• Advances in pediatric surgery
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• v.8 no.1
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• pp.23-27
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• 2002

Infantile hypertrophic pyloric stenosis (IHPS) a common childhood disorders characterized by nonbilious projectile vomiting, an olive shaped mass in the right upper quadrant of the abdomen and visible gastric peristaltic wave in the upper abdomen. Its etiology and pathogenesis are not clear but abnormal nerve distribution of the pylorus has been $postulated^{2-6}$. We performed immunocytochemical staning to the pyloric muscle from 10 IHPS and 3 controls patients, utilizing specific monoclonal antibody to NCAM(neural cell adhesion molecule). In IHPS patients, the number of NCAM protein immunoreactive nerve fibers were less than that in normal subjects. Auerbach myenteric plexuse was well developed and interbundle nerve plexuse was present but nerve fibers supplying individual muscle cells in smooth muscle bundles were poorly developed. These results indicate reduction of innervation in smooth muscles in IHPS patients that possibly contributes to the pathogenesis of IHPS.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.33 no.4
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• pp.340-349
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• 2007

Free flap transplantation with microvascular anastomosis has been successfully performed by development of surgical technique, materials and postoperative monitoring equipments of flap. But success rate of microvascular anastomosis is influenced by various factors, and failure rate is about 5-10%. The most influential factor for success rate is surgical technique and other factors that influence failure of microvascular anastomosis are ischemic time of free flap, thrombus formation of anastomosis region and vascular spasm. In this study, vascular patency and thrombus formation in experimental micro-venous anastomosis, and endothelial repair were observed with histologic analysis, scanning electron microscopy, transmission electron microscopic examination. The results were obtained as follows: 1. In vascular patency test in 30 minute and 7 days after micro-venous anastomosis with heparin irrigation, all of 12 anastomosis site were good vascular patency. 2. In thrombus formation in 2 weeks group(Experimental I), 2 site of 6 cases were observed thrombus, and in 4 weeks group(Experimental II), 1 site of 6 cases were observed thrombus. 3. In histologic examination, normal vein(Control Group) showed continued internal elastic lamina, well formed thick smooth muscle layer and connective tissue. The group of 2 weeks after microvenous anastomosis(Experimental I) showd locally recovered internal lamina, discontinued internal lamina, disorganized smooth muscle cells and granulation tissue around suture silk. In the group of 4 weeks after micro-venous anastomosis(Experimental II), anastomosis site showed almostly continued internal lamina, disorganized smooth muscle cells and cicartrized tissue around suture silk. 4. In scanning electron microscope examination in 2 weeks(Experimental I) after micro-venous anastomosis, mesh fibrin formation showed near to endothelial cells, and in 4 weeks after micro-venous anastomosis(EXperimental II), numerous blood cells and fibrin mesh formation was seen associated with irregular endothelial cell arrangement. 5. In transmission electron microscope examination in 2 weeks after micro-venous anastomosis(Experimental I), irregular arrangement of smooth muscle cells was seen adjacent to collagenized tissue around suture silk. In 4 weeks after micro-venous anastomosis(Experimental II), denuded venous wall composed of relatively well arranged smooth muscle cells was covered by endothelial cells, but fibroblast cells and foreign body giant cells near to suture silk was remained. From the results obtained in this study, results of good vascular patiency and anti-thrombotic effect of heparin were obtained as a local irrigation solution, and repair of venous endothelial cell was observed in 2 weeks after micro-venous anastomosis.

• Journal of Chest Surgery
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• v.40 no.4 s.273
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• pp.256-263
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• 2007

Background: Intimal hyperpiasia is characterized by a proliferation of vascular smooth muscle cells in the intimal layer Epigallocatechin-3-gallate (EGCG) is known to suppress smooth muscle cell proliferation. We propose that EGCG may have a protective effect against the development of intimal hyperplasia through the suppression of smooth muscle cell proliferation. Material and Method: Human umbilical vein endothelial cells (HUVEC) and rat aortic smooth muscle cells (RASMC) were cultured with different concentrations of EGCG, and proliferation and migration speed were measured. In 20 dogs, the autologous jugular veins were interposed into the carotid arteries. For the study group (n=10), the graft was stored for 30 minutes in EGCG solution and 300mM EGCG was applied to the perivascular space after grafting. After 6 weeks, the intimal and medial thickness was measured. Result: The proliferation of RASMC and HUVEC was suppressed with EGCG. The migration of RASMC was suppressed with EGCG, but that of HUVEC was not affected. In the in vivo study, the intimal thickness was thinner in EGCG group than in the control group (p<0.05), but the medial thickness did not show any difference. The intimal/medial thickness ratio was lower in the EGCG group (p<0.05). Conclusion: EGCG suppresses intimal hyperplasia after vascular grafting, and this may be mediated by prevention of migration and proliferation of vascular smooth muscle cells. The use of EGCG may offer new therapeutic modality to prevent intimal hyperplasia.

• Environmental Analysis Health and Toxicology
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• v.19 no.1
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• pp.109-117
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• 2004

The purpose of the present study was to examine the effect of diesel exhaust particles on human aortic vascular smooth muscle cells (VSMCs). DNA synthesis, cell viability and morphology of VSMCs after treatment of diesel exhaust particles (DEP) and fine particulate matter (PM$_{2.5}$) were assayed. PM$_{2.5}$ inhibited the DNA synthesis of VSMCs in a concentration -dependent manner, whereat DEP did not affect VSMCs up to 50$\mu\textrm{g}$/mL. These results were confirmed by morphological examination of VSMCs. PM$_{2.5}$ showed a dose-dependent cytotoxicity of VSMCs by MTT assay. Fraction 4 (organic acids) and fraction 8 (moderately polar compounds) showed the most potent inhibition of DNA synthesis of VSMCs, and fraction 7 (slightly polar compounds), fraction 9 (higher polar compounds), and fraction 6 (aromatic compounds) were next order. These results were confirmed by morphological examination of VSMCs. These results suggest that PM$_{2.5}$ inhibits the DNA synthesis of VSMCs through the cytotoxicity.oxicity.

• Korean Journal of Pharmacognosy
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• v.42 no.2
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• pp.182-186
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• 2011

Houttuynia cordata Thunb.[H.cordata]belonging to Saururaceae, is a wild medicinal herb of perennial plants, and grows well in a place with a lot of shade and moisture. The medical action of H.cordata is reported to have an antitumer effect, toxicity-suppressive effect, antifungal effect, diuretic effect, and antioxidative action, but its effect hasn't been reported on cardiovascular diseases, such as ateriosclerosis and hypertension yet. This study intended to confirm the effect of the water extract of H.cordata on the migration and proliferation of rat aortic smooth muscle cells. Such results show that the water extract of H.cordata suppresses the migration and proliferation of rat aortic smooth muscle cells. It is believed that a useful clue will be offered later to the prevention of cardiovascular diseases such as ateriosclerosis and hypertension, and the development of their medicines on the basis of the fact.

• BMB Reports
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• v.46 no.7
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• pp.352-357
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• 2013

Atherosclerosis, which manifests as acute coronary syndrome, stroke, and peripheral arterial diseases, is a chronic inflammatory disease of the arterial wall. Prunella vulgaris, a perennial herb with a worldwide distribution, has been used as a traditional medicine in inflammatory disease. Here, we investigated the effects of P. vulgaris ethanol extract on TNF-${\alpha}$-induced inflammatory responses in human aortic smooth muscle cells (HASMCs). We found that P. vulgaris ethanol extract inhibited adhesion of monocyte/macrophage-like THP-1 cells to activated HASMCs. It also decreased expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin and ROS, No production in TNF-${\alpha}$-induced HASMCs and reduced NF-${\kappa}B$ activation. Furthermore, P. vulgaris extract suppressed TNF-${\alpha}$-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK). These results demonstrate that P. vulgaris possesses anti-inflammatory properties and can regulate TNF-${\alpha}$-induced expression of adhesion molecules by inhibiting the p38 MAPK/ERK signaling pathway.

• Journal of Life Science
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• v.15 no.2 s.69
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• pp.186-191
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• 2005

Previous studies have demonstrated that expression of galectin-3, a member of family of beta-galactoside-binding animal lectin, is associated with pathological conditions including cancer, atherosclerosis, and viral infection. An increase of this lectin has been observed after infection by Kirsten murine sarcoma, human T lymphotropic virus-l (HTLV-l), and human immunodeficiency virus-l (HIV-l). Viral transactivation protein Tax of HTLV-l mediates the increase in the lectin. In case of HIV-1, there are evidences that Tat would be related with increase in galectin-3. We investigated whether Tat directly induced galectin-3 expression in cells. We found that HIV-l tat gene activated galectin-3 promoter in RAW264.7 cells. To demonstrate direct induction of galectin-3 by HIV-l tat, we transfected the tat into a rabbit smooth muscle cell line (Rb1) and obtained RblTatCl-2, a clone of cell stably transfected with tat gene. The Rb1TatCl-2 cells exhibited activation of LTR promoter and up-regulation of galectin-3 transcript as well as protein. Our results indicate that HIV-l tat alone is sufficient to induce the expression of galectin-3. The Rb1TatCl-2 cells could be valuable for study of the effect of HIV-1 tat on expression of cellular genes.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.2
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• pp.225-232
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• 1998

To investigate the possible involvement of outward potassium ($K^+$) currents in nitric oxide-induced relaxation in intestinal smooth muscle, we used whole-cell patch clamp technique in freshly dispersed guinea-pig ileum longitudinal smooth muscle cells. When cells were held at -60 mV and depolarized from -40 mV to -50 mV in 10 mV increments, sustained outward $K^+$ currents were evoked. The outward $K^+$ currents were markedly increased by the addition of 10 ${\mu}M$ sodium nitroprusside (SNP). 10 ${\mu}M$ S-nitroso-N-acetylpenicillamine (SNAP) and 1 mM 8-Bromo-cyclic GMP (8-Br-cGMP) also showed a similar effect to that of SNP. 1 mM tetraethylammonium (TEA) significantly reduced depolarization-activated outward $K^+$ currents. SNP-enhanced outward $K^+$ currents were blocked by the application of TEA. High EGTA containing pipette solution (10 mM) reduced the control currents and also inhibited the SNP-enhanced outward $K^+$ currents. 5 mM 4-aminopyridine (4-AP) significantly reduced the control currents but showed no effect on SNP-enhanced outward $K^+$ currents. 0.3 ${\mu}M$ apamin and 10 ${\mu}M$ glibenclamide showed no effect on SNP-enhanced outward $K^+$ currents. 10 ${\mu}M$ 1H-[1,2,4]oxadiazolo [4,3-a]quinoxaline-1-one (ODQ), a specific inhibitor of soluble guanylate cyclase, significantly blocked SNP-enhanced $K^+$ currents. We conclude that NO donors activate the $Ca^{2+}-activated$ $K^+$ channels in guinea-pig ileal smooth muscle via activation of guanylate cyclase.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.6
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• pp.547-554
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• 1999

The aim of the present study is to investigate the contribution of $Ca^{2+} ?activated\;K^+\;(K_{Ca})$ channels and delayed rectifier $K^+\;(K_V)$ channels to the resting membrane potential (RMP) in rabbit middle cerebral arterial smooth muscle cells. The RMP and membrane currents were recorded using the whole-cell patch configuration and single $K_{Ca}$ channel was recorded using the outside-out patch configuration. Using the pipette solution containing 0.05 mM EGTA, the RMP was $-25.76{\pm}5.08$ mV (n=12) and showed spontaneous transient hyperpolarizations (STHPs). The membrane currents showed time- and voltage-dependent outward currents with spontaneous transient outward currents (STOCs). When we recorded the membrane potential using the pipette solution containing 10 mM EGTA, the RMP was depolarized and did not show STHPs. The membrane currents showed no STOCs but only showed slowly inactivating outward currents. External TEA (1 mM) reversibly inhibited the STHPs, depolarized the RMP, reduced the membrane currents, abolished STOCs, and decreased the open probability of single $K_{Ca}$ channel. When $K_V$ currents were isolated, the application of 4-AP (5 mM) depolarized the RMP. The important aspect of our results is that $K_{Ca}$ channel is responsible for the generation of the STHPs in the membrane potential and plays an important role in the regulation of the RMP and $K_V$ channel is also responsible for the regulation of the RMP in rabbit middle cerebral arterial smooth muscle cells.

• The Korean Journal of Physiology and Pharmacology
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• v.15 no.1
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• pp.31-36
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• 2011

To understand the roles of purinergic receptors and cellular molecules below the receptors in the vascular inflammatory response, we determined if extracellular nucleotides up-regulated chemokine expression in vascular smooth muscle cells (VSMCs). Human aortic smooth muscle cells (AoSMCs) abundantly express $PSY_1$, $PSY_6$, and $PSY_{11}$ receptors, which all respond to extracellular nucleotides. Exposure of human AoSMCs to $NAD^+$, an agonist of the human $PSY_{11}$ receptor, and $NADP^+$ as well as ATP, an agonist for $PSY_1$ and $PSY_{11}$ receptors, caused increase in chemokine (C-C motif) ligand 2 gene (CCL2) transcript and CCL2 release; however, UPT did not affect CCL2 expression. CCL2 release by $NAD^+$ and $NADP^+$ was inhibited by a concentration dependent manner by suramin, an antagonist of P2-purinergic receptors. $NAD^+$ and $NADP^+$ activated protein kinase C and enhanced phosphorylation of mitogen-activated protein kinases and Akt. $NAD^+$- and $NADP^+$-mediated CCL2 release was significantly attenuated by SP6001250, U0126, LY294002, Akt inhibitor IV, RO318220, GF109203X, and diphenyleneiodium chloride. These results indicate that extracellular nucleotides can promote the proinflammatory VSMC phenotype by up-regulating CCL2 expression, and that multiple cellular elements, including phosphatidylinositol 3-kinase, Akt, protein kinase C, and mitogen-activated protein kinases, are involved in that process.