WordNet

executed with proper legal authority; "a binding contract"
the protective covering on the front, back, and spine of a book; "the book had a leather binding" (同)book binding, cover, back
strip sewn over or along an edge for reinforcement or decoration
the capacity to attract and hold something
match badly; match two objects or people that do not go together
a bad or unsuitable match
any of a large group of nitrogenous organic compounds that are essential constituents of living cells; consist of polymers of amino acids; essential in the diet of animals for growth and for repair of tissues; can be obtained from meat and eggs and milk and legumes; "a diet high in protein"
the 4th letter of the Roman alphabet (同)d
either not matched or unsuitably matched
(of a contest or contestants) not fairly matched as opponents; "vaudeville...waged an uneven battle against the church" (同)uneven

PrepTutorEJDIC

義務的な,拘束力ある / 〈U〉しばること;〈C〉しばる物 / 〈C〉製本,装丁 / 〈U〉縁(‘ふち')取り材料
…‘を'まずく(不釣り合いに)組み合わせる / まずい(不釣り合いな)組み合わせ
蛋白(たんばく)質
deuteriumの化学記号

UpToDate Contents

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1. 失語症患者へのアプローチ approach to the patient with aphasia
2. 大腸癌の分子遺伝学 molecular genetics of colorectal cancer
3. 小児や青年の不安障害：評価および診断 anxiety disorders in children and adolescents assessment and diagnosis
4. 小児や青年の不安障害：疫学、病因、臨床症状、および経過 anxiety disorders in children and adolescents epidemiology pathogenesis clinical manifestations and course
5. ミュアト－ル症候群 muir torre syndrome

English Journal

Mismatch repair protein hMSH2-hMSH6 recognizes mismatches and forms sliding clamps within a D-loop recombination intermediate.

Honda M1, Okuno Y, Hengel SR, Martín-López JV, Cook CP, Amunugama R, Soukup RJ, Subramanyam S, Fishel R, Spies M.Author information 1Department of Biochemistry, University of Iowa, Iowa City, IA 52242.AbstractHigh fidelity homologous DNA recombination depends on mismatch repair (MMR), which antagonizes recombination between divergent sequences by rejecting heteroduplex DNA containing excessive nucleotide mismatches. The hMSH2-hMSH6 heterodimer is the first responder in postreplicative MMR and also plays a prominent role in heteroduplex rejection. Whether a similar molecular mechanism underlies its function in these two processes remains enigmatic. We have determined that hMSH2-hMSH6 efficiently recognizes mismatches within a D-loop recombination initiation intermediate. Mismatch recognition by hMSH2-hMSH6 is not abrogated by human replication protein A (HsRPA) bound to the displaced single-stranded DNA (ssDNA) or by HsRAD51. In addition, ATP-bound hMSH2-hMSH6 sliding clamps that are essential for downstream MMR processes are formed and constrained within the heteroduplex region of the D-loop. Moreover, the hMSH2-hMSH6 sliding clamps are stabilized on the D-loop by HsRPA bound to the displaced ssDNA. Our findings reveal similarities and differences in hMSH2-hMSH6 mismatch recognition and sliding-clamp formation between a D-loop recombination intermediate and linear duplex DNA.
Proceedings of the National Academy of Sciences of the United States of America.Proc Natl Acad Sci U S A.2014 Jan 21;111(3):E316-25. doi: 10.1073/pnas.1312988111. Epub 2014 Jan 6.
High fidelity homologous DNA recombination depends on mismatch repair (MMR), which antagonizes recombination between divergent sequences by rejecting heteroduplex DNA containing excessive nucleotide mismatches. The hMSH2-hMSH6 heterodimer is the first responder in postreplicative MMR and also plays
PMID 24395779

Human CD19 and CD40L deficiencies impair antibody selection and differentially affect somatic hypermutation.

van Zelm MC1, Bartol SJ2, Driessen GJ3, Mascart F4, Reisli I5, Franco JL6, Wolska-Kusnierz B7, Kanegane H8, Boon L9, van Dongen JJ2, van der Burg M2.Author information 1Department of Immunology, Erasmus MC, Rotterdam, The Netherlands. Electronic address: m.vanzelm@erasmusmc.nl.2Department of Immunology, Erasmus MC, Rotterdam, The Netherlands.3Department of Immunology, Erasmus MC, Rotterdam, The Netherlands; Department of Pediatrics, Erasmus MC, Rotterdam, The Netherlands.4Immunobiology Clinic, Hôpital Erasme, and Laboratory of Vaccinology and Mucosal Immunity, Université Libre de Bruxelles, Brussels, Belgium.5Meram Medical Faculty, Department of Pediatric Immunology and Allergy, Necmettin Erbakan University, Konya, Turkey.6Group of Primary Immunodeficiencies, University of Antioquia, Medellín, Colombia.7Department of Immunology, Children's Memorial Health Institute, Warsaw, Poland.8Department of Pediatrics, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Japan.9Bioceros B.V., Utrecht, The Netherlands.AbstractBACKGROUND: Individuals with genetic defects in CD40 ligand (CD40L) or B-cell antigen receptor coreceptor molecules CD19 and CD81 suffer from an antibody deficiency. Still, these patients carry low levels of memory B cells and serum antibodies.
The Journal of allergy and clinical immunology.J Allergy Clin Immunol.2014 Jan 10. pii: S0091-6749(13)01778-8. doi: 10.1016/j.jaci.2013.11.015. [Epub ahead of print]
BACKGROUND: Individuals with genetic defects in CD40 ligand (CD40L) or B-cell antigen receptor coreceptor molecules CD19 and CD81 suffer from an antibody deficiency. Still, these patients carry low levels of memory B cells and serum antibodies.OBJECTIVE: We sought to assess why the remaining memory
PMID 24418477

Tumor mismatch repair immunohistochemistry and DNA MLH1 methylation testing of patients with endometrial cancer diagnosed at age younger than 60 years optimizes triage for population-level germline mismatch repair gene mutation testing.

Buchanan DD1, Tan YY, Walsh MD, Clendenning M, Metcalf AM, Ferguson K, Arnold ST, Thompson BA, Lose FA, Parsons MT, Walters RJ, Pearson SA, Cummings M, Oehler MK, Blomfield PB, Quinn MA, Kirk JA, Stewart CJ, Obermair A, Young JP, Webb PM, Spurdle AB.Author information 1Daniel D. Buchanan, Yen Y. Tan, Michael D. Walsh, Mark Clendenning, Alexander M. Metcalf, Kaltin Ferguson, Sven T. Arnold, Bryony A. Thompson, Felicity A. Lose, Michael T. Parsons, Rhiannon J. Walters, Sally-Ann Pearson, Joanne P. Young, Penelope M. Webb, and Amanda B. Spurdle, QIMR Berghofer Medical Research Institute, Herston; Yen Y. Tan and Andreas Obermair, University of Queensland School of Medicine, Brisbane; Margaret Cummings, University of Queensland Centre for Clinical Research, Herston, Queensland; Martin K. Oehler, Royal Adelaide Hospital, Adelaide, South Australia; Michael A. Quinn, Royal Women's Hospital, Melbourne, Victoria; Judy A. Kirk, Westmead Institute for Cancer Research, Westmead Millennium Institute, University of Sydney, Sydney, New South Wales; Colin J. Stewart, King Edward Memorial Hospital, Perth, Western Australia, Australia; and Penelope B. Blomfield, Royal Hobart Hospital, Hobart, Tasmania.AbstractPURPOSE: Clinicopathologic data from a population-based endometrial cancer cohort, unselected for age or family history, were analyzed to determine the optimal scheme for identification of patients with germline mismatch repair (MMR) gene mutations.
Journal of clinical oncology : official journal of the American Society of Clinical Oncology.J Clin Oncol.2014 Jan 10;32(2):90-100. doi: 10.1200/JCO.2013.51.2129. Epub 2013 Dec 9.
PURPOSE: Clinicopathologic data from a population-based endometrial cancer cohort, unselected for age or family history, were analyzed to determine the optimal scheme for identification of patients with germline mismatch repair (MMR) gene mutations.PATIENTS AND METHODS: Endometrial cancers from 702
PMID 24323032