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1 g locomotor behavior in mice (referred to as arrhythmicity).
2 elated upd3 induction and alleviates cardiac arrhythmicity.
3 r ablation of just six DH44+ PI cells causes arrhythmicity.
4 ne of the pair must be knocked out to confer arrhythmicity.
5 reliably predicted the spontaneous onset of arrhythmicity.
6 ter at higher levels of ZTL, to the point of arrhythmicity.
7 elevated levels of TIM and approximately 50% arrhythmicity.
8 correlated with altered periods or apparent arrhythmicity.
9 ted knockdown of CG17282 produced behavioral arrhythmicity and long periods and high levels of hypoph
10 nt background restored LL-induced behavioral arrhythmicity and wild-type neuronal activity patterns,
11 alizes to nuclei produce dominant behavioral arrhythmicity, and (2) constitutively nuclear PER repres
13 hrony among these regions does not result in arrhythmicity because core body temperature and explorat
14 (LL) can induce behavioral and physiological arrhythmicity by desynchronizing clock cells in the SCN.
17 Mop3), the single knockout of which confers arrhythmicity, despite the presence of its paralog, Bmal
19 PDF-expressing LNv causes initial behavioral arrhythmicity followed by gradual long-term emergence of
20 e age-related transition from rhythmicity to arrhythmicity for each parameter occurs unpredictably, w
21 ptor, PdfR, results in most flies displaying arrhythmicity in activity-rest cycles under constant con
23 rsistent oscillation in constant conditions, arrhythmicity in constant light, resetting by brief ligh
24 role of the engraftment patterns of MSCs on arrhythmicity in controllable in vitro models is investi
26 nd causes long-period behavioral rhythms and arrhythmicity, indicating that cycling vri is required f
27 F in the circadian control circuit overcomes arrhythmicity induced by pdf(01) null mutation, most lik
28 reatretain-->ment counteracted the circadian arrhythmicity induced by the DPS protocol: only 6% of re
32 ture changes, we found that population-level arrhythmicity occurs when certain perturbations cause st
33 rsal neurons 1 (DN1ps), overcomes the severe arrhythmicity of Dh31(#51);Pdf(01) double mutants, sugge
37 d by constant light, resulting in behavioral arrhythmicity or 'splitting' of rhythms of activity and
38 circadian period, and overexpression causes arrhythmicity, suggesting a more comprehensive role for
39 neurons alters tim expression and increases arrhythmicity under standard constant darkness (DD) cond
41 rony within clock nuclei is disrupted during arrhythmicity, whereas neurons in the left and right clo
42 hened significantly, ultimately resulting in arrhythmicity, while blue light-based phase shifts show
43 mozygous viable adults, as well as molecular arrhythmicity, with constitutively high levels of PER pr