1.Pathologic studies on chronic hepatic lesions induced by chloroform.
Ho Seok JEONG ; Dae Young KANG
Journal of the Korean Cancer Association 1991;23(3):544-553
No abstract available.
Chloroform*
2.Study on the Mechanism of Hypoxic Induced Vasodilatation and Vasoconstriction.
Korean Circulation Journal 1998;28(12):2011-2029
BACKGROUND: Although hypoxic pulmonary vasoconstriction (HPC) and hypoxic coronary vasodilatation (HCD) have been recognized by many researchers, the precise mechanism remains unknown. As isolated arteries will constrict or relax in vitro in response to hypoxia, the oxygen sensor/transduction mechanism must reside in the arterial smooth muscle, the endothelium, or both. Unfortunately, much of the current evidence is conflicting, especially concerning to the dependency of HPC and HCD on the endothelium and the role of the K+ channel. Therefore, this experiment was attempted to clarify the dependency of HPC and HCD on the endothelium and the role of the K+ channel on HPC and HCD. METHODS: HPC was investigated in isolated main pulmonary arteries precontracted with norepinephrine (NE). HCD was investigated in isolated left circumflex coronary artery precontracted with prostaglandin F2 alpha. Vascular rings were suspended for isometric tension recording in an organ chamber filled with Krebs-Henseleit solution. Hypoxia was induced by gassing the chamber with 95% N2 +5% CO2, which was maintained for 15 - 25 min. RESULTS: 1)Hypoxia elicited a vasoconstriction in NE-precontracted pulmonary arteries with endothelium, but a vasodilatation in PGF 2 alpha-precontracted coronary arteries with and without endothelium. There was no difference between the amplitude of the HPC and HCD induced by two consecutive hypoxic challenges and the effect of normoxic and hyperoxic control Krebs-Henseleit solution on subsequent response to hypoxia. 2)Inhibition of NO synthesis by the treatment with Nw-nitro-L-arginine reduced HPC in pulmonary arteries, but inhibition of the cyclooxygenase pathway by treatment with indomethacin had no effect on HPC and HCD, respectively. 3)Blockades of the TEA-sensitive K+ channel abolished HPC and HCD. 4)Apamin, a small conductance Ca2+/-activated K+ (KCa) channel blocker, and iberiotoxin, a large conductance KCa channel blocker, had no effect on the HCD. 5)Glibenclamide, an ATP-sensitive K+ (KATP) channel blocker, reduced HCD. 6)Cromakalim, an K(ATP) channel opener, relaxed the coronary artery precontracted with prostaglandin F2 alpha. The degree of relaxation by cromakalim was similar to that by hypoxia and glibenclamide reduced both hypoxia- and cromakalim-induced vasodilations. 7)Verapamil, a Ca2+ entry blocker, caffeine, a Ca2+ emptying drug; and ryanodine, an inhibitor of Ca2+ release from SR, reduced HPC, respectively. CONCLUSION: HPC is dependent on the endothelium and is considered to be induced by inhibition of the mechanisms of NO-dependent vasodilation while HCD is independent of the endothelium and is considered to be induced by activation of the K(ATP) channel.
Anoxia
;
Arteries
;
Caffeine
;
Coronary Vessels
;
Cromakalim
;
Dinoprost
;
Endothelium
;
Glyburide
;
Indomethacin
;
Muscle, Smooth
;
Norepinephrine
;
Oxygen
;
Prostaglandin-Endoperoxide Synthases
;
Prostaglandins F
;
Pulmonary Artery
;
Relaxation
;
Ryanodine
;
Vasoconstriction*
;
Vasodilation*
4.Case of Perforating Osteoma Cutis.
Annals of Dermatology 2003;15(4):153-155
A 24-year-old man presented with a 1.5 × 0.5 cm-sized erythematous nodule with central crust on the forehead since 5 years ago. There was no history of trauma or previous skin disorders. Histopathologic examination showed a typical picture of osteoma cutis. In addition, transepidermal elimination of bony material was observed: red linear plate-like calcified lamella structures had extruded to the skin surface through the perforated epidermis. The perforating type of osteoma cutis was discussed.
Epidermis
;
Forehead
;
Humans
;
Osteoma*
;
Skin
;
Young Adult
5.Teat Shock Response Ingibits IFN-gamma Plus LPS - Induced NO Synthase Expression in Murine Peritoneal Macrophages.
Young Hee JIN ; Young Chul PARK ; Kwang Il KANG ; Ho Sung KANG ; Han Do KIM
Korean Journal of Immunology 1998;20(3):263-268
No abstract available.
Macrophages, Peritoneal*
;
Nitric Oxide
;
Nitric Oxide Synthase*
;
Shock*
;
Tumor Necrosis Factor-alpha
6.Sodium and calcium transport in spherocytic red blood cells.
Shin Heh KANG ; Kir Young KIM ; Young Ho LEE ; Bok Soon KANG
Journal of the Korean Pediatric Society 1991;34(7):978-991
No abstract available.
Calcium*
;
Erythrocytes*
;
Sodium*
;
Spherocytes
7.A Case of Leukemia Cutis.
Eun Seok YANG ; Eun Young KWAK ; Kang Rhun KOO ; Kang Ho KIM ; Young Bong PARK
Journal of the Korean Pediatric Society 1990;33(2):246-251
No abstract available.
Leukemia*
8.Effects of sodium vanadate on contractility of vascular smooth muscle.
Young Kwang YOON ; Chang Hyun MOON ; Young Ho LEE ; Bok Soon KANG ; Doo Hee KANG
Korean Circulation Journal 1993;23(1):104-116
The present study was intended to examine the effect of sodium vanadate on contractility of vascular smooth muscle. Aortic ring preparations were made from the rabbit thoracic aorta and endothelial cells were removed from the ring. The contractility of the aortic ring was measured under various conditions. The results were summarized as follows; 1) Sodium vanadate induced contraction of vascular smooth muscle in a dose-dependent fashion. 2) The contractile effects were not blocked by treatments with adrenergic blocking agent(phentolamine) and indomethacin, indicating the direct action of the drug on vascular smooth muscle. 3) In the presence of ouabain, Na(+)-K(+)-ATPase inhibitor, sodium vanadate still increased the contractility of vascular smooth muscle. 4) Treatment with 4.4'-diisothiocyanostilbene-2.2'-disulfonic acid(DIDS) blocked completely the contractile effects of sodium vanadate. 5) In the presence of verapamil, lanthanum and ryanodine, the contractility of the vascular smooth muscle by sodium vanadate was decreased. From the above results. it was suggested that sodium vanadate acts directly on vascular smooth muscle and causes contraction. It was probably due to inhibition of Ca(++)-ATPase in plasma membrane as well as increasing the release of Ca(++) from sarcoplasmic reticulum and Ca(++) influx across the plasma membrane, but not inhibition of Na(+)-K(+)-ATPase.
Aorta, Thoracic
;
Cell Membrane
;
Endothelial Cells
;
Indomethacin
;
Lanthanum
;
Muscle, Smooth, Vascular*
;
Ouabain
;
Ryanodine
;
Sarcoplasmic Reticulum
;
Sodium*
;
Vanadates*
;
Verapamil
9.A Clinical Study of Pityriasis Versicolor in the Young.
Hyo Jun KANG ; Han Young WANG ; Ho Suk SUNG
Korean Journal of Dermatology 1997;35(3):431-434
BACKGROUND: Pityriasis versicolor(PV) is a superficial mycosis, theoretically unusual in children. Epidemiologic and clinical data for children with PV under 14 years were collected. OBJECTIVE: The purpose of this study was to evaluate the clinical features of PV in the young. METHOD: We included all cases of PV in patients under 14 years of age observed in our department from 1981 to 1995. All cases were diagnosed on the basis of clinical criteria and were confirmed by microscopic examination. RESULTS: From 1981 to 1995 we encountered 32 cases of PV in children, compared with 637 cases in adults; thus children represented 4.7% of all cases. The ratio of male to female was l. 7:1. Among the age groups, the incidence was the highest in the 10-14 years(43%). The monthly prevalence was the highest in August. Distribution of the lesions were the face(40.9%), neck (25%), chest(13.6%), back(11.3%), extremities(6.8%) and abdomen(2.2%). The incidence of hypopigmented lesions was 70.4% and that of hyperpigmented lesions was 29.6%. CONCLUSION: This study confirms that the face is a predilectionl site for PV in children and all facial lesions are hypopigmented. Other clinical features are variable and similar to those of adults.
Adult
;
Child
;
Female
;
Humans
;
Incidence
;
Male
;
Neck
;
Pityriasis*
;
Prevalence
;
Tinea Versicolor*