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1 or the development and maintenance of the DS appendicular skeleton.
2 vitamin in the development of the axial and appendicular skeleton.
3 volved in global patterning of the axial and appendicular skeleton.
4 s with respect to formation of the axial and appendicular skeleton.
5 despread patterning defects of the axial and appendicular skeleton.
6 erichondrium of the craniofacial, axial, and appendicular skeleton.
7 ed form of bone loss affecting the axial and appendicular skeleton.
8 t defects that are largely restricted to the appendicular skeleton.
9 iple defects that include bony fusion of the appendicular skeleton.
10 terior (AP) patterning in both the axial and appendicular skeleton and acts as a regulator of Hox gen
11 abuse include separate frontal views of the appendicular skeleton and frontal and lateral views of t
12 tations in Hoxa13 cause malformations of the appendicular skeleton and genitourinary tract, including
13 e all characterised by the shortening of the appendicular skeleton and loss or abnormal development o
14 lements arise from the paraxial somites, the appendicular skeleton and sternum arise from the somatic
15 s, widespread metaphyseal involvement of the appendicular skeleton, and carpal ossification delay.
16 ns of first and second branchial arches, the appendicular skeleton, and the dermal papillae of the vi
19 thin mesenchymal precursors of the axial and appendicular skeleton, before chondrogenesis occurs.
20 uced an Lrp5 mutation in cells that form the appendicular skeleton but not in cells that form the axi
23 ing an understanding of the way in which the appendicular skeleton has evolved to provide the scaffol
26 limb, where they serve as primordia for the appendicular skeleton, is preceded by the appearance of
27 a hypomorph allele in the development of the appendicular skeleton, kidneys, and female reproductive
28 We observed an increase in the axial and appendicular skeleton lengths, and improvements in dwarf
29 ween these factors during development of the appendicular skeleton, mice were produced with various c
31 s condensations (PCCs) in both the axial and appendicular skeleton of mouse embryos and in committed
35 ion of mammalian stanniocalcin (STC1) in the appendicular skeleton suggests its involvement in the re
36 IFT is essential for normal formation of the appendicular skeleton through disruption of multiple sig
37 FGFR3(K650E) expression was directed to the appendicular skeleton, we show that the mutant receptor
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