were recorded by surface electrodes and normalized by maximal voluntary isometric contraction (MVIC) values. There was no difference in the muscular fatigue of FDS and FCU as determined by the shape of the ultrasound head (p>.05). Without the shape of head, the mean power frequency decreased with the time. There also was no difference in %MVIC of the FDS and FCU as determined by the shape of the ultrasound head (p>.05), but the force exerted exceeded 20%MVIC. There was however a significant difference in the amount of cumulative workload of the FDS and FCU as determined by the shape of ultrasound head (p<.05). The workload was however not affected by the shape of the ultrasound head. Constant static grasp of ultrasound transducer head during ultrasound therapy is considered a high risk factor of work-related musculoskeletal disease.
A bioassay technique and organ bath study were performed to analyze the effects of extracellular $Ca^{2+}$ and $Ca^{2+}$-antagonists on endothelium-derived relaxing factor[s][EDRF] released from the endothelial cells of rabbit aorta. Transverse strips with intact endothelium or damaged endothelium were used for the mechanical contraction experiment using organ bath. Long segment including thoracic and abdominal aorta with endothelium [EDRF donor aorta] was perfused with Tyrode solution which was aerated with 95% $O_2-5%$$CO_2$ mixed gas and kept at 35oC. The perfusate was bioassayed with a transverse strip of thoracic aorta with damaged endothelium. The test strip was contracted with nor-epinephrine and acetylcholine was used to stimulate the release of EDRF from endothelial cells. The results obtained were as follows; 1] The endothelium-dependent relaxation[EDR] induced by acetylcholine was biphasic; an initial rapid relaxation followed by a slow relaxation. 2] EDR induced by acetylcholine was reduced gradually with the decrease in the concentration of extracellular $Ca^{2+}$. The effect of extracellular $Ca^{2+}$ on EDR was more prominent in the late slow relaxation phase. 3] EDR to acetylcholine was not altered by acute exposure to organic $Ca^{2+}$-antagonists. Pretreatment with verapamil to the EDRF donor aortic segment did not alter the magnitude of EDR. 4] Among the inorganic $Ca^{2+}$-antagonists $Mn^{2+}$ and $Cd^{2+}$ did not inhibit EDR, whereas $Co^{2+}$ and $La^{3+}$ inhibited EDR. 5] The inhibitory response of $Co^{2+}$ to EDR developed when infused directly on the test strip. That of $La^{3+}$, however, was evoked when added to solution perfusing the donor aortic segment. The above results suggest that $Ca^{2+}$-antagonists do not affect EDR and the inhibitory effect of $Ca^{2+}$ results from influencing the action of EDRF on vascular smooth muscle, whereas that of $La^{3+}$ results from its action on the release of EDRF from endothelial cells.
Journal of Physiology & Pathology in Korean Medicine
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v.30
no.2
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pp.101-108
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2016
This study is conducted to investigate vasorelaxant effect of Corni Fructus(CF) on rabbit carotid artery. To determine vasorelaxant effect of CF on rabbit carotid artery, arterial sections with intact or removed endothelium were used in this organ bath study. After being contracted by phenylephrine(PE), arterial sections were treated with CF extract in a dose-dependent manner. To identity its mechanism, the contracted arterial sections by PE were pretreated with indomethacin(IM), tetraethylammonium chloride(TEA), Nω-nitro-L-arginine(L-NNA) or methylene blue(MB) and 1.0 ㎎/㎖ CF extract. We also studied to confirm the effect on influx of extracellular calcium chloride(Ca2+) of the CF extract in rabbit carotid artery. To measure the cytotoxicity of the CF extract, cell viability of human umbilical vein endothelial cell(HUVEC) was measured by MTT assay. Generation of nitric oxide(NO) was also measured by Griess reagent. The arterial sections with intact endothelium were relaxed significantly by CF extract, but this effect was inhibited in the arterial sections with damaged endothelium. The vasorelaxant effect was inhibited significantly when arterial sections were pretreated with IM, TEA, L-NNA, MB. In Ca2+-free krebs solution, increasing of arterial contraction by Ca2+ was also inhibited by CF significantly. The treatment of CF extract increased NO concentration in HUVEC. This study suggested that the vasorelaxant effect of CF extract would be related with endothelium derived relaxing factor(EDRF) such as NO, prostacyclin(PGI2), endothelium derived hyperpolarization factor(EDHF).
Kim, Ye-Mi;Park, Jeong-Won;Lee, Chan-Young;Song, Yoon-Jung;Seo, Deok-Kyu;Roh, Byoung-Duck
Restorative Dentistry and Endodontics
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v.33
no.5
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pp.472-480
/
2008
This study was conducted to evaluate the influence of the C-factor on the bond strength of a 6th generation self-etching system by measuring the microtensile bond strength of four types of restorations classified by different C-factors with an identical depth of dentin. Eighty human molars were divided into four experimental groups, each of which had a C-factor of 0.25, 2, 3 or 4. Each group was then further divided into four subgroups based on the adhesive and composite resin used. The adhesives used for this study were AQ Bond Plus (Sun Medical, Japan) and XenoIII (DENTSPLY, Germany). And composite resins used were fantasists (Sun Medical, Japan) and Ceram-X mono (DENTSPLY, Germany). The results were then analyzed using one-way ANOVA, a Tukey's test, and a Pearson's correlation test and were as follows. 1. There was no significant difference among C-factor groups with the exception of groups of Xeno III and Ceram-X mono (p<0.05). 2. There was no significant difference between any of the adhesives and composite resins in groups with C-factor 0.25, 2 and 4. 3. There was no correlation between the change in C-factor and microtensile bond strength in the Fantasista groups. It was concluded that the C-factor of cavities does not have a significant effect on the microtensile bond strength of the restorations when cavities of the same depth of dentin are restored using composite resin in conjunction with the 6th generation self-etching system.
Kim, Chi-Dae;Rhim, Byung-Yong;Hong, Sung-Chul;Hong, Ki-Whan
The Korean Journal of Pharmacology
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v.27
no.2
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pp.125-133
/
1991
In the isolated rabbit mesenteric artery denuded of endothelium, we characterized the identity of the A23187-induced endothelium-dependent relaxing factor (EDRF) released from the endothelium of rabbit aorta, which is distinct from that of acetylcholine-induced relaxing factor. In the normal physiological salt solution (PSS), the dose-response curves to A23187 and acetylcholine were overlapped together. Their effects were also inhibited by methylene blue. Upon application of hypoxanthine and xanthine oxidase into the bath, the phenylephrine-induced precontraction was transiently increased followed by the sustained relaxation. During the burst of hypoxanthine-xanthine oxidase reaction, the $Ca^{++}$ ionophore, A23187 but not acetylcholine was able to cause an immediate relaxation. However, A23187-induced relaxation was not manifested when precontracted by 50 mM $K^+-PSS$. Nevertheless, in the presence of superoxide dismutase, A23187 could produce an immediate relaxation without accompanying the transient contraction as acetylcholine did during the hypoxanthine-xanthine oxidase reaction. On the other hand, acetylcholine-induced relaxation was more sensitively inhibited by phorbol 12-myristate 13-acetate (PMA) than A23187-induced relaxation. Endothelium-independent relaxation to sodium nitroprusside was not affected by PMA. Based on these results it is suggested that both A23187 and acetylcholine cause the methylene blue-inhibitable endothelium-dependent relaxation, and in addition, A23187 may release a stable EDRF which is resistant to superoxide anion and PMA.
Cleft lip and/or palate is the congenital orofacial malformation most commonly occurred in humans, The disease is multifactorial and is probably caused by genetic and/or environmental factors, So, there are many problems in research concerning etiology and in treatment of the disease, Even the most practiced and sophisticated methods of surgical repair are necessarily followed by scar contraction and fibrosis, which result in skeletal defects, dental abnormalities, cosmetic disfigurement, and speech impairment, As a result, Fetal surgery can be considered but practiced rarely when the deformity is not fatal to life, And treatment of cleft palate is performed in the form of medicine projection into uterus in animal experiments, Many studies show that growth factor and its receptor emerge from the developing palate; and the epidermal growth factor receptors have a important role in craniofacial development and in palatal fusion, The palatal morphogenesis of the avine is different from the mammal's; it takes the form of physiologic cleft palate, Recently, cleft palate fusion experiment was performed when the avine were in the period of palate formation through the exogenous TGF-β3 addition, and it showed that the exogenous TGF-β3 makes fusion of divided palate through certain process when cleft palate is occurred in palatal formation, In this study, I had the conformation of the fusion of cleft palate through the addition of TGF-β in case of chicken embryo, and observed the effect of TGF-β in EGF receptor distribution, And the following is the results of this study, 1. In case of the TGF-βl and β3 addition group, there was the decrease of EGFR(Epidermal Growth Factor Receptor) immunoreactivity in mesenchymal cells beneath the medial edge epithelium and also in epithelial mesenchymal interface which is between medial edge epithelium and nasal septum in 72 hours, 2, The immunoreactivity of the control group resembles that of normal chicken embryo palate in development, 3. In the view through fluorescence confocal microscopy, there was confluence in TGF-β3 addition group, This shows that the confluence induced by exogenous TGF-β3 is related to EGFR expression in palate of chicken embryo, which is a physiologic cleft palate model.
Non-neuronal high affinity binding sites for benzodiazepines have been found in many peripheral tissues including cardiac muscle and vascular smooth muscle, and have been designated as 'peripheral benzodiazepine receptor'. Benzodiazepines have been shown to induce relaxation of the ileal, vesical, and uterine smooth muscles. However, it is still unclear about possible involvement of peripheral benzodiazepine receptor on the contractility of trachealis muscle. This study was performed to investigate the role of the peripheral benzodiazepine receptor on the contractility of canine trachealis muscle. Canine trachealis muscle strips of 15 mm long were suspended in an isolated organ bath containing 1 ml of physiological salt solution maintained at $37^{\circ}C$, and aerated with $95%\;O_2/5%\;CO_2$. Isometric myography was performed, and the results of the experiments were as follows: Ro5-4684, FGIN-1-27 and clonazepam reduced a basal tone of isolated canine trachealis muscle strip concentration dependently, relaxant actions of RoS-4684 and FGIN-1-27 were antagonized by PK11195, a peripheral benzodiazepine receptor antagonist. Flumazenil, a central type antagonist, did not antagonize the relaxant action of Peripheral type agonists. Saturation binding assay of [3H]Ro5-4864 showed a high affinity$(Kd=5.33{\pm}1.27nM,\;Bmax=\;867.3{\pm}147.2\;fmol/mg\;protein)$ binding site on the canine trachealis muscle. Ro 5-4684 suppressed the bethanechol-, 5-hydroxyoyptamine- and histamine- induced contractions. Platelet activating factor (PAF) exerted strong and prolonged contraction in trachealis muscle strip. Strong tonic contraction by PAE was attenuated by Ro 5-4684, but not by WEB 2086, a PAF antagonist. Based on these results, it is concluded that the peripheral benzodiazepine receptor mediates the inhibitory regulation of contractilty of canine trachealis muscle.
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