WordNet

exercising influence or control; "television plays a dominant role in molding public opinion"; "the dominant partner in the marriage"
(music) the fifth note of the diatonic scale
(of genes) producing the same phenotype whether its allele is identical or dissimilar
the 16th letter of the Roman alphabet (同)p
of or relating to an autosome; "autosomal gene"

PrepTutorEJDIC

『支配的な』,最も有力な / (位置が)群を抜いて高い,そびえ立つ / (手・目など左右のいずれかが)力のある / (遺伝で)優性の / (音階で)第5度音の,属音の / (遺伝の)優性形質 / 第5度音,属音
parking
phosphorusの化学記号

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

1. 常染色体優性多発性嚢胞腎の診断およびスクリーニング diagnosis of and screening for autosomal dominant polycystic kidney disease
2. 常染色体優性多発性嚢胞腎の経過および治療 course and treatment of autosomal dominant polycystic kidney disease
3. 常染色体優性多発性嚢胞腎の腎症状 renal manifestations of autosomal dominant polycystic kidney disease
4. 常染色体優性多発性嚢胞腎の腎外症状 extrarenal manifestations of autosomal dominant polycystic kidney disease
5. 小児における常染色体優性多発性嚢胞腎 autosomal dominant polycystic kidney disease in children

Utilizing magnetization transfer imaging to investigate tissue remodeling in a murine model of autosomal dominant polycystic kidney disease.

Kline TL1, Irazabal MV2, Ebrahimi B2, Hopp K2, Udoji KN1, Warner JD1, Korfiatis P1, Mishra PK3, Macura SI3, Venkatesh SK1, Lerman LO2, Harris PC2,3, Torres VE2, King BF1, Erickson BJ1.
Magnetic resonance in medicine.Magn Reson Med.2016 Apr;75(4):1466-73. doi: 10.1002/mrm.25701. Epub 2015 May 13.
PURPOSE: Noninvasive imaging techniques that quantify renal tissue composition are needed to more accurately ascertain prognosis and monitor disease progression in polycystic kidney disease (PKD). Given the success of magnetization transfer (MT) imaging to characterize various tissue remodeling path
PMID 25974140

The C-terminal tail of polycystin-1 regulates complement factor B expression by Signal Transducer and Activator of Transcription 1.

Wu M1, Chen M2, Jing Y3, Gu J1, Mei S1, Yao Q1, Zhou J1, Yang M1, Sun L1, Wang W1, Hu H1, Wüthrich RP4, Mei C5.
American journal of physiology. Renal physiology.Am J Physiol Renal Physiol.2016 Mar 16:ajprenal.00428.2015. doi: 10.1152/ajprenal.00428.2015. [Epub ahead of print]
Inhibition of the over-activated alternative complement pathway in autosomal dominant polycystic kidney disease (ADPKD) retards disease progression in animal models, however it remains unknown how complement factor B (CFB) is up-regulated in ADPKD. Here we showed that the overexpression of complemen
PMID 26984954

Intronic PRRT2 mutation generates novel splice acceptor site and causes paroxysmal kinesigenic dyskinesia with infantile convulsions (PKD/IC) in a three generation family.

Weber A1, Kreth J2, Müller U3.
BMC medical genetics.BMC Med Genet.2016 Mar 3;17(1):16. doi: 10.1186/s12881-016-0281-7.
BACKGROUND: Mutations in PRRT2 cause autosomal dominant paroxysmal kinesigenic dyskinesia with infantile convulsions (PKD/IC).CASE PRESENTATION: A previously not recognized intronic PRRT2 mutation (c.880-35G > A; p.S294Lfs*29) was found in an 18 month old girl with IC and in her mother with
PMID 26936445