1.Facial skin graft using preauricular and forehead expansion.
Sang Baek HAN ; Chin Whan KIM ; Chul Gyoo PARK ; Yoon ho LEE ; Kyung Won MINN ; Suk Wha KIM
Journal of the Korean Society of Plastic and Reconstructive Surgeons 1998;25(6):1147-1152
Skin graft has been widely used for facial skin reconstruction. Inguinal area is the common donor site for full-thickness skin graft of various area. Especially for facial skin graft, retroauricular area or upper eyelid skin has been used as a donor site. But these donor sites have some limitations as perfect ones in terms of size, color and texture when applied onto facial area. Even retroauricular skin shows color and texture differences from normal facial skin after it is grafted. Authors performed expansion of the skin of preauricular area or forehead where minimal scars would come out after final operation. We harvested this expanded skin and performed skin graft following excision of nevus, poor scar, or hemangioma in face.We achieved satisfactory results in terms of color and texture by applying this method in 11 clinical cases; 4 cases of hemangioma, 4 nevus, and 3 cases of traumatic scar. Donor site scars were clinically inspicuous in all these 11 cases.
Cicatrix
;
Eyelids
;
Forehead*
;
Hemangioma
;
Humans
;
Nevus
;
Skin*
;
Tissue Donors
;
Transplants*
2.Drug - Induced Esophageal Ulcers.
Han Lim MOON ; In Sik CHUNG ; Sang Hong BAEK ; Kyu Sik SHIM ; Chang Don LEE ; Suk Won HAN ; Kyu Won CHUNG ; Hee Sik SUN ; Whan Kook CHUNG
Korean Journal of Gastrointestinal Endoscopy 1985;5(1):11-15
Over 26 kinds of tablets and capsules, such as Tetracycline, Quinidine and Potassium preparations were reported to cause esopbageal ulcerations, eharacterized in various size, shape and number, ind sually in mid-esophagus, Recently authors experienced 10 cases of drug-induced esophageal ulcerations due to antibiotics and antiinflammatory agents such as Tetracycline, Aspirin, etc. Four cases were men and six were women. Four cases were in third dades, three in fourth cleeades, two in fifth decades and one in sixth decades. Presenting symptoras were odynophagia(4/10), dysphagia(3/10), substernal pain(7/10) and epigastric pain(3/10). Endoscopic examination of the esophgus showed single or multiple, small and shallow ulcers on the mid-esophgeal mucosa at the level of 30cm from the ineisor in eight cases, one Iarge and deep ulcer at the level of 40cm from incisor in one patient and one amall, shallow and one large, deep ulcers at the same time. in one patient The shape of alcers were various from a round to a large horseshoe shaped one. The clinical course was mild without complications. It was suggested that drug-induced esophsgeal ulcers with antibiotics and antiinflammatory agents could be found frequently and they had benign and mild clinicalc ourse,
Anti-Bacterial Agents
;
Anti-Inflammatory Agents
;
Aspirin
;
Capsules
;
Female
;
Humans
;
Incisor
;
Male
;
Mucous Membrane
;
Potassium
;
Quinidine
;
Tablets
;
Tetracycline
;
Ulcer*
3.The Regulation of Cyclooxygenase-2 Expressionby Interleukin-1beta in WISH cells.
Young Jin CHANG ; Yoon Ki PARK ; Suk Whan BAEK ; Young Ki LEE ; Dong Hyuk LEE ; Hyun Woo LEE
Korean Journal of Obstetrics and Gynecology 2001;44(8):1393-1400
OBJECTIVE: To determine of the regulation of cyclooxygenase-2 (COX-2) expression by Interleukin-1beta in WISH cells. METHODS: Amnion WISH cells were incubated in media containing increasing concentrations of IL-1beta or with various inhibitors. Increased COX-2 expression was determined by Western blot analysis with anti-COX-2 antibody. Concomitant measurements of culture media PGE2 were made by an enzyme immunoassay. RESULTS: The COX-2 and prostaglandin E2 production induced by IL-1beta increased in a dose- and time-dependent manner. One of the regulating factors that induced COX-2 by IL-1beta was protein kinase C (PKC). PKC inhibitor, Ro 31-8220 was pretreated and continued treating by IL-1beta. Then, PKC inhibitor completely blocked COX-2 protein induction by IL-1beta. In contrast, COX-2 induction by IL-1beta after pretreating PKC stimulator, phobol 12-myristate 13-acetate was potentiated with synergism. Another factor in controlling COX-2 protein induction was identified as phosphatidylinositol 3-kinase (PI 3K). COX-2 protein induction by IL-1beta after pretreating PI 3K inhibitors, wortmannin and LY294002 strongly increased. This kind of result reflected that PI 3K act as negative regulator. COX-2 induction by IL-1beta was known to be regulated in not only transcription step, but also translation step after performing experiment of actinomycin and cycloheximide treatment. CONCLUSION: COX-2 protein and prostaglandin E2 production induced by IL-1beta were controlled by many factors in amnion cell. Among those factors, PKC and PI 3K have an important role, but their control mechanism act as positive and negative, respectively.
Amnion
;
Blotting, Western
;
Culture Media
;
Cycloheximide
;
Cyclooxygenase 2*
;
Dactinomycin
;
Dinoprostone
;
Immunoenzyme Techniques
;
Interleukin-1beta*
;
Phosphatidylinositol 3-Kinase
;
Protein Kinase C
4.Comparison of Maternal Serum Screening Test Efficacy for Down Syndrome.
Chung No LEE ; Yong Won LEE ; Hye Sun JUN ; Suk Whan LEE ; Kyung Lyul KIM ; Kwang Eun CHA ; Kyung Sub CHA ; Jin Young BAEK
Korean Journal of Obstetrics and Gynecology 1997;40(4):721-731
Maternal serum alpha-feto protein(MSAFP) screening test has provided high sensitivity and specificity in detecting neural tube defects(NTD). Approximately 80~90% of NTD can be identified by this screening test.Prospective studies have shown that low levels of MSAFP can be used for Down syndrome screening test, but the detection rate for Down syndrome in combination with age is only 20% in younger women, making this screening test relatively insensitive. However recently some studies have suggested that the triple marker test with MSAFP, unconjugated estriol, beta-human chorionic gonadotropin achieved higher detection rate for Down syndrome. The purpose of present study is to compare the positive predictive values of both MSAFP and Triple test. We had 6,436 cases of MSAFP test during the year of 1994 and 7,077 cases for triple test during the year of 1995. We analyzed data with positive results by screening both tests, since our purpose is to compare positive value. The number of positive results were 290(triple test) and 206(AFP) respectively. With this study, we concluded that positive predictive value of triple marker test is 4.17 times greater than of the MSAP test.
Chorionic Gonadotropin
;
Down Syndrome*
;
Estriol
;
Female
;
Humans
;
Mass Screening*
;
Neural Tube
;
Sensitivity and Specificity
5.Comparison of Maternal Serum Screening Test Efficacy for Down Syndrome.
Chung No LEE ; Yong Won LEE ; Hye Sun JUN ; Suk Whan LEE ; Kyung Lyul KIM ; Kwang Eun CHA ; Kyung Sub CHA ; Jin Young BAEK
Korean Journal of Obstetrics and Gynecology 1997;40(4):721-731
Maternal serum alpha-feto protein(MSAFP) screening test has provided high sensitivity and specificity in detecting neural tube defects(NTD). Approximately 80~90% of NTD can be identified by this screening test.Prospective studies have shown that low levels of MSAFP can be used for Down syndrome screening test, but the detection rate for Down syndrome in combination with age is only 20% in younger women, making this screening test relatively insensitive. However recently some studies have suggested that the triple marker test with MSAFP, unconjugated estriol, beta-human chorionic gonadotropin achieved higher detection rate for Down syndrome. The purpose of present study is to compare the positive predictive values of both MSAFP and Triple test. We had 6,436 cases of MSAFP test during the year of 1994 and 7,077 cases for triple test during the year of 1995. We analyzed data with positive results by screening both tests, since our purpose is to compare positive value. The number of positive results were 290(triple test) and 206(AFP) respectively. With this study, we concluded that positive predictive value of triple marker test is 4.17 times greater than of the MSAP test.
Chorionic Gonadotropin
;
Down Syndrome*
;
Estriol
;
Female
;
Humans
;
Mass Screening*
;
Neural Tube
;
Sensitivity and Specificity
6.Expression and Regulation of Endothelial Nitric Oxide Synthase by Vascular Endothelial Growth Factor in ECV 304 Cells.
Jong Seon PARK ; Gu Ru HONG ; Suk Whan BAEK ; Dong Gu SHIN ; Young Jo KIM ; Bong Sup SHIM
Journal of Korean Medical Science 2002;17(2):161-167
Nitric oxide (NO) seems to play a pivotal role in the vascular endothelial growth factor (VEGF)-induced endothelial cell proliferation. This study was designed to investigate the role and intracellular signal pathway of endothelial nitric oxide synthase (eNOS) activation induced by VEGF. ECV 304 cells were treated with betaVEGF(165) and then cell proliferation, eNOS protein and mRNA expression levels were analyzed to elucidate the functional role of eNOS in cell proliferation induced by VEGF. After exposure of cells to betaVEGF(165) , eNOS activity and cell growth were increased by approximately two-fold in the betaVEGF(165) -treated cells compared to the untreated cells. In addition, VEGF stimulated eNOS expression at both the mRNA and protein levels in a dose-dependent manner. Phosphatidylinositol-3 kinase (PI-3K) inhibitors were used to assess PI-3K involvement in eNOS regulation. LY294002 was found to attenuate VEGF-stimulated eNOS expression. Wortmannin was not as effective as LY294002, but the reduction effect was detectable. Cells activated by VEGF showed increased ERK1/2 levels. Moreover, the VEGF-induced eNOS expression was reduced by the PD98059, MAPK pathway inhibitor. This suggests that eNOS expression might be regulated by PI-3K and the ERK1/2 signaling pathway. In conclusion, betaVEGF(165) induces ECV 304 cell proliferation via the NO produced by eNOS. In addition, eNOS may be regulated by the PI-3K or mitogen-activated protein kinase pathway.
1-Phosphatidylinositol 3-Kinase/*antagonists & inhibitors
;
Cell Division/drug effects
;
Cell Line
;
Endothelial Growth Factors/*metabolism/pharmacology
;
Endothelium, Vascular/cytology
;
*Gene Expression Regulation, Enzymologic
;
Lymphokines/*metabolism/pharmacology
;
MAP Kinase Signaling System
;
Mitogen-Activated Protein Kinase 1/*antagonists & inhibitors
;
Mitogen-Activated Protein Kinase 3
;
Mitogen-Activated Protein Kinases/*antagonists & inhibitors
;
Nitric Oxide Synthase/*genetics/metabolism
;
Nitric Oxide Synthase Type III
;
Signal Transduction
;
Vascular Endothelial Growth Factor A
;
Vascular Endothelial Growth Factors