WT症候群
WordNet
- the 23rd letter of the Roman alphabet (同)w, double-u
- a pattern of symptoms indicative of some disease
- a complex of concurrent things; "every word has a syndrome of meanings"
PrepTutorEJDIC
- Watt / West; Western
- wolfram(=tungsten)の原子記号
- (疾患の徴候となる一群の)症徴候,症候群 / (事件・社会的状態などのパターンを示す)徴候形態
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English Journal
- Intraperitoneal adoptive transfer of mesenchymal stem cells enhances recovery from acid aspiration acute lung injury in mice.
- Mauri T1, Zambelli V2, Cappuzzello C3, Bellani G2, Dander E3, Sironi M4, Castiglioni V5, Doni A4, Mantovani A4, Biondi A2,3, Garlanda C4, D'amico G3, Pesenti A6,7.
- Intensive care medicine experimental.Intensive Care Med Exp.2017 Dec;5(1):13. doi: 10.1186/s40635-017-0126-5. Epub 2017 Mar 6.
- PMID 28265979
- Aging rather than aneuploidy affects monoamine neurotransmitters in brain regions of Down syndrome mouse models.
- Dekker AD1, Vermeiren Y2, Albac C3, Lana-Elola E4, Watson-Scales S4, Gibbins D4, Aerts T5, Van Dam D2, Fisher EMC6, Tybulewicz VLJ7, Potier MC3, De Deyn PP8.
- Neurobiology of disease.Neurobiol Dis.2017 Sep;105:235-244. doi: 10.1016/j.nbd.2017.06.007. Epub 2017 Jun 15.
- PMID 28624415
- The effect of fibroblast growth factor 15 deficiency on the development of high fat diet induced non-alcoholic steatohepatitis.
- Schumacher JD1, Kong B1, Pan Y2, Zhan L3, Sun R2, Aa J2, Rizzolo D1, Richardson JR1, Chen A4, Goedken M1, Aleksunes LM1, Laskin DL1, Guo GL5.
- Toxicology and applied pharmacology.Toxicol Appl Pharmacol.2017 Sep 1;330:1-8. doi: 10.1016/j.taap.2017.06.023. Epub 2017 Jul 1.
- PMID 28673684
Japanese Journal
- 骨髄異形成症候群に合併したクームス陰性自己免疫性溶血性貧血
- 永井 正,上原 英輔,斉藤 桐子,亀崎 豊実,小澤 敬也,室井 一男,神田 善伸
- 日本輸血細胞治療学会誌 61(4), 468-473, 2015
- … に重要である.今回,MDSにクームス陰性AIHAを合併した症例を経験した.MDSに対してDNAメチル化阻害薬azacitidineの投与を行ったところ,造血不全の著明な改善,末梢血芽球の消失およびMDSの進行マーカーであるWT1 mRNAの低下を認めた.興味深いことに,azacitidine療法の過程で溶血所見が著明に改善し,azacitidineによりAIHAも同時に改善したものと考えられた.MDSに溶血性貧血を合併した例では,直接クームス試験陰性の場合 …
- NAID 130005100034
- The Susceptibilities of Human Ether-à-Go-Go-Related Gene Channel with the G487R Mutation to Arrhythmogenic Factors
- Hisajima Nozomi,Hata Yukiko,Kinoshita Koshi [他],Fukushima Toshiki,Nishida Naoki,Kano Masanobu,Tabata Toshihide
- Biological and Pharmaceutical Bulletin 38(5), 781-784, 2015
- … hERG mutation may cause hERG channel malfunction, leading to long QT syndrome and other arrhythmic disorders. … Here we used a voltage-clamp technique to compare the effects of the major arrythmogenic factors on wild-type hERG [hERG(WT)] and hERG(G487R) channel currents (IhERG) in HEK-293T cells. …
- NAID 130005068093
- Opposing Roles of Nitric Oxide and Rho-Kinase in Lipid Metabolism in Mice
- Noda Kazuki,Godo Shigeo,Saito Hiroki,Tsutsui Masato,Shimokawa Hiroaki
- The Tohoku Journal of Experimental Medicine 235(3), 171-183, 2015
- … Nitric oxide (NO) exerts beneficial effects on lipid metabolism through activation of hepatic sterol regulatory element-binding protein (SREBP)-2, a transcriptional factor for cholesterol metabolism and expression of LDL receptor, while Rho-kinase, an effecter protein of small G protein, RhoA, contributes to the pathogenesis of metabolic syndrome through suppressing the whole body energy consumption. … In the present study, we used male wild-type (WT) mice and mice lacking three isoforms of NO synthase (NOSs−/−). …
- NAID 130004822441
Related Links
- WT limb blood syndrome symptoms, causes, diagnosis, and treatment information for WT limb blood syndrome (WT limb blood syndrome) with alternative diagnoses, full-text book chapters, misdiagnosis, research treatments ...
- 1. Acta Paediatr Jpn. 1995 Feb;37(1):108-12. A patient with WT syndrome and Castleman disease. Vergin C, Cetingül N, Kavakli K, Oztop S, Ozkinay F, Coker M, Nişli G, Soydan S, Balik E, Akar O. Faculty of Medicine, Department ...
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- 英
- WT syndrome
参考
- The WT syndrome--a "new" autosomal dominant pleiotropic trait of radial/ulnar hypoplasia with high risk of bone marrow failure and/or leukemia.
- Gonzalez CH, Durkin-Stamm MV, Geimer NF, Shahidi NT, Schilling RF, Rubira F, Opitz JM.AbstractWe report 2 families with an autosomal dominant syndrome of limb and hematologic abnormalities. The W Family was ascertained through AW, a 13-year-old girl, who was purportedly born without congenital anomalies and who was normal until 11 1/2 years when she developed acute lymphoblastic leukemia. She died 2 years later with CNS involvement. Her chromosomes, studied in the first weeks after diagnosis of the disease, were apparently normal. Her father had clinodactyly of both 5th fingers and was found to have panmyelocytopenia refractory to all treatment at 26 years. He died within a year of the onset of his anemia. This man's oldest brother was born with congenital malformations of the elbows and the hands and was healthy until 38 years when he was also found to have an "idopathic anemia" and panmyelocytopenia which was refractory to treatment except for transfusions; he died at age 42 years. Both men were initially thought to have the Fanconi anemia syndrome. Their mother died at 71 years of leukemia. DT, the propositus of the second family, was noted to have malformations of both hands at birth. At 21 months he had anemia for which he received transfusions. Family history reveals that several people on the paternal side have severe hand anomalies and a history of childhood anemia. The paternal grandfather died at age 51 of acute monocytic leukemia. Barring genetic heterogeneity, we think that the trait in the W and T families in the same. It is a pleiotropic autosomal dominant mutant which affects radial and ulnar development of the upper limbs and is associated with a relatively high risk of transient or permanent bone marrow arrest with or without leukemia. We propose the hypothesis that apparently increased risk of leukemia to Fanconi heterozygotes actually represents admixture with the WT syndrome and that Fanconi heterozygotes may not have an increased risk of leukemia.
- Birth defects original article series.Birth Defects Orig Artic Ser.1977;13(3B):31-8.
- We report 2 families with an autosomal dominant syndrome of limb and hematologic abnormalities. The W Family was ascertained through AW, a 13-year-old girl, who was purportedly born without congenital anomalies and who was normal until 11 1/2 years when she developed acute lymphoblastic leukemia. Sh
- PMID 890097
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- 関
- wild strain、wild type、wild-type、wild-type strain、wildtype
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