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1 have ectopic Shh and Ptch1 expression in the anterior limb.
2 Hand2 likely mediates Gli3 repression in the anterior limb.
3 ssively by power-strokes of each of the more anterior limbs.
5 ctyly phenotype with loss of digits from the anterior limb, although the development of more proximal
6 bers descend in the internal capsule (SMA in anterior limb and genu; M1 in posterior limb) and traver
7 ing activity, leading to derepression of the anterior limb and induction of polarizing zone marker ge
8 n mouse led to ectopic Shh expression in the anterior limb bud and a preaxial polydactyly (PPD) skele
10 duced extra, sometimes multiple digits, from anterior limb bud demonstrating the negative role in Shh
12 nges in the regulation of development of the anterior limb bud resulting in ectopic expression of sig
13 Ectopic Ihh expression in the distal and anterior limb bud results in the ectopic activation of s
14 The polydactyly was preceded by unexpected anterior limb bud transcription of Shh, so one function
15 al cells, including mesenchymal cells in the anterior limb bud, and mice homozygous for targeted disr
20 function abrogates ectopic Shh expression in anterior limb buds, limits overexpression in the zone of
21 ons in the Shh limb enhancer lead to similar anterior limb defects, highlight the importance of Shh r
23 the pathways were widespread, involving the anterior limb, genu and posterior limb with the M3 proje
26 Beads soaked in Shh-N do not induce Shh in anterior limb mesenchyme ruling out direct propagation o
27 ch are known repressors of Shh expression in anterior limb mesenchyme, strongly enhances the anterior
28 Msx-2 during normal limb development in the anterior limb mesoderm, the posterior necrotic zone, and
30 integrity in the fibers that are part of the anterior limb of internal capsule (ALIC) in MDD and diab
32 ubcortical, 188 x 10(-5) mm(2)/sec at birth; anterior limb of internal capsule, 130 x 10(-5) mm(2)/se
34 (-0.01; p = .02) of the corpus callosum and anterior limb of the internal capsule (-0.02; p =.01) at
36 study of DBS targeting the ventral striatum/anterior limb of the internal capsule (VS/ALIC) in 10 pa
37 uced fractional anisotropy (FA) in the right anterior limb of the internal capsule and right uncinate
39 nteers revealed that fiber tracts within the anterior limb of the internal capsule have a significant
40 ateral lesions in the ventral portion of the anterior limb of the internal capsule over a 20-year per
41 primates form a well defined and topographic anterior limb of the internal capsule, the specific loca
42 re also associated with abnormalities in the anterior limb of the internal capsule, the white matter
47 , a small region of increased atrophy in the anterior limb of the left internal capsule adjacent to t
48 to sham deep brain stimulation (DBS) in the anterior limb of the ventral capsule/ventral striatum (V
49 esults explain why GLI3 is required only for anterior limb patterning and why GLI2 can compensate for
50 nd Shh gene dosage improves the integrity of anterior limb structures, validating the importance of t
51 he involvement of inhibitory pathways in the anterior limb that prevent secondary polarizing zone for
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