• Journal of Chest Surgery
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• 제30권4호
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• pp.363-372
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• 1997

본 연구는 1986년 6월 3일부터 1995년 12월 31일까지 서울대학교 어린이 병원 흉부외과에서 경험한 144례의 대동맥 교약증 환아를 대상으로, 술후 결과에 영향을 미치는 여러 가지 요소들을 분석하였다. 환아의 평균 연령은 15.73+32.43(범 위 0.1-191.0, 중앙값=3.3)개월이 었고, 이중 11)례(78.5%)의 환아는 영아, 25례(17.4%)는 신생아였다. 환아를 대동맥궁 협 착 부위와 동반 심기형에 따라(제 1형:국소 협착, 제2형:대동맥 헙부 협착, 제3형 :대동맥 협부 및 횡대동맥궁 협착, h:심실중격결손증 동반, B:기타 복 잡 심기 형 동반) 9가지로 분류한 결과, 1, IA, IB, I, IIA, IIB, III, IIIA, IIIB형이 각각 25, 9, 6, 24, 35, 15, 4, 19, 7례 였다. 수술방법은 쇄골하동맥편 교약성형술(subclavian-flap coarctoplasty, SFC: 60례), 절단 및 문합술(resection and anastomo sis, R&A: 44례), 확장된 대동맥성형술(extended aortoplasty, Ex-Ao: 26 례), 덮개포편술(onlay patch, Onlay: 14례)이 사용되었다. 총수술 사망률은 16.0%(23/144)였고, 수술 사망률을 높이는 인자로 협착부위(I, II, III형) 동반 심기형(0, A, B), 환아의 연령, 수술방법, 단계수술 \ulcorner부 등이 분석되었는데 이중 횡대동맥궁협착을 동반하는 III형(I형 사망률=2.5%(1/40), II형=17.6% (13/74), III형=30%(9/30); p(0.01), B형(0형 사망률=3.8%(2/53), A형 =15.9%(10/63), B형 =39.3%(11/28); p(0.01) 등이 의미있는 위험 인자였다. 생존환아 121례는 술후 평균 29.1+28.8(범위 0-129.2)개월 외래 추 적되 었으며 이중 술후 협착을 보였던 경우는 18례로 14.9%의 헙착률은 보였다. 생존환자중 77례의 환자 (I형 20명. ll형 42명, 111형 15명)에서 술전, 술후 3개월 이내, 술후 6개월이후의 심에코도상의 대동맥 각 부위 크기에 관한 자료의 입수가 가능하였으며 이를토대로무명동맥 직근위부의 상행대동맥 직경에 대 한 대동맥협부 직경의 비율(대동맥협부지수)및 경동맥부위의 횡대동맥 직경비율(횡대동맥지수)을구하 여 형태 별로 술전, 수술 직후 6개월이상 경과후의 대동맥 크기 변화의 양상을 관찰하였다. 제 I, II, III형 모두에서 술전에 비하여 술후 평균 대동맥협부지수의 의미있는 증가가 관찰되었으며(p<0.01),제 III형에서는 횡대동맥지수의 의미있는 증가도 관찰되었다(p<0.01). 재헙착으로 진단된 I, II형의 수술직후 대 동맥협부지수와 111형의 횡대동맥 지수는 비협착군에 비하여 의미있게 작았는데 이는 아마도수술 당시 협 착 부위의 완전제거가 이루어지지 않은 것이 원인이라고 사료되었다. 본 분석에서는 어린 연령(3개월 이하), 3개월이하에 시행한 쇄골하동맥편 교약성형술이 의미있는 재협착의 위험요소로 밝혀졌다. 결론 적으로 저자등은 본연구를 통하여 대동맥협부지수, 횡대동맥 지수 등이 개개 대동맥교약 환아의 해부학 적, 임상적 특징을 파악하는데 도움이 되는 도구라는 사실을 발견하였고 아울러 교약의 해부학적 특성, 동반 심기 형, 연령, 수술방법 등이 수술사망 및 재협착에 영향한다는 사실을 입증하였다.

• Journal of Periodontal and Implant Science
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• 제42권3호
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• pp.73-80
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• 2012

Purpose: The purpose of this study was to investigate the effects of the immunosuppressants FK506 and cyclosporin A (CsA) on the osteogenic differentiation of rat mesenchymal stem cells (MSCs). Methods: The effect of FK506 and CsA on rat MSCs was assessed in vitro. The MTT assay was used to determine the deleterious effect of immunosuppressants on stem cell proliferation at 1, 3, and 7 days. Alkaline phosphatase (ALP) activity was analyzed on days 3, 7, and 14. Alizarin red S staining was done on day 21 to check mineralization nodule formation. Real-time polymerase chain reaction (RT-PCR) was also performed to detect the expressions of bone tissue-specific genes on days 1 and 7. Results: Cell proliferation was promoted more in the FK506 groups than the control or CsA groups on days 3 and 7. The FK506 groups showed increased ALP activity compared to the other groups during the experimental period. The ALP activity of the CsA groups did not differ from the control group in any of the assessments. Mineralization nodule formation was most prominent in the FK506 groups at 21 days. RT-PCR results of the FK506 groups showed that several bone-related genes-osteopontin, osteonectin, and type I collagen (Col-I)-were expressed more than the control in the beginning, but the intensity of expression decreased over time. Runx2 and Dlx5 gene expression were up-regulated on day 7. The effects of 50 nM CsA on osteonectin and Col-I were similar to those of the FK506 groups, but in the 500 nM CsA group, most of the genes were less expressed compared to the control. Conclusions: These results suggest that FK506 enhances the osteoblastic differentiation of rat MSCs. Therefore, FK506 might have a beneficial effect on bone regeneration when immunosuppressants are needed in xenogenic or allogenic stem cell transplantation to treat bone defects.

• Archives of Reconstructive Microsurgery
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• 제6권1호
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• pp.29-38
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• 1997

A peripheral nerve when approximation of the ends imparts tension at the anastomosis and with a relatively long segment defect after excision of neuroma and neurofibroma cannnot be repaired by early primary suture. The one of the optimistic reconstruction method of severed peripheral nerves is to restore tension-free continuity at the repair site putting an autogenous nerve graft into the neural gap despite of ancipating motor or sensory deficit of the donor nerve area. To overcome the deficit of the autogenous nerve graft, several other conduits supplying a metabolically active environment which is able to support axon regeneration and progression, providing protection against scar invasion, and guiding the regrowing axons to the distal stump of the nerve have been studied. An author have used ipsilateral femoral vein, ipsilateral femoral vein filled with fresh thigh muscle, and autogenous sciatic nerve for the sciatic nerve defect of around 10 mm in length to observe the regeneration pattern in rat by light and electron microscopy. The results were as follows. 1. Light microscopically regeneration pattern of nerve fibers in the autogenous graft group was more abundant than vein graft and vein filled with muscle group. 2. On ultrastructural findings, the proxial end of the graft in various groups showed similar regenerating features of the axons, myelin sheaths, and Schwann cells. The fascicular arrangement of the myelinated and unmyelinated fibers was same regardless of the type of conduits. There were more or less increasing tendency in the number and the diameter of myelinated fibers correlated with the regeneration time. 3. In the middle of the graft, myelinated nerve fibers of vein filled with muscle group were more in number and myelin sheath was thinner than in the venous graft, but the number of regenerating axons in autogenous nerve graft was superior to that in both groups of the graft. The amount of collagen fibrils and amorphous materials in the endoneurial space was increased to elapsed time. 4. There was no difference in regenerating patterns of the nerve fibers of distal end of the graft. The size and shape of the myelinated nerve fbers were more different than that of proximal and middle portion of the graft. From the above results, the degree of myelination and regenerating activity in autogenous nerve is more effective and active in other types of the graft and there were no morphological differences in either ends of the graft regardless of regeneration time.

• Journal of Periodontal and Implant Science
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• 제45권1호
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• pp.30-35
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• 2015

Purpose: Implant beds with an insufficient amount of cortical bone or a loss of cortical bone can result in the initial instability of a dental implant. Thus, the objective of this study was to evaluate the effect of bone cement grafting on implant initial stability in areas with insufficient cortical bone. Methods: Two different circumferential defect depths (2.5 mm and 5 mm) and a control (no defect) were prepared in six bovine rib bones. Fourteen implants of the same type and size ($4mm{\pm}10mm$) were placed in each group. The thickness of the cortical bone was measured for each defect. After the implant stability quotient (ISQ) values were measured three times in four different directions, bone cement was grafted to increase the primary stability of the otherwise unstable implant. After grafting, the ISQ values were measured again. Results: As defect depth increased, the ISQ value decreased. In the controls, the ISQ value was $85.45{\pm}3.36$ ($mean{\pm}standard$ deviation). In circumferential 2.5-mm and 5-mm defect groups, the ISQ values were $69.42{\pm}7.06$ and $57.43{\pm}6.87$, respectively, before grafting. These three values were significantly different (P<0.001). After grafting the bone cement, the ISQ values significantly increased to $73.72{\pm}8.00$ and $67.88{\pm}10.09$ in the 2.5-mm and 5.0-mm defect groups, respectively (P<0.05 and P<0.001). The ISQ value increased to more than double that before grafting in the circumferential 5-mm defect group. The ISQ values did not significantly differ when measured in any of the four directions. Conclusions: The use of bone cement remarkably increased the stability of the implant that otherwise had an insufficient level of stability at placement, which was caused by insufficient cortical bone volume.

• International Journal of Oral Biology
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• 제32권3호
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• pp.85-91
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• 2007

Dlx3 is a homeodomain protein and is known to playa role in development and differentiation of many tissues. Deletion of four base pairs in DLX3 (NT3198) is causally related to tricho-dento-osseous (TDO) syndrome (OMIM # 190320), a genetic disorder manifested by taurodontism, hair abnormalities, and increased bone density in the cranium. Although the observed defects of TDO syndrome involves bone, little is known about the role of Dlx3 in bone remodeling process. In this study, we examined the effect of wild type DLX3 (wtDlx3) expression on osteoclast differentiation and compared it with that of 4-BP DEL DLX3 (TDO mtDlx3). To examine whether Dlx3 is expressed during RANKL-induced osteoclast differentiation, RAW264.7 cells were cultured in the presence of receptor activator of nuclear factor-B ligand (RANKL). Dlx3 protein level increased slightly after RANKL treatment for 1 day and peaked when the fusion of prefusion osteoclasts actively progressed. When wtDlx3 and TDO mtDlx3 were overexpressed in RAW264.7 cells, they enhanced RANKL-induced osteoclastogenesis and the expression of osteoclast differentiation marker genes such as calcitonin receptor, vitronectin receptor and cathepsin K. Since osteoclast differentiation is critically regulated by the balance between RANKL and osteoprotegerin (OPG), we examined the effect of Dlx3 overexpression on expression of RANKL and OPG in C2C12 cells in the presence of bone morphogenetic protein 2. Overexpression of wtDlx3 enhanced RANKL mRNA expression while slightly suppressed OPG expression. However, TDO mtDlx3 did not exert significant effects. This result suggests that inability of TDO mtDlx3 to regulate expression of RANKL and OPG may contribute to increased bone density in TDO syndrome patients. Taken together, it is suggested that Dlx3 playa role as a positive regulator of osteoclast differentiation via up-regulation of osteoclast differentiation-associated genes in osteoclasts, as well as via increasing the ratio of RANKL to OPG in osteoblastic cells.

• Journal of Periodontal and Implant Science
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• 제32권2호
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• pp.389-402
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• 2002

BMP can induce ectopic bone formation when implanted into sites such as rat muscle and can greatly enhance healing of bony defects when applied exogenously. In addition, BMP stimulated osteoblastic differentiation in vitro in various types of cells. The aim of this study was to investigate the effect of recombinant human bone morphogenetic protein(rhBMP-2) on the proliferation and osteoblastic differentiation of human periodontal ligament cells and gingival fibroblasts. The cell number and alkaline phosphatase activity were measured in 3 experimental groups of human periodontal ligament cells and gingival fibroblasts (control group, rhBMP-2 50ng/ml group, and rhBMP-2 100ng/ml group) at 1 and 2 weeks after culture. At the same time, total RNA of cultured cells were extracted and reverse trascription polymerase chain reaction(RT-PCR) was performed to determine the expression of mRNA of bone matrix protein. RhBMP-2 had no effect on the cell proliferation of human periodontal ligament cells and gingival fibroblasts. Alkaline phosphatase activity was elevated significantly by rhBMP-2 in both cells. And periodontal ligament cells showed significantly higher alkaline phosphatase activity than gingival fibroblasts. ${\beta}$-actin, type I collagen, alkaline phosphatase, BMP-2 mRNA were expressed in all of the samples. Osteopontin, osteocalcin mRNA were expressed in all periodontal ligament cell groups, and rhBMP-2 50ng/ml group, rhBMP-2 100ng/ml group of 2 week culture period of gingival fibroblasts. Bone sialoprotein mRNA was only expressed in rhBMP-2 50ng/ml group and rhBMP-2 100ng/ml group of 2-week culture period. These results suggest that rhBMP-2 stimulates osteoblastic differentiation in human periodontal ligament cells and gingival fibroblasts in vitro.

• Journal of Periodontal and Implant Science
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• 제35권2호
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• pp.345-357
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• 2005

Prostaglandin plays a significant role in the local control of bone metabolism associated with periodontal disease. ${\Delta}^{12}-PGJ_2$ is a natural $PGD_2$ metabolite that is formed in vivo in the presence of plasma. It is known for ${\Delta}^{12}-PGJ_2$ to stimulate calcification in osteoblastic cells. Bone morphogenetic protein(BMP) stimulated osteoblastic differentiation in various types of cells and greatly enhanced healing of bony defects. The purpose of this study was to evaluate the effect of rhEMP-2 on ${\Delta}^{12}-PGJ_2$ induced osteoblastic differentiation and mineralization in vitro. A human osteosarcoma cells line Saos-2 were cultured. In the test groups, 10-7M of ${\Delta}^{12}-PGJ_2$ or mixture of 10-8M of ${\Delta}^{12}-PGJ_2$ and 100ng/ml of rhBMP-2 or 100ng/ml of rhEMP-2 were added to culture media. After 1 day, 2 days and 4 days of culture period, the cell number was measured. Alkaline phosphatase activity was measure at 3 days. Reverse transcription polymerase chain reaction(RT-PCR) was performed to determine the expression of mRNA of bone matrix protein at 8 hours, 1 day and 7 days. The ability to produce mineralized nodules in rat osteoblasts(MC3T3-E1) was evaluated at 21 days. The results were as follows : 1. rhEMP-2 or mixture of rhBMP-2 and ${\Delta}^{12}-PGJ_2$ inhibited cell proliferation of human osteosarcoma cells. 2. rhEMP-2 or mixture of rhBMP-2 and ${\Delta}^{12}-PGJ_2$ stimulated alkaline phosphatase activity significantly higher than ${\Delta}^{12}-PGJ_2$ alone. 3. rhBMP-2 or mixture of rhEMP-2 and ${\Delta}^{12}-PGJ_2$ stimulated mineralization compared to ${\Delta}^{12}-PGJ_2$ alone. 4. mRNA of alkaline phosphatase, BMP-2, cbfa 1, Type I collagen were detected in the group treated with ${\Delta}^{12}-PGJ_2$/rhBMP-2, rhBMP-2 alone, ${\Delta}^{12}-PGJ_2$ alone. These results show that mixture of ${\Delta}^{12}-PGJ_2$ and rhBMP-2 causes more bone formation than ${\Delta}^{12}-PGJ_2$ alone while the bone formation effects of mixture of ${\Delta}^{12}-PGJ_2$ and rhBMP-2 are less than those of rhBMP-2 alone. Further researches would be necessary to clarify the interactions of these agents.

• Archives of Plastic Surgery
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• 제37권6호
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• pp.823-826
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• 2010

Purpose: Meningomyelocele is the most common type of neural tube defect disease. Early surgical treatment is recommended to prevent central nervous system infection. Several reconstruction methods were reported previously regarding surgical wound defect closure following meningomyelocele excision. In this article, we report two successful patients using the bilateral fasciocutaneous sliding V-Y advancement flap as a covering for meningomyelocele defects. Methods: Two patients with meningomyelocele were evaluated. Both patients were male and received their operations on the 1st and 4th day of life. After neurosurgeons completed their part of the operation, the V-Y advancement flap was used to close the defect. Initially a bilateral V-shape incision design was made on the skin such that the base of the V-flap measures identical to the size of the wound defect. An incision was made down to the fascia in order to allow the V-flaps to slide into the defect. Subfascial dissection was performed up to 1/3 to 1/4 the length of the V-flap from the wound while minimizing injury to the perforating vessels. Results: Both patients were treated successfully and there was no evidence of complication in 2 months follow up. Conclusion: Several reconstruction methods such as local flaps, skin graft and myocutaneous flaps were reported regarding meningomyelocele surgical wound defect closure. Bilateral fasciocutaneous sliding V-Y advancement flap is an easy method without involving the underlying muscles or a secondary skin graft in a short operation time. Therefore we recommend this treatment option for reconstruction of the wound defect following meningomyelocele excision.

• 한국표면공학회:학술대회논문집
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• 한국표면공학회 2018년도 춘계학술대회 논문집
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• pp.102-102
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• 2018

Electronic industry had required the finer size and the higher performance of the device. Therefore, 3-D die stacking technology such as TSV (through silicon via) and micro-bump had been used. Moreover, by the development of the 3-D die stacking technology, 3-D structure such as chip to chip (c2c) and chip to wafer (c2w) had become practicable. These technologies led to the appearance of HBM (high bandwidth memory). HBM was type of the memory, which is composed of several stacked layers of the memory chips. Each memory chips were connected by TSV and micro-bump. Thus, HBM had lower RC delay and higher performance of data processing than the conventional memory. Moreover, due to the development of the IT industry such as, AI (artificial intelligence), IOT (internet of things), and VR (virtual reality), the lower pitch size and the higher density were required to micro-electronics. Particularly, to obtain the fine pitch, some of the method such as copper pillar, nickel diffusion barrier, and tin-silver or tin-silver-copper based bump had been utillized. TCB (thermal compression bonding) and reflow process (thermal aging) were conventional method to bond between tin-silver or tin-silver-copper caps in the temperature range of 200 to 300 degrees. However, because of tin overflow which caused by higher operating temperature than melting point of Tin ($232^{\circ}C$), there would be the danger of bump bridge failure in fine-pitch bonding. Furthermore, regulating the phase of IMC (intermetallic compound) which was located between nickel diffusion barrier and bump, had a lot of problems. For example, an excess of kirkendall void which provides site of brittle fracture occurs at IMC layer after reflow process. The essential solution to reduce the difficulty of bump bonding process is copper to copper direct bonding below $300^{\circ}C$. In this study, in order to improve the problem of bump bonding process, copper to copper direct bonding was performed below $300^{\circ}C$. The driving force of bonding was the self-annealing properties of electrodeposited Cu with high defect density. The self-annealing property originated in high defect density and non-equilibrium grain boundaries at the triple junction. The electrodeposited Cu at high current density and low bath temperature was fabricated by electroplating on copper deposited silicon wafer. The copper-copper bonding experiments was conducted using thermal pressing machine. The condition of investigation such as thermal parameter and pressure parameter were varied to acquire proper bonded specimens. The bonded interface was characterized by SEM (scanning electron microscope) and OM (optical microscope). The density of grain boundary and defects were examined by TEM (transmission electron microscopy).

• Journal of Microbiology and Biotechnology
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• 제26권8호
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• pp.1446-1451
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• 2016

Clostridium difficile toxin A causes acute gut inflammation in animals and humans. It is known to downregulate the tight junctions between colonic epithelial cells, allowing luminal contents to access body tissues and trigger acute immune responses. However, it is not yet known whether this loss of the barrier function is a critical factor in the progression of toxin A-induced pseudomembranous colitis. We previously showed that NADH:quinone oxidoreductase 1 (NQO1) KO (knockout) mice spontaneously display weak gut inflammation and a marked loss of colonic epithelial tight junctions. Moreover, NQO1 KO mice exhibited highly increased inflammatory responses compared with NQO1 WT (wild-type) control mice when subjected to DSS-induced experimental colitis. Here, we tested whether toxin A could also trigger more severe inflammatory responses in NQO1 KO mice compared with NQO1 WT mice. Indeed, our results show that C. difficile toxin A-mediated enteritis is significantly enhanced in NQO1 KO mice compared with NQO1 WT mice. The levels of fluid secretion, villus disruption, and epithelial cell apoptosis were also higher in toxin A-treated NQO1 KO mice compared with WT mice. The previous and present results collectively show that NQO1 is involved in the formation of tight junctions in the small intestine, and that defects in NQO1 enhance C. difficile toxin A-induced acute inflammatory responses, presumably via the loss of epithelial cell tight junctions.