192 research outputs found

    Hydrated copper and gold monovalent cations: Ab initio study

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    To understand the hydration phenomena of noble transition metals, we investigated the structures, hydration energies, electronic properties, and spectra of the Cu+(H3O)(1-6) and Au+ (H2O)(1-6) clusters using ab initio calculations. The coordination numbers of these clusters are found to be only two, which is highly contrasted to those of Ag+ (H2O)(n) (which have the coordination numbers of 3-4) as well as the hydrated alkali metal ions (which have the coordination numbers of similar to6). For the possible identification of their interesting hydration structures, we predict their IR spectra for the OH stretch modes. (C) 2005 American Institute of Physics.open384

    Allelic and Haplotypic Diversity of HLA-A, -B, -C, and-DRB1 Genes in Koreans Defined by High-resolution DNA Typing

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    ๋ฐฐ๊ฒฝ : HLA ํ˜•๋ณ„์€ ํ˜ˆ์ฒญํ•™์  ์ˆ˜์ค€(generic level)์—์„œ๋„ ๋‹คํ˜•์„ฑ์ด ์‹ฌํ•˜์ง€๋งŒ ๋Œ€๋ฆฝ์œ ์ „์ž ์ˆ˜์ค€์—์„œ๋Š” ๋”์šฑ ์‹ฌํ•œ ๋‹คํ˜•์„ฑ์„ ๋ณด์ด๊ณ  ์ธ์ข… ๊ฐ„์— ํฐ ์ฐจ์ด๋ฅผ ๋‚˜ํƒ€๋‚ด๋Š” ๊ฒƒ์œผ๋กœ ์•Œ๋ ค์กŒ๋‹ค. ๋ณธ ์—ฐ๊ตฌ์—์„œ๋Š” ๊ณ ํ•ด์ƒ๋„ DNA ๊ฒ€์‚ฌ๋ฒ•์„ ์ด์šฉํ•˜์—ฌ ํ•œ๊ตญ์ธ์—์„œ HLA๋Œ€๋ฆฝ์œ ์ „์ž ํ˜•๋ณ„๊ณผ ์ผ๋ฐฐ์ฒดํ˜•์˜ ์ข…๋ฅ˜ ๋ฐ ๋นˆ๋„๋ฅผ ์•Œ์•„๋ณด๊ณ ์ž ํ•˜์˜€๋‹ค. ๋ฐฉ๋ฒ• : ๊ฑด๊ฐ•ํ•œ ํ•œ๊ตญ์ธ 474๋ช…์„ ๋Œ€์ƒ์œผ๋กœ HLA-A, -B, -C, -DRB1 ์œ ์ „์ž์— ๋Œ€ํ•ด ๋‘ ๋‹จ๊ณ„์˜ ๊ฒ€์‚ฌ๋กœ ๋Œ€๋ฆฝ์œ ์ „์ž(4์ž๋ฆฌ์ˆ˜) ํ˜•๋ณ„ ๋ถ„์„์„ ์‹ค์‹œํ•˜์˜€๋‹ค. 1๋‹จ๊ณ„๋กœ ํ˜ˆ์ฒญํ•™์  ์ˆ˜์ค€์˜ ํ˜•๋ณ„๊ฒ€์‚ฌ๋ฅผ ํ˜ˆ์ฒญํ•™์  ๊ฒ€์‚ฌ๋ฒ•์ด๋‚˜ sequence-specific oligonucleotide(PCR-SSO) ๋ฐฉ๋ฒ•์œผ๋กœ ์‹œํ–‰ํ•˜์˜€๊ณ , ๊ทธ ๋‹ค์Œ ๋‹จ๊ณ„๋กœ ๋Œ€๋ฆฝ์œ ์ „์ž ํ˜•๋ณ„๊ฒ€์‚ฌ๋ฅผ class I์€ exon 2์™€ exon3, DRB1์€ exon 2์— ๋Œ€ํ•ด single-strand conformation polymorphism (PCR-SSCP) ๋˜๋Š” ์ง์ ‘์—ผ๊ธฐ์„œ์—ด๋ถ„์„๋ฒ•์„ ์ด์šฉํ•˜์—ฌ ์‹ค์‹œํ•˜์˜€๋‹ค. HLA ๋Œ€๋ฆฝ ์œ ์ „์ž์˜ ์œ ์ „์ž ๋นˆ๋„, ์ผ๋ฐฐ์ฒดํ˜• ๋นˆ๋„, ์—ฐ์‡„๋ถˆํ‰ํ˜• ๊ฐ’์€ maximum likelihood ์›๋ฆฌ์— ๊ทผ๊ฑฐํ•œ ์ œ11์ฐจ ๊ตญ์ œ์กฐ์ง์ ํ•ฉ์„ฑ์›Œํฌ์ˆ ์ปดํ“จํ„ฐ ํ”„๋กœ๊ทธ๋žจ์„ ์ด์šฉํ•˜์—ฌ ์‚ฐ์ถœํ•˜์˜€๋‹ค. ๊ฒฐ๊ณผ : ํ•œ๊ตญ์ธ์—์„œ ๊ฒ€์ถœ๋œ HLA-A, -B, -C, DRB1 ๋Œ€๋ฆฝ์œ ์ „์ž ํ˜•๋ณ„์€ ๊ฐ๊ฐ 21, 40, 22, 29์ข…์ด์—ˆ๋‹ค. ์ด ์ค‘์— ์œ ์ „์ž ๋นˆ๋„ 10% ์ด์ƒ์„ ๋ณด์ธ ๋Œ€๋ฆฝ์œ ์ „์ž ํ˜•๋ณ„(๋นˆ๋„์ˆœ ๋‚˜์—ด)์€ A*02:01, A*24:02, A*33:03; B*51:01; C*01:02, C*03:03; RB1*09:01๋“ฑ์ด์—ˆ๋‹ค. HLA ์ผ๋ฐฐ์ฒดํ˜•์˜ ๋ถ„์„ ๊ฒฐ๊ณผ 0.5% ์ด์ƒ์˜ ๋นˆ๋„๋ฅผ ๋‚˜ํƒ€๋‚ด๋Š” 2-์œ ์ „์ž์ขŒ ์ผ๋ฐฐ์ฒดํ˜•์€ A-C 44์ข…, B-C 42์ข…, A-B 51์ข…, B-DRB1 52์ข…์ด์—ˆ๊ณ , 3-์œ ์ „์ž์ขŒ ์ผ๋ฐฐ์ฒดํ˜•์€ A-C-B 42์ข…, A-B-DRB1 34์ข…์ด์—ˆ๋‹ค. ํ•œ๊ตญ์ธ์—์„œ ๋นˆ๋„ 1% ์ด์ƒ์˜ A-B-DR ์ผ๋ฐฐ์ฒดํ˜•์€ 13์ข…์œผ๋กœ, ์ „์ฒด ์ผ๋ฐฐ์ฒดํ˜•์˜ 26.0%๋ฅผ ์ฐจ์ง€ํ•˜์˜€๊ณ , 2% ์ด์ƒ์œผ๋กœ ๊ฐ€์žฅ ํ”ํ•œ A-B-DR ์ผ๋ฐฐ์ฒดํ˜•์€ A*33:03-B*44:03-DRB1*13:02 (3.7%), A*33:03-B*44:03-DRB1*07:01 (3.0%), A*33:03-B*58:01-DRB1*13:02 (3.0%), A*24:02-B*07:02-DRB1*01:01 (2.8%), A*30:01-B*13:02-DRB1* 07:01 (2.3%), A*11:01-B*15:01-DRB1*04:06 (2.2%) ๋“ฑ 6์ข…์ด์—ˆ๋‹ค. ๊ฒฐ๋ก  : ๋ณธ ์—ฐ๊ตฌ๋ฅผ ํ†ตํ•ด ํ•œ๊ตญ์ธ์˜ ๋Œ€๋ฆฝ์œ ์ „์ž ์ˆ˜์ค€์˜ HLA ํ˜•๋ณ„๊ณผ HLA ์ผ๋ฐฐ์ฒดํ˜• ๋นˆ๋„์— ๋Œ€ํ•œ ์ž๋ฃŒ๋ฅผ ์ œ์‹œํ•˜์˜€์œผ๋ฉฐ, ๋ณธ ์—ฐ๊ตฌ์˜ ๊ฒฐ๊ณผ๋Š” ํ•œ๊ตญ์ธ์—์„œ ์žฅ๊ธฐ์ด์‹, ์งˆํ™˜์—ฐ๊ด€์„ฑ ์—ฐ๊ตฌ, ์ธ๋ฅ˜์œ ์ „ํ•™์  ์—ฐ๊ตฌ ๋“ฑ์—์„œ ์ค‘์š”ํ•œ ๊ธฐ์ดˆ์ž๋ฃŒ๋กœ ์ด์šฉ๋  ์ˆ˜ ์žˆ์„ ๊ฒƒ์œผ๋กœ ๊ธฐ๋Œ€๋œ๋‹ค. Background : In this study, we used high-resolution DNA typing to investigate the distribution of HLA alleles and haplotypes in Koreans. Methods : HLA-A, -B, -C, and -DRB1 alleles were genotyped at the allelic (4-digit) level in 474 healthy Koreans. HLA genotyping was performed in two steps. Initially, serologic typing or generic-level DNA typing was performed using the FOR-sequence-specific oligonucleotide method, and then allelic DNA typing (exons 2 and 3 for class I, and exon 2 for DRB1) was carried out using the FOR-single-strand conformation polymorphism method or sequence-based typing. HLA allele and haplotype frequencies and linkage disequilibrium values were calculated by the maximum likelihood method using a computer program developed for the 11th International Histocompatibility Workshop. Results : A total of 21 HLA-A, 40 HLA-B, 22 HLA-C, and 29 HLA-DRB1 alleles were found in Koreans. The most frequent alleles in each locus with frequencies of >= 10% were, in decreasing order of frequency, as follows: A star 24:02, A star 02:01, A(star)33:03; B(star)51:01; C(star)01:02, C(star)03:03; and DRB1(star)09:01. The numbers of two- and three-locus haplotypes with frequencies of >0.5% were as follows: 44 A-C, 42 B-C, 51 A-B, 52 B-DRB1, 42 A-C-B, and 34 A-B-DRB1. Thirteen A-B-DRB1 haplotypes with frequencies of >= 1.0% comprised 26.0% of the total haplotypes. The six most common haplotypes were as follows: A(star)33:03-B(star)44:03-DRB1(star)3:02 (3.7%), A(star)33:03-B(star)44:03-DRB1(star)07:01 (3.0%), A(star)33:03-B(star)58: 01-DRB1(star)13:02 (3.0%), A(star)24:02-B(star)07:02-DRB1(star)01:01 (2.8%), A(star)30:01-B(star)13:02-DRB1(star)07:01 (2.3%), and A(star)11:01-B(star)15:01-DR81(star)04:06 (2.2%). Conclusions : The information obtained in this study can be used as basic data for Koreans in the fields of organ transplantation, disease association, and anthropologic studies. 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    A Case of Hypersensitivity to Mosquito Bite Associated with Epstein-Barr Viral Infection and Natural Killer Cell Lymphocytosis

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    Hypersensitivity to mosquito bites (HMB) is a disorder characterized by a necrotic skin reaction and generalized symptoms subsequent to mosquito bites. It has been suggested that HMB is associated with chronic Epstein-Barr virus (EBV) infection and natural killer cell leukemia/lymphoma. We describe here a Korean child who had HMB associated with chronic EBV infection and natural killer cell lymphocytosis. A 5-yr-old boy was suffered from necrotic skin lesions on the right ear lobe. Type A EB virus was detected from hlood cells and bone marrow biospy recognized hemophagocyrosis

    Evaluation of 28 Human Embryonic Stem Cell Lines for Use as Unrelated Donors in Stem Cell Therapy: Implications of HLA and ABO Genotypes

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    For human embryonic stem cells (hESCs) to be used clinically, it is imperative that immune responses evoked by hESCs and their derivates after transplantation should be prevented. Human leukocyte antigens (HLA) and ABO blood group antigens are important histocompatibility factors in graft rejection. HLA matching between recipient and unrelated donors, in particular, is important in improving outcomes in hematopoietic cell transplantation (HCT). We have established and successfully maintained 29 hESC lines and analyzed the HLA and ABO genotypes of these lines. HLA-A, -B, -C and -DR (DRB1) genotyping was performed by polymerase chain reaction (PCR) sequence-based typing and ABO genotyping was carried out by PCR restriction fragment length polymorphism methods. To determine what proportion of the Korean population would be covered by these cell lines in organ transplantation, 27 cell lines with HLA-A, -B, and -DR data were evaluated for HCT (cord blood) donors and 28 cell lines with HLA-DR and ABO data were evaluated for solid organ (kidney) transplantation donors, and then compared the data with those from 6,740 donated cord bloods. When <= 2 HLA mismatches are allowed for HCT, as currently accepted for cord blood transplantation, it was estimated that about 16% and 25% of the possible recipients can find one or more donor cell lines with mismatches at A, B, DRB1 allele level and at A, B antigen/DRB1 allele level, respectively. When HLA-DR antigen level matching and ABO compatibility was considered for solid organ (kidney) transplantation, it was estimated that about 29% and 96% of the possible recipients can find one or more ABO-compatible donor cell lines with 0 and 1 DR mismatches, respectively. We provided the first report on the HLA and ABO genotypes of hESC lines, and estimated the degree of HLA and ABO matching in organ transplantation for the Korean population.Yu JY, 2009, SCIENCE, V324, P797, DOI 10.1126/science.1172482Kaji K, 2009, NATURE, V458, P771, DOI 10.1038/nature07864Lee JY, 2010, FERTIL STERIL, V93, P976, DOI 10.1016/j.fertnstert.2008.10.017Holdsworth R, 2009, TISSUE ANTIGENS, V73, P95, DOI 10.1111/j.1399-0039.2008.01183.xLehec SC, 2009, CELL TRANSPLANT, V18, P941, DOI 10.3727/096368909X471323Oishi K, 2009, CELL TRANSPLANT, V18, P581Molne J, 2008, TRANSPLANTATION, V86, P1407, DOI 10.1097/TP.0b013e31818a6805Fernandes AM, 2010, CELL TRANSPLANT, V19, P509, DOI 10.3727/096368909X485067Stadtfeld M, 2008, SCIENCE, V322, P945, DOI 10.1126/science.1162494Wang GW, 2005, BIOCHEM BIOPH RES CO, V330, P934, DOI 10.1016/j.bbrc.2005.03.058Hoffman LM, 2005, NAT BIOTECHNOL, V23, P699, DOI 10.1038/nbt1102Li Y, 2005, BIOTECHNOL BIOENG, V91, P688, DOI 10.1002/bit.20536Vallier L, 2005, J CELL SCI, V118, P4495, DOI 10.1242/jcs.02553Taylor CJ, 2005, LANCET, V366, P2019Boyd AS, 2005, ADV DRUG DELIVER REV, V57, P1944, DOI 10.1016/j.addr.2005.08.004Ludwig TE, 2006, NAT BIOTECHNOL, V24, P185, DOI 10.1038/nbt1177Drukker M, 2006, STEM CELLS, V24, P221, DOI 10.1634/stemcells.2005-0188Priddle H, 2006, STEM CELLS, V24, P815, DOI 10.1634/stemcells.2005-0356Reubinoff BE, 2000, NAT BIOTECHNOL, V18, P399Amit M, 2000, DEV BIOL, V227, P271Xu CH, 2001, NAT BIOTECHNOL, V19, P971Drukker M, 2002, P NATL ACAD SCI USA, V99, P9864, DOI 10.1073/pnas.142298299Richards M, 2002, NAT BIOTECHNOL, V20, P933, DOI 10.1038/nbt726Bradley JA, 2002, NAT REV IMMUNOL, V2, P859, DOI 10.1038/nri934Amit M, 2003, BIOL REPROD, V68, P2150, DOI 10.1095/biolreprod.102.012583Li L, 2004, STEM CELLS, V22, P448Drukker M, 2004, TRENDS BIOTECHNOL, V22, P136, DOI 10.1016/j.tibtech.2004.01.003Thomson JA, 1998, SCIENCE, V282, P1145Petersdorf EW, 1999, CURR OPIN IMMUNOL, V11, P521Bodnar MS, 2004, STEM CELLS DEV, V13, P243Koivisto H, 2004, REPROD BIOMED ONLINE, V9, P330Rocha V, 2004, NEW ENGL J MED, V351, P2276Laughlin MJ, 2004, NEW ENGL J MED, V351, P2265Lee JB, 2005, BIOL REPROD, V72, P42, DOI 10.1095/biolrepod.104.033480Xu RH, 2005, NAT METHODS, V2, P185, DOI 10.1038/NMETH744Beattie GM, 2005, STEM CELLS, V23, P489, DOI 10.1634/stemcells.2004-0279Genbacev O, 2005, FERTIL STERIL, V83, P1517, DOI 10.1016/j.fertnstert.2005.01.086Oh SKW, 2006, CLIN EXP PHARMACOL P, V33, P489Skottman H, 2006, FEBS LETT, V580, P2875, DOI 10.1016/j.febslet.2006.03.083Xiao L, 2006, STEM CELLS, V24, P1476, DOI 10.1634/stemcells.2005-0299Stussi G, 2006, TRANSFUS APHER SCI, V35, P59, DOI 10.1016/j.transci.2006.05.009Takahashi K, 2006, CELL, V126, P663Guhr A, 2006, STEM CELLS, V24, P2187, DOI 10.1634/stemcells.2006-0053Klumpp TR, 2006, BONE MARROW TRANSPL, V38, P615, DOI 10.1038/sj.bmt.1705496Nakajima F, 2007, STEM CELLS, V25, P983, DOI 10.1634/stemcells.2006-0566Huangfu DW, 2008, NAT BIOTECHNOL, V26, P1269, DOI 10.1038/nbt.1502Petersdorf EW, 2008, CURR OPIN IMMUNOL, V20, P588, DOI 10.1016/j.coi.2008.06.014Chen YT, 2008, STEM CELLS DEV, V17, P853, DOI 10.1089/scd.2007.0226Park IH, 2008, CELL, V134, P877, DOI 10.1016/j.cell.2008.07.041Swijnenburg RJ, 2008, P NATL ACAD SCI USA, V105, P12991, DOI 10.1073/pnas.0805802105Unger C, 2008, HUM MOL GENET, V17, pR48, DOI 10.1093/hmg/ddn079Drukker M, 2008, SEMIN IMMUNOL, V20, P123, DOI 10.1016/j.smim.2007.11.002Revazova ES, 2008, CLONING STEM CELLS, V10, P11, DOI 10.1089/clo.2007.0063Mountford JC, 2008, TRANSFUSION MED, V18, P1, DOI 10.1111/j.1365-3148.2007.00807.xPark IH, 2008, NATURE, V451, P141, DOI 10.1038/nature06534Nakagawa M, 2008, NAT BIOTECHNOL, V26, P101, DOI 10.1038/nbt1374Buzzeo MP, 2008, CELL TRANSPLANT, V17, P489Kamani N, 2008, BIOL BLOOD MARROW TR, V14, P1, DOI 10.1016/j.bbmt.2007.11.003Saric T, 2008, CELLS TISSUES ORGANS, V188, P78, DOI 10.1159/000118784Navarro-Alvarez N, 2008, CELL TRANSPLANT, V17, P27KASTENBERG ZJ, 2008, TRANSPLANT REV ORLAN, V22, P215Lee SJ, 2007, BLOOD, V110, P4576, DOI 10.1182/blood-2007-06-097386Shaw BE, 2007, BLOOD, V110, P4560, DOI 10.1182/blood-2007-06-095265Strom S, 2007, HUM REPROD, V22, P3051, DOI 10.1093/humep/dem35Lin G, 2007, CELL RES, V17, P999, DOI 10.1038/cr.2007.97Crook JM, 2007, CELL STEM CELL, V1, P490Helming AM, 2007, PEDIATR BLOOD CANCER, V49, P313, DOI 10.1002/pbc.21025Cabrera CM, 2007, CELL BIOL INT, V31, P1072, DOI 10.1016/j.cellbi.2007.03.015Lei T, 2007, CELL RES, V17, P682, DOI 10.1038/cr.2007.61Okita K, 2007, NATURE, V448, P313, DOI 10.1038/nature05934Wernig M, 2007, NATURE, V448, P318, DOI 10.1038/nature05944Maherali N, 2007, CELL STEM CELL, V1, P55, DOI 10.1016/j.stem.2007.05.014Eapen M, 2007, LANCET, V369, P1947

    Effects of Korean Red Ginseng (Panax ginseng), urushiol (Rhus vernicifera Stokes), and probiotics (Lactobacillus rhamnosus R0011 and Lactobacillus acidophilus R0052) on the gutโ€“liver axis of alcoholic liver disease

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    AbstractBackgroundRoles of immune reaction and toll-like receptor-4 (TLR-4) have widely been established in the pathogenesis of alcoholic liver disease (ALD).MethodsWe evaluated the biologic efficacy of Korean Red Ginseng (KRG), urushiol, and probiotics (Lactobacillus rhamnosus R0011 and Lactobacillus acidophilus R0052) in mouse models of ALD. Sixty C57BL/6 mice were equally divided into six feeding groups for 10 weeks: normal diet, alcohol, control, alcoholย +ย KRG, alcoholย +ย urushiol, and alcoholย +ย probiotics. Alcohol was administered via a Lieberโ€“DeCarli liquid diet containing 10% alcohol. TLR-4 expression, proinflammatory cytokines, and histology, as well as the results of liver function tests were evaluated and compared.ResultsNo between-group differences were observed with regard to liver function. TLR-4 levels were significantly lower in the KRG, urushiol, and probiotics groups than in the alcohol group (0.37ย ยฑย 0.06ย ng/mL, 0.39ย ยฑย 0.12ย ng/mL, and 0.33ย ยฑย 0.07ย ng/mL, respectively, vs. 0.88ย ยฑย 0.31ย ng/mL; pย <ย 0.05). Interleukin-1ฮฒ levels in liver tissues were decreased among the probiotics and KRG groups. The tumor necrosis factor-ฮฑ level of liver tissue was decreased in the KRG group.ConclusionThe pathological findings showed that alcohol-induced steatosis was significantly reduced by KRG and urushiol. As these agents improve immunologic capacity, they may be considered in potential anti-ALD treatments

    Pattern of Hepatitis A Incidence According to Area Characteristics Using National Health Insurance Data

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    Objectives: Over the past several years, the incidence of hepatitis A infection has been increasing rapidly in the young-adult population in Korea. We examined the effects of area-level socioeconomic status and environmental hygiene on the incidence of hepatitis A. Methods: This study is based on the registered national population of Korea and the national health insurance data from 2004 to 2008. A total of 73 459 individuals were confirmed to have had hepatitis A. The standardized incidences of hepatitis A in 232 districts adjusted for sex and age of people were calculated for each year, and the rate ratios of the incidence rates were estimated according to area-level socioeconomic status and environmental hygiene using multiple Poisson regression models. Results: The incidence rates of hepatitis A infection were 15.6 (per 100 000) in 2004, 19.0 (per 100 000) in 2005, 27.2 (per 100 000) in 2006, 25.1 (per 100 000) in 2007, and 61.7 (per 100 000) in 2008. The analysis of the area-level effects showed that residential areas of the less deprived than other regions, areas with higher levels of education, and heavily populated areas were significantly associated with increased risk. Conclusions: There is a very strong possibility that both area-level socioeconomic status and environmental hygiene play a role in increasing the risk of hepatitis A infection in Korea. Therefore, to reduce hepatitis A infection, we need a nationwide strategy that considers these area-level characteristics
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