문자패턴의 특징지도 추출을 위한 상대유사 경쟁학습 알고리즘

유영재,이진,장영학,김성환 국립7개대학공동논문집간행위원회 2001 공업기술연구 Vol.1 No.-

In this paper, we propose a new competitive learning algorithm for unsupervised learning neural network to extract a feature map from letter patterns. The proposed learning algorithm is based on relative similarity, which is similarity measure between input data and cluster group. So, the proposed network and algorithm is called relative similarity network(RSN) and learning algorithm. According to the definition of similarity and learning rule, the structure of RSN is designed and the pseudo code of the algorithm is described. In the extraction of a feature map. RSN, in spite of deletion of learning rate, resulted in the identical performance with those of WTA, and SOM. Thus, it is shown that RSN is useful to extract a feature map of letter patterns.

문자패턴의 특징지도 추출을 위한 상대유사 경쟁학습 알고리즘

유영재,이진,장영학,김성환 木浦大學校 應用科學硏究院 2001 應用科學硏究誌 Vol.1 No.-

In this paper, we propose a new competitive learning algorithm for unsupervised learning neural network to extract a feature map from letter patterns. The proposed learning algorithm is based on relative similarity, which is similarity measure between input data and cluster group. So, the proposed network and algorithm is called relative similarity network (RSN) and learning algorithm. According to the definition of similarity and learning rule, the structure of RSN is designed and the pseudo code of the algorithm is described. In the extraction of a feature map. RSN, in spite of deletion of learning rate, resulted in the identical performance with those of WTA, and SOM. Thus, it is shown that RSN is useful to extract a feature map of letter patterns.

Smad에 의한 alkaline phosphatase 유전자의 발현 조절기전

김난진,류현모,김현정,김영진,남순현 대한소아치과학회 2001 大韓小兒齒科學會誌 Vol.28 No.2

본 실험은 탁월한 골유도능으로 관심의 대상이 되고 있는 RMP의 세포내 신호 전달자로 알려진 Smad 1과 Smad 5가 조 골세포 초기 분화표지인자인 ALP 유전자의 발현에 미치는 영향 및 그 조절기전을 알아보고자 하였다. BMP 처리 없이도 Smad에 의해 ALP가 발현되는가를 알아보기 위해 Smad 1과 Smad 5가 각각 stably transfection된 C2C12 세포를 3일간 배양후 histochemical assay를 하였고, Smad 1과 Smad 5의 expression vector와 ALP promoter vector를 transient co-transfectiongksgn ALP promoter activity를 측정하였다. Smad에 의한 BMP의 효과를 알아보기 위해서 100ng/ml의 BMP-2를 처리한 군과 처리하지 않은 군으로 나누어 세포를 배양한후 ALP 유전자의 발현을 northern blot analysis로 확인하였다. Smad가 ALP 유전자의 발현을 직접적으로 조절하는가를 알아보기 위여서는 단백질 합성억제제인 cycloheximide를 전처리하여 ALP 유전자의 발현을 northern blot analysis하였다. 이상의 실험결과 다음과 같은 결론을 얻었다. ·Smad 1과 Smad 5가 과발현된 세포에서는 BMP 처리없이도 ALP가 발현된다. ·Smad 1과 Smad 5가 과발현된 세포에서 RMP 처리후 ALP 발현 증가율이 대조군 보다 현저히 높게 나타나 Smad가 BMP 효과를 증가시킨다는 것을 알수있다. ·Smad는 새로운 단백질의 합성을 통해 ALP 유전자를 발현시킨다. Bone morphogenetic proteins(BMPs), members of the transforming growth factor β(TGF-β) superfamily were first identified as the factors that induce ectopic bone formation in vivo, when implanted into muscular tissue. Especially BMP-2 inhibits terminal differentiation of C2C12 myoblasts and converts them into osteoblast lineage cells. In the molecular mechanism of the signal transduction of TGF-β and related factors, intracellular signaling proteins were identified as Smad. In previous study, it has been reported that Smad 1 and Smad 5, which belong to the R-Smad family mediate BMP signaling, were involved in the induction of osteoblast differentiation in C2C12 cells. To understnad the role of Smads involved in osteogenic transdifferentiation in C2C12 cell, in present study, after we stably transfected C2C12 cells with each. Smad(Smad 1, Smad 5) expression vector, cultured for 3 days and stained for alkaline phophatase activity. ALP activity positive cells appeared in the Smad 1, Smad 5 stably transfected cell even in the abscence of BMP. After transiently co-transfected C2C12 cells with each Smad expression vector and ALP promoter, it was excence of MBP. These result suggested that both Smad 1 and Smad 5 were involved in the intracellular BMP signals which induce osteoblast differentiation in C2C12 cells. The effect of BMP on C2C12 cells with Smad 1, Smad 5 transfected were studied by using northern blot analysis. the treatment of BMP upregulated ALP mRNA level in three groups, especially upregulation of ALP was larger in Smad 1, Smad 5 transfected cell than control group. Pretreatment with cycloheximide(10㎍/ml), a protein synthesis inhibitor resulted in blocking the ALP gene expression even in BMP(100ng/ml) treated cell. These results suggested that Smad increased the level of ALP mRNA via the synthesis of a certain transcriptional regulatory protein.

자발성 뇌지주막하출혈 환자에서 Cardiac Troponin Ⅰ를 이용한 심근손상의 발생율

김용권,류진호,소정일,문원식,전병조,허탁,민용일 대한응급의학회 1999 대한응급의학회지 Vol.10 No.4

Background : More than 90% of acute stroke patients have measurable cardiovascular sequelae, but we have been often overlooked in formal discussions of treatment. If we estimate the incidence of myocardial injury in patients with spontaneous SAH, we may figure the possibility of cardiac dysfunction in such patients. This study was designed to investigate the incidence of myocardial injury in patients with spontaneous SAH using cardiac troponin I(cTnI). Methods : A prospective single emergency center study was performed to determined preoperative incidence of unrecognized cardiac injury in patients suffering spontaneous SAH. We include the spontaneous SAH patients who underwent serum measurements of the cardic troponin I immediately upon admission last six month period. ECG, CK, CK-MB and myoglobin were also performed at admission. We excluded the spontaneous SAH patients who had past history of myocardial ischemia and ECG abnormality. Results : Fifty-two patients(34 females, 18 males) with spontaneous SAH were studied prospectively. 18 patients(34.6% of the total study population) had cTnI level above 0.5ng/ml. ECG was performed in 52 patients and was abnormal in 15 of the 52 patients(28.8%). Conclusion : The measurement of cTnI has provided physicians with a myocardial marker that has a cardiac sensitivity for cardiac injury equal to that of CK-MB yet with greater specificity. So, cardiac troponin I is useful to estimate the incidence of myocardial injury in patients with spontaneous SAH. And we may estimate the possibility of cardiac dysfunction in such patients. This knowledge will hopefully aid in the care and improve the outcome.

Mouse의 치아 발육시 Runx2의 발현 양상

김태완,류현모,남순현,김영진,김현정 大韓小兒齒科學會 2004 大韓小兒齒科學會誌 Vol.31 No.4

Runx2는 runt gene family에 속하는 전사조절 인자로써 뼈의 형성과 골아세포의 분화에 중요한 역할을 담당하고 있다. Runx2-haploinsufficency는 쇄골의 저형성 및 두개 봉합의 지연을 특징으로 하는 쇄골두개 이형성증을 일으키며, 치아에 있어서는 법랑질의 저형성, 영구치 맹출지연 등을 보인다. 이에, 치아의 발육 및 맹출에 미치는 Runx2의 영향을 알아보기 위해 in situ hybridization 방법으로 태생 1, 4, 7, 14. 21일 된 쥐의 하악 및 제1대구치를 사용하여 실험을 실시하였다. Runx2-full length는 태생 1일과 4일에 치낭 및 주위조직에 보이지만 Runx2-typeⅡ는 보이지 않았다. Runx2-full length는 태생 7일에 치관 교합면 부위의 법랑모세포에 발현하였고, 1주일 후인 태생 14일에는 백악법랑경계 상방의 치관인 접면 법랑모세포에서 발현되었다. 이에 반해 Runx2-typeⅡ는 법랑모세포에서 발현하지 않았다. 또한 태생 21일에서는 두가지 이성질체가 모두 하악골에서 발현을 보였다. 이런 결과를 종합해볼 때, Runx2-full length는 치아의 맹출과 연관이 있으며, 법랑모세포의 분화 및 이로 인한 법랑질형성에 영향을 주지만 Runx2-typeⅡ는 하악골의 형성에만 영향을 미치는 것으로 사료된다. Runx2 is a transcription factor in homologous with Drosophila runt gene and it is essential for bone formation during embryogenesis and a critical gene for osteoblast differentiation and osteoblast function. Runx2-haploinsufficency causes cleidocranial dysplasia (CCD). CCD is an autosomal-dominant inherited disorder characterized by hypoplastic clevicle and delayed ossification in fontanelles and wormian bones. Dental defects are possibly shown to CCD patients : multiple supernumerary teeth, irregular and compressed permanent tooth crowns, hypoplastic and hypomineralized defects in enamel and dentin, an excess of epithelial root remnants, the absence of cellular cementum, and abnormally shaped roots. In addition, delayed eruption of the secondary dentition is a constant finding. The aim of this study is to evaluate the role of Runx2 in the tooth development and eruption through analyzing the expression pattern of Runx2 by in situ hybridization during crown (late bell stage) and root formation of tooth, using postnatal day 1, 4, 7, 14 and 21 mice mandibular molar teeth. mRNA of Runx2-full length is expressed in dental follicle and surrounding tissue at postnatal day1 and 4. At post-natal day 7, it is expressed in ameloblasts of occlusal surface of enamel and bone area surrounding the tooth. In comparison with previous stage, at postnatal day 14, it is expressed in ameloblasts of proximal surface of enamel. At postnatal day 21 it's expression is observed only in bone area. mRNA of Runx2-typeⅡ is not expressed At postnatal day 1 and 7. At postnatal day 14 and 21, it's expression is observed in the bone area. In this study, we suggest that Runx2 have a relation of ameloblasts differentiation and an important role to tooth eruption made by dental follicle during intraosseous eruption stage. Also we can confirm that Runx2 has a role to bone formation.

Bisphosphonate가 조골세포 분화에 미치는 영향

이인순,김현정,류현모,김영진,남순현 대한소아치과학회 2000 大韓小兒齒科學會誌 Vol.27 No.2

본 실험은 bisphosphonate가 조골세포 분화 및 파골세포 분화에 미치는 영향을 알아보고자, etidronate와 alendronate를 조골세포에 투여하여 조골세포 전사인자인 Cbfa1, 조골세포 표시인자의 발현, 석회화된 골결절 형성을 평가하였다. Bisphosphonate가 조골세포의 석회화된 골결절 형성에 미치는 영향을 평가하기 위하여 배양액에 □ M의 etidronate 및 □ M의 alendronate를 첨가하였으며, 배양 15일 후에 alizarin red로 염색하여 관찰하였다. 또 조골세포의 분화에 미치는 bisphosphonate의 영향을 평가하고자 백서 두개관에서 얻은 조골세포에 etidronate □ M 및 alendronate □ M을 투여하고 배양 8일 후 총RNA를 수집하였고, 전기영동 및 Northern blot hybridization하여 Cbfa1, alkaline phosphatase, type Ⅰ collagen, osteopontin, osteocalcin의 발현을 조사하였다. 이상의 실험결과 다음과 같은 결론을 얻었다. 1.Etidronate는 농도 의존적으로 골결절 석회화를 억제하였으나, alendronate는 골석회화를 억제하지 않았다. 2.Etidronate는 Cbfa1의 발현을 농도 의존적으로 억제하였으나, alendronate는 오히려 촉진하였다. 3.Etidronate는 type Ⅰ collagen, osteocalcin 및 osteopontin의 발현을 농도 의존적으로 억제하였으나, alendronate는 오히려 증가시켰다. 4.Alkaline phosphatase의 발현은 사용된 etidronate와 alendronate에 의해 영향 받지 않았다. 이상의 결과에서 etidronate는 조골세포의 전사인자인 Cbfa1의 발현을 억제하며, 이에 의하여 조골세포의 분화표지인자인 type Ⅰ collagen, osteopontin 및 osteocalcin의 합성이 억제되고, 결과적으로 석회화된 골결절의 형성을 억제하는 것으로 사료된다. 주요어 : bisphosphonate, 조골세포, Cbfa1, Type Ⅰ교원질, alkaline phosphatase, osteopontin, osteocalcin, 석회화된 골결절

외상 후 뇌 지방색전증 1예

문정미,소정일,김용권,류진호,허탁,서정진,민용일 대한응급의학회 2001 대한응급의학회지 Vol.12 No.2

Post-traumatic fat embolism was first reported by Zenker in 1862, Von Bergmann reported the first clinical diagnosis of the fat embolism syndrome in 1873. Fat embolism has been associated with traumatic or non-traumatic disorders. Fat embolization after long bone trauma is probably common as a subclinical event. The diagnosis of fat embolism syndrome is based on the patient's history, is supported by clinical signs of pulmonary, cerebral, and cutaneous dysfunction, and is confirmed by the demonstration of arterial hypoxemia in the abscence of other disorders. Two different mechanisms cause fat to embolize: direct entry of deposit fat into the blood stream and agglutination of endogenous or exogenous plasma fat. MRI can detect a cerebral fat embolism with a higher sensitivity than cerebral CT. We report a case of post-traumatic cerebral fat embolism without pulmonary involvement, and we present a review of the literature. A 16-year girl had a traffic accident and pelvic bone fracture. Forty eight hours later severe trauma become stuporous without a focal neurological deficit. The patient received supportive therapy, and her condition improved throughout her hospital course. She was discharged with good condition after a 30-day hospital stay.

FGF signaling이 연골 형성에 미치는 영향

박충제,이상원,남순현,김영진,류현모,김현정 大韓小兒齒科學會 2003 大韓小兒齒科學會誌 Vol.30 No.4

막내골화와 연골내골화 등의 정상적인 골격 성장은 섬유아세포 성장인자 (FGF) 와 이들 수용체들 (FGFR) 에 의한 신호전달체계에 의해 조절된다. 또한 전사조절인자인 Runx2 (Cbfa1/Pebp2αA/AML3) 는 골아세포분화 뿐만 아니라 골형성에도 필수적인 유전자로 알려져 있다. FGF signaling이 mouse의 두 개관과 하악에서의 연골 형성에 어떤 영향을 미치고 있으며, 이 과정에서 Runx2의 연관성을 알아보고자 in vivo 및 in vitro 실험을 시행하여 다음과 같은 결과를 얻었다. 두 개관의 하악을 Alcian blue 염색한 결과 시상두개봉합부 연골은 태생16일부터, Meckel's 연골은 태생11일부터 형성되기 시작하였다. 이들 연골세포들의 성사을 알아보기위한 in situ hybridization 결과 시상두개봉합부 연골 및 Meckel's 연골 모두에서 type Ⅱ collagen은 발현되었으나, Type X collagen은 발현되지 않았다. Runx2 mRNA는 시상두개봉합부 연골과 Meckel's 연골 모두에서 발현되지 않았지만, 이들 연골들의 가장자리를 둘러싸고 있는 독특한 발현양상을 나타내었다. 두개 봉합부에서의 FGF2 protein의 국소적 적용은 두개봉합부 하방의 연골형성을 억제하였다. 또한 하악의 Meckel's 연골 발생부위에 FGF2 protein의 국소적 적용 역시 Meckel's 연골의 형성을 억제하였다. FGF2 protein은 시상두개봉합부상의 bead 주위로 Runx2의 발현을 유도하였다. 이 결과들을 종합해볼 때, FGF signaling은 골아세포와 연골아세포가 공존하고 있는 조직에서의 연골 형성을 억제하고 있음을 시사해 주고 있으며, 이 과정에서 FGF signaling은 부분적으로 Runx2 유전자의 발현을 조절하므로써 연골세포의 증식과 분화에 관여할 것으로 사료된다. Figroblast growth factor (FGF) / FGF receptor (FGFR) mediated signaling is required for skeletogenesis including intramembranous and endochondral ossifications. Runx2 (Cbfa1/Pebp2αA/AML3) is an essential transcription factor for osteoblast differentiation and bone formation. Murine calvaria and mandible are concurrently undergoing both intramembranous bone and cartilage formations in the early development stage. However the mechanism by which these cartilage formations are regulated remains unclear. To elucidate the effect of FGF signaling on development of cranial sutural catilage and Meckel's cartilage and to understand the role of Runx2 in these processs, we have done both in vivo and in vitro experiments. Alcian blue staining showed that cartilage formation in sagittal suture beings from embryonic state 16 (E16), Meckel's cartilage formation in mandible from E12. We analyzed by in situ hybridization the characteristics of cartilage cells that type Ⅱ collagen, not type X collagen, was expressed in sagittal sutural cartilage and Meckel's cartilage. In addition, Runx2 was not expressed in Meckel's cartialge as well as sagittal sutural cartilage, except specific expression pattern only surrounding both cartilages. FGF signaling pathway was further examined in vitro. Beads soaked in FGF2 placed on the sagittal suture and mandible inhibited both sutural and Meckel's cartilage formations. We next examined whether Runx2 gene lies in FGF siganling pathway during regulation of catilage formation. These results suggest that FGF signaling inhibits formations of sagittal sutural and Meckel's cartilages, also propose that FGF siganling is involved in the proliferation and differentiation of chondroblasts through regulating the transcription factor Runx2.

두개골 및 두개봉합부 초기발육과정에서의 전사조절인자인 Msx2와 DIx5의 역할

송민호,박미현,남순현,김영진,류현모,김현정 大韓小兒齒科學會 2003 大韓小兒齒科學會誌 Vol.30 No.3

두개봉합부의 조기융합으로 일컬어지는 craniosynostosis는 두개봉합부에서의 골아세포의 조기분화 및 석회화의 결과로 나타나는 선천성 발육이상이다. 최근 유전학적 연구에 의하면 homeobox gene인 Msx2의 변이에 의해 Boston-type craniosynostosis가 야기되며, 또한 Dlx5 homozygote mutant mouse의 표현형에서 두개골의 골화지연을 포함한 다양한 두개안면부위의 이상을 발견하였다는 보고가 있었다. 게다가 Msx2와 Dlx5 homeodomain protein의 상호작용에 의해 성숙골아세포의 표지자인 osteocalcin의 전사를 조절할 수 있다는 사실이 알려져 있다. 이러한 일련의 결과들은 Msx2, Dlx5 및 osteocalcin 유전자들이 두개골의 골화과정과 두개봉합부의 형태발생에 중요한 역할을 담당하고 있음을 제시해주고 있다. 두개골의 성장과 두개봉합부의 형태발생시 이러한 유전자들의 기능을 알아보기위해 mouse의 태생기 (E15-E18) 동안 osteocalcin, Msx2, 및 Dlx5 유전자들의 발현양상을 조사하였다. Osteocalcin은 E15부터 두정골의 골막에서 관찰되었으며, 발생시기가 후기일수록 강한 발현양상을 나타내었다. Msx2는 시상봉합부의 미분화간엽조직과 osteogenic front에서 강하게 발현되었으며 경막과 hair follicle에서도 관찰되었다. Dlx5는 osteogenic front를 포함한 두정골의 골막에서 강하게 발현되었으나 시상봉합부의 미분화간엽조직에서는 발현되지않아, Msx2와는 발현양상의 차이를 나타내었다. 이 결과들을 종합해볼 때, Msx2와 Dlx5 유전자는 두개골과 두개봉합부의 성장발육과정에 중요한 역할을 담당하고 있으며, BMP signaling은 두 전사조절인자들을 조절하므로써 두개골의 골화과정과 두개봉합부의 형태발생 및 유지에 관여하고 있음을 제시해주고 있다. 특히 BMP signaling에 specific downstream gene인 Msx2 및 Dlx5의 발현양상의 차이는 골아세포의 분화시 이들 유전자가 각각의 독특한 기능을 가지고 있음을 시사해주고 있다. Craniosynostosis, known as a premature fusion of cranial sutures, is a developmental disorder characterized by precocious differentiation and mineralization of osteoblasts in the calvarial sutures. Recent genetic studies have demonstrated that mutation in the homeobox gene Msx2 causes Boston-type human craniosynostosis. Additionally, the phenotype of Dlx5 homozygote mutant mouse presents craniofacial abnormalities including a delayed ossification of calvarial bone. Furthemore transcription of osteocalcin, a mature osteoblast marker, is reciprocally regulated by the nomeodomain proteins Msx2 and Dlx5. These facts suggest important roles of osteocalcin, Msx2 and Dlx5 genes in the calvarial bone growth and suture morphogenesis. To elucidate the function of these molecules in the early morphogenesis of mouse cranial sutures, wer have first analyzed by in situ hybridization the expression of osteocalcin, Msx2 and Dlx5 genes in the developing parietal bone and sagittal suture of mouse calvaria during the embryonic (E15-E18) stage. Osteocalcin mRNA was found in the periosteum of parietal bones from E15, and gradually more highly expressed with aging. Msx2 mRNA was intensely expressed in the sutural mesenchyme, osteogenic fronts and midly expressed in the dura mater during the embryonic stage. Dlx5 mRNA was intensely expressed osteogenic fronts and the periostem of parietal bones. To further examine the upstream signaling molecules of transcription factor Msx2 and Dlx5, we have done in vitro experiments in E15.5 mouse calvarial explants. Interestingly, implantation of BMP2-, BMP4-soaked beads onto the osteogenic fronts after 48 hours organ culture induced etopic expressions of Msx2 and Dlx5 genes. On the other hand, overexpression of TGFβ1, GDF-6, -7, FGF-2, -4 and Shh did not induce the expression of Msx2 and Dlx5. Taken together, these data indicate that transcription factor Msx2 and Dlx5 play critical roles in the calvarial bone and suture development, and that BMP siganling is involved in the osteogenesis of calvarial bones and the maintenance of cranial sutures through these two transcriotpn factors. Furthermore, different expression patterns between Msx2 and Dlx5 suggest their specific functions in the osteoblast differentiation.

젊은 성인에게서 발생한 담낭선종 1례

류승환,김인호,오경석,이상혁,설상영,정정명,최하진,최영길,한상석 인제대학교 1995 仁濟醫學 Vol.16 No.1

담낭 선종의 빈도는 드물지만 악성변이의 가능성을 가지고 있다. 저자들은 젊은 성인에게서 초음파로 진단된 다양한 크기(0.3-2.5cm)의 담낭용종을 악성종양으로 의심하여 외과적 절제술을 시행한 결과 악성의 증거가 없었던 담낭선종 1례를 경험하였기에 이에 보고하는 바이다. Gall bladder adenoma is very rare, but it has possibility of malignant transformation. We had experienced a case of large gall bladder adenoma in young adult, iris finding was multiple variable sized(0.3-2.5cm), fixed echogenic density without sonic shadow in ultra sonogram. Because it had been highly suspected malignancy, surgical intervention was done. Postoperative microscopic finding shows compact glandular structure intervening delicate fibrous stroma, and there is no evidence of malignant characteristics such as stromal invasion or anaplasia. So, we report one case of large gall bladder adenoma treated by surgical intervention.