• Proceedings of the Korean Institute of Electrical and Electronic Material Engineers Conference
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• 2008.06a
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• pp.202-202
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• 2008

실리콘 기판 위에 성장된 세륨 산화막(CeO2)은 고품질의 SOI(Silicon on Insulator)나 혹은 안정한 캐패시터 소자와 같은 반도체 소자에 대한 응용 가능성이 높아 여러 연구가 진행되어 왔다. 세륨 산화막은 형석 구조, 다시 말해서 대칭적인 큐빅 구조이며 화학적으로 안정한 물질이다. 또한, 세륨 산화막의 격자상수 (a = $5.411\AA$)는 실리콘의 격자상수 (a = $5.430\AA$) 와 비슷하며 큰 밴드갭(6eV) 및 높은 유전상수 ($\varepsilon$ = 26), 높은 열적 안전성을 지니고 있어 실리콘 기판에 사용된 기존 절연막인 사파이어나 질코늄 산화막보다 우수한 특성을 지니고 있다. 본 논문에서는 스퍼터링을 이용하여 세륨 산화막을 실리콘 기판 위에 형성하면서 기판가열 온도 조건을 각각 상온, $100^{\circ}C$, $200^{\circ}C$로 설정하였으며, 세륨 산화막의 증착 두께 조건을 각각 80nm, 120nm로 설정한 다음 퍼니스를 이용하여 $1100^{\circ}C$에서 1시간 동안 열처리를 거친 세륨 산화막의 결정화 형태 및 박막의 막질 상태를 각각 X선 회절 장치 (XRD) 및 주사전자현미경 (SEM)으로 관찰하였다.

• Journal of the korean academy of Pediatric Dentistry
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• v.35 no.3
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• pp.539-547
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• 2008

Apert syndrome is an autosomal dominant condition characterized by craniosynostosis, midface hypoplasia, and syndactyly of the hands and feet. It occurs in about 1 of every 65,000 to 160,000 births and is caused by a mutation in the fibroblast growth factor receptor 2(FGFR2) gene. Apert syndrome typically produces acrobrachycephaly(tower skull). The occiput is flattened, and there is a tall appearance to the fore head. Ocular proptosis is a characteristic finding, along with hypertelorism and downward slanting lateral palpebral fissures. The middle third of the face is markedly retruded and hypoplastic, resulting in a relative mandibular prognathism. The reduced size of the nasopharynx and narrowing of the posterior choana can lead to mouth breathing, contributing to an open-mouth apprance. Three fourths of all patients exhibit either a cleft of the soft palate or a bifid uvula. The maxillary hypoplasia leads to a V-shaped arch and crowding of the teeth. A 6-year-old male patient visited to the Department of Pediatric dentistry, Kangnung National University of Dental Hospital. He visited the hospital to get treatment of carious teeth. The purpose of this report is to present a specific dental manifestations about the apert syndrome.

• Journal of Applied Biological Chemistry
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• v.57 no.4
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• pp.379-386
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• 2014

Chromatin is an instructive DNA structure that can widely respond to external signals. An important change of chromatin is the modifications of histone for this regulation. There are accumulating lists of these modifications and the complexity of their action is gradually understood. It is evident that histone modifications play important roles in most biological processes that are involved in the expression or repression of DNA. The surface of nucleosomes is susceptible to multiplicity of modifications. Chromatin modifications can play either by eliminating chromatin contacts or by recruiting non-histone proteins to chromatin. Many of these regulations seem to be epigenetically inherited. Thus, histone modifications are closely correlated with many fundamental biological processes in animal, plant and microbial kingdoms. Failures of histone modification lead, in general, to defective chromosome condensation or decondensation, impeding many biological functions including development, maturation, and protection against various diseases.

• Korean Journal of Ichthyology
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• v.9 no.2
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• pp.228-234
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• 1997

This study was carried out to confirm the taxonomical status by comparison of morphological and chromosomal charateristics and cross breeding in the two types of black and yellow body color of Korean mandarin fish, Siniperca sherzeri from Han River, Korea. Black and yellow types of Korean mandarin fish were similar in having 90-98 lateral line scale pores, 13 dorsal fin rays and XII XIII spines, 9 anal fin rays and 15 pectoral fin rays, but yellow type was differ from blacks type by yellow body color pattern. Diploid chromosome and arm number (fundamental number, NF) of the two types were the same to 2n=48 and NF=52. Karyotypes in the two types are consisted of 2 pairs submetacentric chromosome and 22 pairs of acro and/or telocentric chromosome. The black type females of Siniperca scherzeri were artificially crossed with yellow type males and black type males, respectively. The progenies from each cross breeding produced the normal individuls that possessed with parent types in the body color pattern. These data suggest that two types of Korean mandarin fish were same species, and yellow type was mutant by albino.

• Clinical and Experimental Pediatrics
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• v.51 no.7
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• pp.771-774
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• 2008

Familial hypokalemic periodic paralysis (hypoPP) is a rare inherited channelopathy that often presents with episodic weakness accompanied by hypokalemia. Thus far, mutations in the gene encoding two ion channels (CACNL1A3, L-type calcium channel alpha-1 subunit and SCN4A, a sodium channel type IV alpha subunit) have been identified. Several cases of familial hypoPP in children have been reported in Koreans, but there are only a few cases with identified mutations. We report a 12-year-old boy and his affected mother with hypoPP who has a heterozygous G to A substitution at codon 1239 in exon 30 of the CACNL1A3 gene that causes a change from arginine to histidine (Arg1239His, CACNL1A3). This mutation is common among Caucasians; however, it has not yet been reported in Koreans. The patients were treated with oral acetazolamide and potassium replacement and were instructed to avoid precipitating factors. After the medication and lifestyle modification, the paralytic attacks significantly decreased.

• Journal of Life Science
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• v.19 no.10
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• pp.1484-1488
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• 2009

Familial hypokalemic periodic paralysis (HOKPP) is an autosomal dominant muscle disorder characterized by episodic attacks of muscle weakness with concomitant hypokalemia. Mutations in either a calcium channel gene (CACNA1S) or a sodium channel gene (SCN4A) have been shown to be responsible for this disease. The combination of sarcolemmal depolarization and hypokalemia has been attributed to abnormalities of the potassium conductance governing the resting membrane potential. To understand the pathophysiology of this disorder, we examined both mRNA and protein levels of delayed rectifier potassium channel genes, KCNQ3 and KCNQ5, in skeletal muscle fibers biopsied from patients with HOKOur results showed an increase in the cytoplasmic level of KCNQ3 protein in patients' cells exposed to 50 mM external concentration of potassium. However, mRNA levels of both channel genes did not show significant change in the same condition. Our results suggest that long term exposure of skeletal muscle cells in HOKPP patients to high extracellular potassium alters the KCNQ3 localization, which could possibly hinder the normal function of this channel protein. These findings may provide an important clue to understanding the molecular mechanism of familial hypokalemic periodic paralysis.

• Journal of Sasang Constitutional Medicine
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• v.12 no.1
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• pp.84-100
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• 2000

Are the body and th spirit to different things? How individual ability and feeling displays in a human being and what correation between the two lise physiologically? Namely, what determines the external and the internal world? By what physiological functions and circulations, it makes possible to indciate individual's characteristic? These kinds of questions in constitutional medicine is able us lead to the following approach.

• Journal of Life Science
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• v.20 no.3
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• pp.457-461
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• 2010

Familial hypokalemic periodic paralysis (HOKPP) is an autosomal dominant disorder characterized by reversible flaccid paralysis and intermittent hypokalemia. Although it has been reported that decreased activity in the $K_{ATP}$ channels of the skeletal muscle cell membrane plays a role in the pathogenesis of HOKPP, a clear mechanism has not yet been established. This study aimed to investigate the molecular biological mechanism underlying the decreased activity of $K_{ATP}$ channels in the skeletal muscles of familial HOKPP patients by studying the levels of the $K_{ATP}$ channel subunit Kir6.2. We found that when cells obtained from healthy individuals (normal cells) and HOKPP patients (patient cells) were treated with 4 mM potassium buffer, there was no quantitative change in the KCNJ11 mRNA levels and no difference in the Kir6.2 protein expression in the cytosol and cell membrane. On the other hand, when 1 mM potassium buffer was used, normal cells showed decreased expression of KCNJ11 mRNA as well as decreased expression of Kir6.2 protein in the cell membrane. However, patient cells treated with the same buffer showed no quantitative change in the levels of KCNJ11 mRNA or in the levels of Kir6.2 protein in the cytosol and cell membrane. Thus, in HOKPP patients, the Kir6.2 protein cannot be transported from the cell membrane to the cytosol, leading to closure of the $K_{ATP}$ channels, induction of depolarization, and subsequently, to the paralytic symptoms observed in the patient. Our findings thus provide new insights into the pathogenesis of HOKPP.