1.Urgent Application of Extracorporeal Membrane Oxygenation in Amniotic Fluid Embolism.
Korean Journal of Critical Care Medicine 2016;31(3):179-180
No abstract available.
Amniotic Fluid*
;
Embolism, Amniotic Fluid*
;
Extracorporeal Membrane Oxygenation*
;
Female
;
Pregnancy
2.Statutory Communicable Diseases in 2003.
Journal of the Korean Medical Association 2004;47(5):479-483
No abstract available.
Communicable Diseases*
3.Statutory Communicable Diseases in 2003.
Journal of the Korean Medical Association 2004;47(5):479-483
No abstract available.
Communicable Diseases*
4.Infection Control Program in Yonsei Medical Center.
Eun Suk PARK ; Young Suk KIM ; June Myung KIM
Korean Journal of Nosocomial Infection Control 1999;4(1):51-57
No Abstract available.
Infection Control*
5.Comparisons of the Ratio of Pulmonary to Systemic Blood Flow(Qp/Qs) Determined by Non-invasive Doppler Echocardiography and Radionuclide-Angiocardiography in Congenital Heart Diseases.
Jung Suk LEE ; Chul Wo PARK ; Hyang Suk YOON
Journal of the Korean Pediatric Society 1989;32(7):943-950
No abstract available.
Echocardiography, Doppler*
;
Heart Diseases*
;
Heart*
7.Tendocutaneous free flap transfer from the dorsum of the foot.
Kwang Suk LEE ; Jae Suk CHANG ; Hae Il PARK
The Journal of the Korean Orthopaedic Association 1993;28(4):1413-1418
No abstract available.
Foot*
;
Free Tissue Flaps*
8.Reversal Effects of Neostigmine, Edrophonium and 4-aminopyridine of Verapamil Pretreatment on Pipecuronium Induced Neuromuscular Blockade in Rat-Hemidiaphragm.
Korean Journal of Anesthesiology 1997;33(2):228-236
BACKGROUND: It has been shown that L-type calcium channel blockers increase the muscle relaxation effects of non-depolarizing neuromuscular blocking agents whereas the potentiated neuromuscular blocking effects by L-type calcium channel blocker are resistant to reversal by neostigmine. The aims of this study were 1) to see whether the pretreatment of L-type calcium channel blocker, such as verapamil, aggravates the pipecuronium-induced muscle relaxation, 2) if so, to see whether these effects are reversed by anticholinesterase, such as neostigmine and edrophonium or potassium channel blocker, such as 4-aminopyridine. METHODS: The rat-phrenic nerve-hemidiaphragms (n=60) were prepared. Twenty microgram of pipecuronium was administered to all organ bath. All samples were divided into two groups according to the administration of 10uM of verapamil i.e. verapamil pretreated, non-pretreated group. The amounts of administered pipecuronium were gradually increased by 4ug until the force of twitch decreased to 10% of control value in both groups. Each group was subdivided into three groups according to the administration of 0.75 M of neostigmine, 12.4 uM of edrophonium or 40uM of 4-aminopyridine. RESULTS: The dose of pipecuronium required for the decrease of contractile force to 10% of control value was less in verapamil pretreated group than in non-pretreated group. And, the decrease of contractile force in both groups was more effectively reversed by 4-aminopyridine than neostigmine and edrophonium. CONCLUSIONS: Verapamil potentiates the pipecuronium-induced neuromuscular blockade and 4-aminopyridine is more effective to reverse verapamil pretreated, pipecuronium induced neuromuscular blockade.
4-Aminopyridine*
;
Baths
;
Calcium Channels, L-Type
;
Edrophonium*
;
Muscle Relaxation
;
Neostigmine*
;
Neuromuscular Blockade*
;
Neuromuscular Blocking Agents
;
Pipecuronium*
;
Potassium Channels
;
Verapamil*
9.The Effects of Rehabilitation Excercise Program on Physical Function and Mental Health Status in Patients with Hemiparesis Following Chronic Stroke.
Journal of Korean Academy of Community Health Nursing 2006;17(2):166-175
No abstract available.
Humans
;
Mental Health*
;
Paresis*
;
Rehabilitation*
;
Stroke*
10.Effect of Methylmercury in Cultured Rat Myocardial Cells.
Hyang Suk YOON ; Seung Taeck PARK
Korean Circulation Journal 1996;26(4):894-900
BACKGROUND: It is known that methylmercury poisoning, Minamata disease is very toxic to human body. But, cardiotoxic mechanism of methylmercury is left unknown, Recent study has been reported that the cleavage of methylmercury produce oxygen radicals as well as methyl radicals, and also these radicals induce the release of excitotoxic amino acids(EAAs). So, oxygen radicals and EAA are regarded as a causative factors in the various diseases such as heart disease induced by toxicity of methylmercury. We studied to know the cardiotoxic effect of methylmercury on cultured myocardial cells derived from neonatal rat in order to evaluate the toxic mechanism of methylmercury. METHODS: Myocardial cells of neonatal rat were incubated with various concentrations of methylmercuric chloride for 1-96 hours. MTT90 and MTT50 values were measured and cell viability was determined by MTT assay. In addition, morphological study was performed by light microscope after cultured myocardial cells that were exposed to methymercuric chloride. RESULTS: MTT90 and MTT50 values were 1microM and 15microM of methylmercuric chloride in cultured myocardial cells of neonatal rat respectively. Exposure of cultured rat myocardial cells to methylmercuric chloride resulted in a significant cell death in a time-dependent manner. In the observation of morphological changes, cultured cells treated with methlymercuric chloride showed decrease of cell number and disconnection between cultured myocardial cells. CONCLUSION: These observation suggest that methylmercury has a severe myocardiotoxicity on cultured myocardial cells derived from neonatal rat by the decrease of cell viability and morphological changes.
Animals
;
Cell Count
;
Cell Death
;
Cell Survival
;
Cells, Cultured
;
Heart Diseases
;
Human Body
;
Mercury Poisoning, Nervous System
;
Poisoning
;
Rats*
;
Reactive Oxygen Species
Result Analysis
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