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      • 비등방성 확산 필터링된 영상 슬라이스들의 볼륨 렌더링에 관한 연구

        신문걸,김태형,박용기,김두영 동아대학교 정보기술연구소 2001 情報通信硏究所論文誌 Vol.9 No.1

        The goals of this paper are not only to reduce of noise using anisotropic diffusion filter post-processing but also to represent 3-D image using 2-D image slices by volume rendering. A 3D shape image can be obtained as the 2-D images are continuously acquired, during the object is removed noise by filtering. The 3-D shape images are displayed on computer monitor by use of OpenGL Software.

      • KCI등재

        항정신병약물 사용 중인 정신분열병 환자에서 올란자판으로의 교체 방법에 관한 연구(II) : Comparison of Safety 안전성 비교

        안용민,권용실,권준수,민성호,박두병,양문정,소형석,송종호,신윤식,우행원,유범희,이홍석,정한용,한창환,김용식 大韓神經精神醫學會 2002 신경정신의학 Vol.41 No.5

        연구목적: 이 다기관 공동임상연구는 사용 중인 항정신병약물을 ’직접 교체 방법’또는 ’시작-감량 교체 방법’중 한 가지 방법으로 올란자핀으로 교체한 후, 안정성 측면에서 두 교체 방법 간의 비교와 교체후의 변화를 관찰하기 위한 것이다. 방법: 국내 13개 병원의 입원 및 외래에 내원한 환자들 중 ICD-10 지단기준으로 정신분열병에 해당되며, 임상적으로 항정신병약물 교체가 필요한 환자를 대상으로 하였다. 두 가지 교체 방법 중 한 가지를 무작위로 피험자에 적용하였으며, ’직접 교체 방법’에 배정된 경우에는 사용중인 항정신병약물을 일시에 중단하고 10㎎의 올란자핀을 바로 투여하였고, ’시작-감량 교체 방법’에 배정된 경우는 10㎎의 올란자핀 투여하고 2주에 걸쳐서 기존 약물을 감량하여 중단하였다. 올란자핀 사용기간은 총 6주이며, 용량은 5∼20㎎ 범위로 제한하였다. 한정성 평가를 위해서 체중, 생명징후, 자발적인 이상반응 복, 실험실 검사 그리고 Simpson-Angus Scale(SAS), Barnes akathisia rating scale(BARS), Abnormal involuntary movement scale(AIMS). Liverpool University neuroleptic side effect rating scale(LUNSERS)등을 이용하였다. 결과: 총 103명의 정신분열병 환자를 대상으로 하였다. 사용한 올란자핀의 용량, 벤조디아제핀의 병용률, 탈락률과 탈락 사유, 자발적인 이상반응 보고, 생명징후, 실험실 검사 그리고 대부분의 부작용 척도 상에서 임상적으로 의미 있는 차이를 두 교체 방법간에 발견하지 못하였다. 다만 AIMS의 감소는 ’직접 교체 방법’군에서 보다 적었고, 항콜린제의 병용률은 ’시작-감량 교체 방법’군에서 보다 많았다. 기저 상태에서 전체 피험자의 SAS와 BARS 점수는 각각 3.5점과 1.8점이었으며 70% 이상의 피험자가 고프로락틴 혈증을 보였다. 올란자핀으로 교체한 후, SAS, BARS, AIMS 점수의 유의한 감소가 있었으며 고프로락틴 혈증을 보인 피험자 분율도 약 30%이하로 감소하였다. 그러나 교체 방법과 상관없이 올란자핀 교체 후 유의한 체중 증가가 있었다. 결론: 이 연구를 통해 교체 방법에 관계없이 비교적 안전하고 용이하게 올란자핀으로 교체 할 수 있음을 알 수 있었다. 그리고 기존 항정신병약물을 올란자핀으로 교체함으로써 일부 부작용들을 줄일 수 있음을 간접적으로 관찰할 수 있었다. 하지만 이 연구는 여러 제한점과 문제점을 지니고 있기 때문에 보다 체계적인 연구를 통해 검정이 필요하리라 생각된다. Objectives: This multicenter clinical trial involving 13 hospital sites compared the safely of switching to olanzapine between ’direct switching method’ and ’start-tapering switching method’. Method: This study included both inpatients and outpatients who fulfilled the criteria for schizophrenia as defined in the ICD-10, and were in need to be appropriate for switching antipsychotics. Subjects were randomly assigned to one of the two switching methods. For ’direct switching method’group, previous antipsychotics were abruptly discontinued and 10㎎ of olanzapine was administered, and previous antipsychotics was gradually tapered for 2 weeks. Olanzapine was used for 6 weeks and the dose was adjusted within the range of 5-20㎎. The safety of switching to olanzapine was measured with vital sings including body weight, adverse events reported spontaneously, laboratory tests, and various scales such as Simpson-Angus Scale(SAS), Barnes Akathisia Rating Scale(BARS). Abnormal Involuntary Movement Scale(AIMS), and Liverpool University Neuroleptic Side Effect Rating Scale(LUNSERS). Results: 103 patients were switched to olanzapine in this study. The comparison between two switching methods did not show any significant difference in the dosage of olanzapine used, the concomitant use of benzodiazepine, the rate and reasons of drop-out, the adverse events, vital signs, laboratory tests, and most scales for measuring side-effects. However, the decrease in AIMS scores was significantly lower in ’direct switching method’ group, and the concomitant use of anticholinergics was comparatively greater in ’start-tapering switching method’ group. At baseline, SAS and BARS scores were 3.5 and 1.8 points respectively, and more than 70% of the subjects showed hyperprolactinemia. After switching to olanzapine, SAS, BARS, and AIMS scores were significantly decreased and the proportion of the patients with hyperprolactinemia was also decreased to less than 30%. However significant weight gain after the treatment of olanzapine was observed regardless of switching method. Conclusion: This study may suggest that switching to olanzapine can be done with relatively high safety regardless of switching methods and olanzapine can significantly decrease some side-effects induced by other antipsychotics.

      • KCI등재SCISCIE

        Novel Promoter Polymorphism in RUNX2 Is Associated with Serum Triglyceride Level.

        Shin, Hyoung Doo,Jeon, Jae-Pil,Park, Byung Lae,Bae, Joon Seol,Nam, Hye-Young,Shim, Sung-Mi,Park, Kyong Soo,Han, Bok-Ghee Korean Society for Molecular Biology 2008 Molecules and cells Vol.26 No.5

        <P>Much research evidence supports the hypothesis that chronic, low-grade inflammation related to innate immunity may play an important role in the pathophysiology of type 2 diabetes mellitus (T2DM). Runt-related transcription factor 2 (RUNX2; MIM# 600211) acts as a scaffold that controls the integration, organization, and assembly of nucleic acids. To examine whether the novel promoter variant in RUNX2 is associated with the risk of T2DM and related phenotypes, RUNX2-742G > T was genotyped in 378 T2DM patients and 382 normal controls recruited in the Korean T2DM Study. Statistical analysis revealed that RUNX2-742G > T was associated with serum triglyceride level (TG) in nondiabetic controls, although it was not associated with the risk of T2DM. Individuals who carry T/T, T/G, and G/G genotypes had the highest (2.061 +/- 0.20), intermediate (2.01 +/- 0.19), and the lowest (1.97 +/- 0.18) levels of log [TG (mmol/l)] (P = 0.007), respectively. Our data on this important variant of RUNX2 suggest that lipid metabolism might be affected by genetic polymorphisms in the promoter region.</P>

      • Replication of the genetic effects of IFN regulatory factor 5 ( <i>IRF5</i> ) on systemic lupus erythematosus in a Korean population

        Shin, Hyoung Doo,Sung, Yoon-Kyoung,Choi, Chan-Bum,Lee, Soo Ok,Lee, Hye Won,Bae, Sang-Cheol BioMed Central 2007 Arthritis research & therapy Vol.9 No.2

        <P>Recently, two studies provided convincing evidence that IFN regulatory factor 5 (<I>IRF5</I>) gene polymorphisms are significantly associated with systemic lupus erythematosus (SLE) in several white populations. To replicate the association with SLE in an Asian population, we examined the genetic effects in our SLE cohort from a Korean population. A total of 1,565 subjects, composed of 593 cases and 972 controls, were genotyped using the TaqMan<SUP>® </SUP>(Applied Biosystems, Foster City, CA, USA) method. The genetic effects of polymorphisms on the risk of SLE were evaluated using χ<SUP>2 </SUP>tests and a Mantel–Haenszel meta-analysis. Statistical analysis revealed results in the Korean population were similar to the previous reports from white populations. The rs2004640 T allele had a higher frequency in SLE cases (0.385) than controls (0.321; odds ratio (OR) = 1.32, <I>P </I>= 0.0003). In combined analysis, including all seven independent cohorts from the three studies so far, robust and consistent associations of the rs2004640 T allele with SLE were observed. The estimate of risk was OR = 1.44 (range, 1.34–1.55), with an overall <I>P </I>= 1.85 × 10<SUP>-23 </SUP>for the rs2004640 T allele. The haplotype (rs2004640T–rs2280714T) involved in both the alternative splice donor site and the elevated expression of IRF5 also had a highly significant association with SLE (pooled, <I>P </I>= 2.11 × 10<SUP>-16</SUP>). Our results indicate that the genetic effect on the risk of SLE mediated by IRF5 variants can be generally accepted in both white and Asian populations.</P>

      • SCIESCOPUSKCI등재
      • Association between colony-stimulating factor 1 receptor gene polymorphisms and asthma risk

        Shin, Eun Kyong,Lee, Shin-Hwa,Cho, Sung-Hwan,Jung, Seok,Yoon, Sang Hyuk,Park, Sung Woo,Park, Jong Sook,Uh, Soo Taek,Kim, Yang Ki,Kim, Yong Hoon,Choi, Jae-Sung,Park, Byung-Lae,Shin, Hyoung Doo,Park, Ch Springer-Verlag 2010 HUMAN GENETICS Vol.128 No.3

        <P>Colony-stimulating factor 1 receptor (<I>CSF1R</I>) is expressed in monocytes/macrophages and dendritic cells. These cells play important roles in the innate immune response, which is regarded as an important aspect of asthma development. Genetic alterations in the <I>CSF1R</I> gene may contribute to the development of asthma. We investigated whether <I>CSF1R</I> gene polymorphisms were associated with the risk of asthma. Through direct DNA sequencing of the <I>CSF1R</I> gene, we identified 28 single nucleotide polymorphisms (SNPs) and genotyped them in 303 normal controls and 498 asthmatic patients. Expression of <I>CSF1R</I> protein and mRNA were measured on CD14-positive monocytes and neutrophils in peripheral blood of asthmatic patients using flow cytometry and real-time PCR. Among the 28 polymorphisms, two intronic polymorphism (+<I>20511C</I>><I>T</I> and +<I>22693T</I>><I>C</I>) were associated with the risk of asthma by logistic regression analysis. The frequencies of the minor allele at <I>CSF1R</I> +<I>20511C</I>><I>T</I> and +<I>22693T</I>><I>C</I> were higher in asthmatic subjects than in normal controls (4.6 vs. 7.7%, <I>p</I> = 0.001 in co-dominant and dominant models; 16.4 vs. 25.8%, <I>p</I> = 0.0006 in a recessive model). <I>CSF1R</I> mRNA levels in neutrophils of the asthmatic patients having the +<I>22693CC</I> allele were higher than in those having the +<I>22693TT</I> allele (<I>p</I> = 0.026). Asthmatic patients with the +<I>22693CC</I> allele also showed significantly higher <I>CSF1R</I> expression on CD14-positive monocytes and neutrophils than did those with the +<I>22693TT</I> allele (<I>p</I> = 0.045 and <I>p</I> = 0.044). The +<I>20511C</I>><I>T</I> SNP had no association with <I>CSF1R</I> mRNA or protein expression. In conclusion, the minor allele at <I>CSF1R</I> +<I>22693T</I>>C may have a susceptibility effect in the development of asthma, via increased <I>CSF1R</I> protein and mRNA expression in inflammatory cells.</P><P><B>Electronic supplementary material</B></P><P>The online version of this article (doi:10.1007/s00439-010-0850-3) contains supplementary material, which is available to authorized users.</P>

      • Independent Association of Tumor Necrosis Factor Polymorphism with Type 1 Diabetes Susceptibility

        Shin, Hyoung Doo,Yang, Sei Won,Kim, Duk Hee,Park, Yongsoo Wiley (New York Academy of Sciences) 2008 Annals of the New York Academy of Sciences Vol.1150 No.1

        <P>The contribution of SNPs in TNF genes to type 1 diabetes (T1D) is not well established and may be confounded by the linkage disequilibrium within the HLA genes. Seven SNPs in the TNF genes (TNFA and TNFB) were genotyped in a Korean cohort (398 T1D patients and 1422 nondiabetic controls), along with HLA DRB1, DQB1, and MICA (MHC class I chain-related genes). Among them, three SNPs (TNFB+318, TNFA-857, and TNFA-308) and two common TNF haplotypes showed significant association with the risk of T1D (P= 5 x 10(-3)-10(-5)). T1D patients were more often heterozygous for the alleles at the TNFB+318 (OR = 1.7, P= 10(-3)) and TNFA-308 (OR = 1.7, P < 10(-5)) than were the controls. Genetic association analyses of the DRB1, DQB1, and MICA alleles with the risk of T1D revealed dramatic associations in several alleles as expected. Independent analyses to discern the genetic effects of TNF polymorphisms on the risk of T1D suggested that these genetic influences might be not totally dependent on the nearby HLA genes. Our results support the hypothesis that two susceptibility loci in the MHC (one in the HLA class II and another in the central MHC region) act epistatically to increase susceptibility to T1D.</P>

      • Association of ZDHHC8 polymorphisms with smooth pursuit eye movement abnormality

        Shin, Hyoung Doo,Park, Byung Lae,Bae, Joon Seol,Park, Tae Joon,Chun, Ji Yong,Park, Chul Soo,Sohn, Jin-Wook,Kim, Bong-Jo,Kang, Yeo-Hwa,Kim, Jae Won,Kim, Ki-Hoon,Shin, Tae-Min,Woo, Sung-Il Wiley Subscription Services, Inc., A Wiley Company 2010 American Journal of Medical Genetics. Part B Vol.b153 No.6

        <P>The zinc finger DHHC domain-containing protein 8 (ZDHHC8) is located in the 22q11 microdeletion region and may contribute to the behavioral deficit associated with 22q11 deletion syndrome. Although polymorphisms of ZDHHC8 have been reported to be associated with the risk of schizophrenia, those associations are still controversial. This study was performed to validate the genetic association of ZDHHC8 polymorphisms with the risk of schizophrenia, and also to scrutinize the association with smooth pursuit eye movement (SPEM) abnormality in a Korean population. Five SNPs of ZDHHC8 were genotyped by TaqMan assay. Their genetic effects on the risk of schizophrenia were analyzed in 354 patients and 396 controls using allele-based χ<SUP>2</SUP> analyses. Association of ZDHHC8 polymorphisms with SPEM abnormality among 166 schizophrenic patients were analyzed using multiple regressions. No ZDHHC8 polymorphisms were found to be associated with the risk of schizophrenia. However, four SNPs and one haplotype (ht4) were strongly associated with the risk of SPEM abnormality even after multiple correction (P = 0.00005–0.0007, P<SUP>corr</SUP> = 0.0001–0.002). The results of the present study provide the first evidence that ZDHHC8 on the 22q11 locus might have influence on SPEM function of schizophrenia patients in a Korean population and may provide a new clue for understanding differential effects of candidate genes in schizophrenia. © 2010 Wiley-Liss, Inc.</P>

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