• Journal of Yeungnam Medical Science
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• v.19 no.2
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• pp.99-106
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• 2002

Background: Simple ventricular septal defect(VSD) is the most common congenital heart disease. Although closure of VSD is currently associated with a relatively low risk, experience with younger and smaller infants has been variably less satisfactory. We assessed the results of surgical closure of VSD in infant. Materials and Methods: Between 1996 and 2000, 45 non-restrictive VSD patients underwent patch repair and retrospective analysis was done. Patients were divided into two groups based on weight: group I infants weighed 5kg or less(n=16), and group II infants weighed more than 5kg(n=29). Both groups had similar variation in sex, VSD location, aortic cross clamp time and total bypass time. But combined diseases (ASD, PDA, MR) were more in group I. We closed VSD with patch and used simple continuous suture method in all patients. Results: There were no operative mortality, no reoperation for hemodynamically significant residual shunt and no surgically induced complete heart block. As a complication, pneumonia(group I: 2 cases, group II: 2 cases), transient seizure(group II: 2), wound infection(group I: 1, group II: 1), urinary tract infection(group I: 1) and chylopericardium(group I: 1) developed, and there was no significant difference between two groups(p>0.05). Conclusion: Early primary closure with simple continuous suture method was applicable in all patients with non-restrictive VSD without any serious complications.

• Progress in Medical Physics
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• v.15 no.4
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• pp.220-227
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• 2004

In N-type $Ca^{2＋}$ channels, the mechanism of inactivation - decline of inward current during a depolarizing voltage step- is still controversial between voltage-dependent inactivation and $Ca^{2＋}$ -dependent inactivation. In the previous paper we demonstrated that fast component of inactivation of N-type calcium channels does not involve classic $Ca^{2＋}$ -dependent mechanism and the slowly inactivating component could result from a $Ca^{2＋}$ -dependent process. However, there should be signal transduction pathway which enhances inactivation no matter what the inactivation mechanism is. We have investigated the effect of phosphorylation on calcium channels of rat sympathetic neurons. Intracellular dialysis with the phosphatase inhibitors okadaic acid markedly enhanced the inactivation. The rapidly inactivating component is N-type calcium current, which is blocked by $\omega$-conotoxin GVIA. Staurosporine, a nonselective protein kinase inhibitor, prevented the action of okadaic acid, suggesting that protein phosphorylation is involved. More specifically lavendustin C, inhibitor of CaM kinase II, prevented the action of okadaic acid, suggesting that calmodulin dependent pathway is involved in inactivation process. It is not certain to this point whether phosphorylation process is inactivation itself. Molecular biological research regarding binding site should be followed to address the question of how the divalent cation binding site is related to phoshorylation process.

• Journal of Ginseng Research
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• v.24 no.4
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• pp.168-175
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• 2000

Relatively little is known about the signaling mechanism of ginseng saponins (ginsenosides), active ingredients of ginseng, in non-neuronal cells. Here, we describe that ginsenosides utilize a common pathway of receptor-mediated signaling pathway in Xenopus oocytes: increase in intracellular $Ca^{2+}$ concentration via phospholipase C (PLC) and $Ca^{2+}$ mobilization. Ginsenosides induced a marked and robust artivation of $Ca^{2+}$-activated Cl- channels in Xenopus oocytes. The effect of ginsenosides was completely reversible, in a dose-dependent manner with EC$_{50}$ of 4.4 $\mu\textrm{g}$/mi, and specifically blocked by niflumic acid, an inhibitor of $Ca^{2+}$-activated Cl- channel. Intracellular injection of BAPIA abolished the effect of ginsenosides. Intracellular injection of GTP${\gamma}$S also abolished the effect of ginsenosides. The effect of gin senosides on $Ca^{2+}$-activated Cl- currents was greatly reduced by the intracellular injection of heparin, an IP$_3$ receptorantagonist or the pretreatment of PLC inhibitor. These results indicate that ginsenosides activate endogenous $Ca^{2+}$-activated Cl- channels via the activation of PLC and the release of $Ca^{2+}$ from the IP$_3$-sensitive intracellular store following the initial interaction with membrane component(s) from extracellular side. This signaling pathway of ginsenosides may be one of the action mechanisms for the pharmacological effects of ginseng.ts of ginseng.

• Journal of Ginseng Research
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• v.36 no.1
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• pp.55-60
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• 2012

In a previous report, we demonstrated that ginsenoside Rc, one of major ginsenosides from Panax ginseng, enhances ${\gamma}$-aminobutyric acid (GABA) $receptor_A$ ($GABA_A$)-mediated ion channel currents. However, little is known about the effects of ginsenoside metabolites on $GABA_A$ receptor channel activity. The present study investigated the effects of ginsenoside metabolites on human recombinant $GABA_A$ receptor (${\alpha}_1{\beta}_1{\gamma}_{2s}$) channel activity expressed in Xenopus oocytes using a two-electrode voltage clamp technique. M4, a metabolite of protopanaxatriol ginsenosides, more potently inhibited the GABA-induced inward peak current ($I_{GABA}$) than protopanaxadiol (PPD), a metabolite of PPD ginsenosides. The effect of M4 and PPD on $I_{GABA}$ was both concentration-dependent and reversible. The half-inhibitory concentration ($IC_{50}$) values of M4 and PPD were 17.1${\pm}$2.2 and 23.1${\pm}$8.6 ${\mu}M$, respectively. The inhibition of $I_{GABA}$ by M4 and PPD was voltage-independent and non-competitive. This study implies that the regulation of $GABA_A$ receptor channel activity by ginsenoside metabolites differs from that of ginsenosides.

• Journal of the korean academy of Pediatric Dentistry
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• v.40 no.2
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• pp.98-105
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• 2013

The purpose of this study was to investigate the mesiodistal widths at the cervical level of primary second molars in Korean children, and to compare them with commercial rubber dam clamps commonly used in pediatric dentistry. Dental casts of 115 primary and mixed dentition children were studied. Cervical mesiodistal width (C-MD) was measured at the clinical cervical level of each primary second molar from buccal and lingual sides using a digital caliper (Absolute, Mitutoyo, Kawasaki, Japan). The data were compared with mesiodistal widths of rubber dam clamps #203/204, #10/11, and #205 (Dentech, Japan). C-MDs of primary mandibular second molars were larger than those of primary maxillary second molars, and C-MDs at buccal sides were larger than those of lingual sides. All C-MDs showed statistically significant discrepancies to corresponding widths on clamps (p < 0.05). However the amount of discrepancy was mild in maxillary teeth, while up to 1 mm of discrepancy was shown in mandibular teeth. In conclusion, C-MDs measured in this study imply a relatively fair fit of #10/#11 or #203/#204 clamps on primary maxillary second molars, while suggesting our need for a better clamp with proper size for primary mandibular second molars.

• Journal of Ginseng Research
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• v.26 no.3
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• pp.132-138
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• 2002

To study the effect of Korea red ginseng (KCG) on the skin and cerebral blood flow, we evaluated the change of skin perfusion rate and cerebral perfusion rate after the intravenous, intraperitoneal, and oral administration of crude saponin (CS) and saponin-free fraction (SFF) of KRG in the rats. The change of skin perfusion rate and cerebral perfusion rate was measured laser doppler flowmetry. The intravenous injections of CS or SFF of KRG and intraperitoneal injection of SFF of KRG did not change the relative skin and cerebral blood flow in the rats. When the rats were treated by the intraperitoneal injection of CS of KRG, relative cerebral blood flow was significantly increased with a time-dependent manner, however, relative skin blood flow was not influenced by the them. Oral administration of CS of KRG slightly increased skin blood flow in the rats. Also, the change of cerebral blood flow by transient bilateral carotid arterial clamp in the CS-treated rats was significantly decreased, compared with control groups. From the above results, it was suggested that Korea red ginseng have a increasing property of cerebral blood flow in the rats.

• Proceedings of the Korean Biophysical Society Conference
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• 1999.06a
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• pp.61-62
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• 1999

;The mechanisms inducing hypertension are actively investigated and are still challenging topics. Basically hypertension must be caused by the disorder of $Ca^{2+}$ metabolism in vascular smooth muscle, such as the increase of $Ca^{2+}$ influx, the decrease of ci+ efflux, or the change of sensitivity of contractile protein etc. The one of cause of the increase of ci+ influx may be the change of ci+ channel activity. Even though the relationships of ci+ channel activity and hypertension were studied using various hypertension models, still it is not clear how much change of $Ca^{2+}$ channel activity in diabetes mellitus (DM) induced hypertension is occurred. We induced DM hypertension in SD rat and compared the $Ca^{2+}$ channel activity with age-matched normotensive SD rat. For inducing DM hypertension, left kidney was removed with 200 gm rat and, after 1 month, 60 mg/kg of streptozotocin was injected into peritoneal space to induce diabetes mellitus. Usually after 4-6 weeks, hypertension was fully induced. For isolating vascular smooth muscle cells (VSMC), we used mesenteric arteriole (3rd - 4th branch of mesenteric artery) of which diameter is below 150 urn. VSMCs were isolated enzymatically. $Ca^{2+}$ current was measured using whole cell patch clamp technique. All experiments were performed at $37^{\circ}C$. The cell membrane area of VSMC of DM hypertensive rat is larger than that of control VSMC($36.6{\pm}3.64{\;}pF{\;}vs{\;}22.4{\pm}1.29{\;}pF, {\;}mean{\pm}S.E.$) When we compared the current amplitude, the $Ca^{2+}$ current amplitude in VSMC of DM hypertensive rat is much larger than that in VSMC of normotensive age-matched rat. After $Ca^{2+}$ current amplitude was normalized by cell membrane area, the current amplitude in DM hypertension is increased to $249.1{\pm}15.9{\;}%{\;}(mean{\pm}S.E.M)$, which means the ;absolute current amplitude is about 4 times larger in DM hypertension. When we compared the steady state activation and inactivation. there were no noticeable differences. From these results. one of cause of the DM hypertension is due to the increase of $Ca^{2+}$ current amplitude. But it need further study why the $Ca^{2+}$ current is so large in VSMC of DM hypertension and how much $Ca^{2+}$ influx through $Ca^{2+}$ channel contribute to the increase of intracellular $Ca^{2+}$ and eventually contribute to development of hypertension.ypertension.

• Tuberculosis and Respiratory Diseases
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• v.54 no.5
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• pp.532-541
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• 2003

Background : Phospholipase $A_2$ ($PLA_2$) has been known to be involved in the pathogenesis of acute lung injury (ALI) including ARDS. Since doxycycline has the property of inhibiting secretory group II $PLA_2$, the therapeutic effect of doxycycline hyclate was investigated for gut ischemia/reperfusion (I/R)-induced ALI in Sprague-Dawley rats. Methods : ALI was induced in Sprague-Dawley rats by clamping of the superior mesenteric artery for 60 min, followed by 120 min of reperfusion. To confirm the pathogenetic mechanisms of this ALI associated with neutrophilic oxidative stress, we measured bronchoalveolar lavage (BAL) protein content and lung MPO, and performed cyto-chemical electron microscopy for detection of free radicals, assay of $PLA_2$ activity and cytochrome-c reduction assay. Results : In gut I/R-induced ALI rats, protein leakage, pulmonary neutrophil accumulation, free radical production and lung $PLA_2$ activity were all increased. These effects were reversed by doxycycline hyclate. Conclusion : Doxycycline appears to be effective in ameliorating the gut I/R-induced ALI by inhibiting $PLA_2$, thereby decreasing the production of free radicals from neutrophils.

• Journal of Conservation Science
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• v.28 no.4
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• pp.353-366
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• 2012

This study was interpreted the making techniques of the Four Guardian Statues in Wanju Songkwangsa Temple, and retained basic data necessary for conservation treatment and restoration of the same material by estimating the soil source. The molding clay used in the Statues showed a variety of material characteristics according to different layers. The first and mid layers estimated as the original molding clay are composed of the same kind of soil. The soil of the finish layer was also confirmed to be genetically similar to that of the first and mid layers, despite little discrepancy. The former restoration layer was inconsistent in material characteristics with the original molding clay in every result of analysis. As a result of gamma radiography, making techniques of the Statues were able to identify the figure of the frame connecting the woods of main pillar frame to sub-frame and steel wire with ㄷ-clamp, nails and straw ropes, and the molding clay constructed upon the frame. Meanwhile, provenance interpretation confirmed that the soil of the estimated provenance area is of the same origin as the soil of the finish layer, and therefore is an appropriate material for conservation treatment. This result will contribute to the research on making techniques of the molding clay Statues.

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.1
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• pp.33-40
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• 2000

This study was designed to clarify the mechanism of the inhibitory action of a nitric oxide (NO) donor, 3-morpholino-sydnonimine (SIN-1), on contraction, cytosolic $Ca^{2+}$ level $([Ca^{2+}]_i)$ and ionic currents in guinea-pig ileum. SIN-1 $(0.01{\sim}100\;{\mu}M)$ inhibited 25 mM KCl- or histamine $(10\;{\mu}M)-induced$ contraction in a concentration-dependent manner. SIN-1 reduced both the 25 mM KCl- and the histamine-stimulated increases in muscle tension in parallel with decreased $[Ca^{2+}]_i.$ Using the patch clamp technique with a holding potential of -60 mV, SIN-1 $(10\;{\mu}M)$ decreased peak Ba currents $(I_{Ba})$ by $30.9{\pm}5.4%$ (n=6) when voltage was stepped from -60 mV to +10 mV and this effect was blocked by ODQ $(1\;{\mu}M),$ a soluble guanylyl cyclase inhibitor. Cu/Zn SOD (100 U/ml), the free radical scavenger, had little effect on basal $I_{Ba},$ and SIN-1 $(10\;{\mu}M)$ inhibited peak $I_{Ba}$ by $32.4{\pm}5.8%$ (n=5) in the presence of Cu/Zn SOD. In a cell clamped at a holding-potential of -40 mV, application of $10\;{\mu}M$ histamine induced an inward current. The histamine-induced inward current was markedly and reversibly inhibited by $10\;{\mu}M$ SIN-1, and this effect was abolished by ODQ $(1\;{\mu}M).$ In addition, SIN-1 markedly increased the depolarization-activated outward $K^+$ currents in the all potential ranges. We concluded that SIN-1 inhibits smooth muscle contraction mainly by decreasing $[Ca^{2+}]_i$ resulted from the inhibition of L-type $Ca^{2+}$ channels and the inhibition of nonselective cation currents and/or by the activation of $K^+$ currents via a cGMP-dependent pathway.