Biomedical subjects

Duck Sun Ahn

Publications and source records attributed to Duck Sun Ahn.

5 recordsLinked to original sources

PubMed2006

Augmented sphingosylphosphorylcholine-induced Ca2+-sensitization of mesenteric artery contraction in spontaneously hypertensive rat.

Sphingosylphosphorylcholine (SPC) is a vasoconstricting lysosphingolipid, and the RhoA/Rho-kinase pathway plays an important role in SPC-induced contraction. Since RhoA/Rho-kinase-mediated signaling is involved in the generation and/or maintenance of hypertension, we compared the effect of SPC on the contractility of endothelium-denuded small mesenteric arteries in spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY). Fura-2 Ca2+ signals, contractile responses, and phosphorylation of 20-kDa myosin light chains (MLC20) were measured. Ten microM SPC induced a gradual and sustained vasoconstriction, which was greater in arteries of the SHR (82.5 +/- 4.3%, n=9) than in those of the WKY (26.7 +/- 4.5%, n=10). In Ca2+-free media, SPC gradually increased vascular tone in the SHR, but caused little vasoconstriction in the WKY. In the SHR and WKY, SPC evoked a greater vasoconstriction than did high K+ depolarization at a given Ca2+ ratio, and the Ca2+ ratio-tension curve induced by SPC was significantly shifted to the left compared with that induced by high K+ depolarization. However, the magnitude of shift to the left was greater in the SHR than in the WKY. The Rho-kinase inhibitor Y-27632 significantly inhibited SPC-induced contractions, but neither the protein kinase C inhibitor calphostin-C nor PD98059, which inhibits activation of some mitogen-activated protein kinases, had any effect on the SHR or the WKY. SPC significantly increased the phosphorylation of MLC20 in both the SHR and the WKY, and Y-27632 inhibited the SPC-induced increase in MLC(20) phosphorylation in the SHR. Our results suggest that SPC induces greater vascular tone in the SHR than in the WKY. Furthermore, our results indicate that activation of the Rho-kinase pathway plays an important role in the SPC-induced Ca2+ sensitization in the SHR.

Amides↗

PubMed2005

C2-ceramide induces vasodilation in phenylephrine-induced pre-contracted rat thoracic aorta: role of RhoA/Rho-kinase and intracellular Ca2+ concentration.

It is known that ceramide may play an important regulatory role in vascular tone although its effect on vascular tone and the mechanisms involved are controversial. The present study was designed to investigate the effects of ceramide and its key initial regulators, TNF-alpha and neutral sphingomyelinase (SMase), on vascular tone of isolated rat thoracic aortic rings and elucidate the mechanisms involved in the changes in vascular tone induced by ceramide. Contractile responses and Fura-2 Ca2+ signals were measured in rat thoracic aortic rings or strips. 10(-5) M C2-ceramide, 0.1 U/ml neutral sphingomyelinase (SMase), and 5x10(-7) g/ml TNF-alpha had no effect on resting tone in rat thoracic aortic rings. However, in phenylephrine-induced pre-contracted rings, treatment with ceramide, SMase, and TNF-alpha evoked a gradual but sustained vasodilation. Vasodilation effect in response to 10(-5) M C2-ceramide was not significantly changed by the absence or presence of endothelium, a cyclooxygenase pathway inhibitor (10(-6) M indomethacin), or PKC inhibitors (10(-5) M H-7 & 5x10(-7) M calphostin-C). Pretreatment with 1 microM Y-27632, a RhoA/Rho-kinase inhibitor, significantly inhibited the phenylephrine-induced contraction itself as well as the C2-ceramide-induced vasodilation. Pre-treatment with 10(-5) M C2-ceramide had no effect on phasic rise in [Ca2+]i and tension evoked by stimulation with 10(-8) M phenylephrine, but post-treatment of C2-ceramide significantly reduced the phenylephrine-induced secondary tonic [Ca2+]i and tension plateau. Our results indicate that C2-ceramide induces vasodilation in phenylephrine-induced pre-contracted rat thoracic aorta. Furthermore, inhibition of phenylephrine-induced activation of RhoA/Rho-kinase pathway as well as phenylephrine-induced elevations in [Ca2+]i are clearly a key factors in C2-ceramide-induced vasodilation.

Animals↗

PubMed2002

Role of protein kinase C- or RhoA-induced Ca(2+) sensitization in stretch-induced myogenic tone.

OBJECTIVE: It has been suggested that Ca(2+) sensitization mechanisms might contribute to myogenic tone. However, specific mechanisms have yet to be fully identified. Therefore, we investigated the role of protein kinase C (PKC)- or RhoA-induced Ca(2+) sensitization in myogenic tone of the rabbit basilar vessel. METHODS: Myogenic tone was developed by stretch of rabbit basilar artery. Fura-2 Ca(2+) signals, contractile responses, PKC immunoblots, translocation of PKC and RhoA, and phosphorylation of myosin light chains were measured. RESULTS: Stretch of the resting vessel evoked a myogenic contraction and an increase in the intracellular Ca(2+) concentration ([Ca(2+)](i)) only in the presence of extracellular Ca(2+). Stretch evoked greater contraction than high K(+) at a given [Ca(2+)](i). The stretch-induced increase in [Ca(2+)](i) and contractile force were inhibited by treatment of the tissue with nifedipine, a blocker of voltage-dependent Ca(2+) channel, but not with gadolinium, a blocker of stretch-activated cation channels. The PKC inhibitors, H-7 and calphostin C, and a RhoA-activated protein kinase (ROK) inhibitor, Y-27632, inhibited the stretch-induced myogenic tone without changing [Ca(2+)](i). Immunoblotting using isoform-specific antibodies showed the presence of PKCalpha and PKCepsilon in the rabbit basilar artery. PKCalpha, but not PKCepsilon, and RhoA were translocated from the cytosol to the cell membrane by stretch. Phosphorylation of the myosin light chains was increased by stretch and the increased phosphorylation was blocked by treatment of the tissue with H-7 and Y-27632, respectively. CONCLUSIONS: Our results are consistent with important roles for PKC and RhoA in the generation of myogenic tone. Furthermore, enhanced phosphorylation of the myosin light chains by activation of PKCalpha and/or RhoA may be key mechanisms for the Ca(2+) sensitization associated myogenic tone in basilar vessels.

Animals↗

PubMed2002

Correction of blepharoptosis in oculopharyngeal muscular dystrophy.

Oculopharyngeal muscular dystrophy is a hereditary, autosomal dominant, slowly progressive disorder with onset that occurs during middle age. Major symptoms are ptosis and dysphagia resulting primarily from selectively involved levator palpebrae and the pharyngeal muscles. Progressive, usually symmetrical blepharoptosis, with or without dysphagia, appears during middle age. Muscular weakness in the limbs can be noted in some patients. The guidelines for surgery in myopathic ptosis are conservative in view of the increased risk of postoperative corneal complications. However, orbicularis function remains intact in oculopharyngeal muscular dystrophy; therefore, corrective surgery is performed in most patients. This report describes four cases of ptosis correction in patients with oculopharyngeal muscular dystrophy in one family. The frontalis action was very poor to qualify for frontalis transfer; therefore, the authors performed moderate to large levator resection in all patients. The follow-up results 5 years postoperatively are promising to date and all the patients are satisfied with the results.

Adult↗

PubMed2002

Curriculum design for problem-based learning on a volunteer basis: a Yonsei approach.

Innovative new medical programs such as Problem Based Learning (PBL) are being developed worldwide. An increasing number of medical schools are starting to introduce these programs into or even to replace the existing curriculum. At Yonsei University College of Medicine (YUCM), we developed our own PBL curriculum and evaluation method. In order to develop a program suitable for our school, we suggest that for trial purposes, a small number of student and teacher volunteers should be selected and that the tutors involved in the program be given adequate training.

Education, Medical↗