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1 in both growth plate chondrocytes and in the perichondrium.
2 ciated with ectopic bone collars in adjacent perichondrium.
3 elated protein (PTHrP), in the periarticular perichondrium.
4 hat block a Wnt5a autoregulatory loop in the perichondrium.
5 s in the fetal cartilage and its surrounding perichondrium.
6 nhibit a Wnt5a positive-feedback loop in the perichondrium.
7 onal Ext1 deficiency in the growth plate and perichondrium.
8 nse preceded by ectopic BMP signaling within perichondrium.
9 sed in both the stacked chondrocytes and the perichondrium.
10 rentiation in the bone-forming region in the perichondrium.
11 pic cartilaginous tissues protruded into the perichondrium.
12 tal analysis showed to be dependent upon the perichondrium.
13  Cre activity in chondrocytes but not in the perichondrium.
14 en chondrocytes and cells in the surrounding perichondrium.
15 nchymal stem cells (MSCs) in bone marrow and perichondrium.
16 ite of bone collar formation in the adjacent perichondrium.
17 unding the early cartilage template form the perichondrium.
18 n level of several BMP genes in the adjacent perichondrium.
19 s synthesized by chondrogenic mesenchyme and perichondrium.
20 amma, while RARbeta expression was strong in perichondrium.
21 on in both growth plate cartilage and in the perichondrium.
22                                          The perichondrium, a structure made of undifferentiated mese
23 ssive intramembranous ossification along the perichondrium, accompanied by excessive Patched-1 expres
24 ssive intramembranous ossification along the perichondrium, accompanied by local expression of the he
25 ing so intimately associated with cartilage, perichondrium acquires and maintains its distinct phenot
26   The tumors originate from the growth plate perichondrium along skeletal elements, appear first as e
27 ytes incorporating BrdU, indicating that the perichondrium also negatively regulates the proliferatio
28 ubsets of chondrocytes without affecting the perichondrium and found that Smo removal led to localize
29 to follow the fate of cells derived from the perichondrium and from the vasculature.
30 icroscopy is used to image through an intact perichondrium and into the cartilage of anesthetized mic
31 ression in hypertrophic chondrocytes and the perichondrium and is sufficient to induce Vegf expressio
32         Indeed, conditional Ext1 ablation in perichondrium and lateral chondrocytes flanking the epip
33  a third paralogue is expressed later in the perichondrium and mandibular arch.
34 at the histologically distinct layers of the perichondrium and periosteum are associated with distinc
35 letal tissues, we generated microarrays from perichondrium and periosteum cDNA libraries and used the
36  Previously, we observed that removal of the perichondrium and periosteum from tibiotarsi in organ cu
37                                          The perichondrium and periosteum have recently been suggeste
38                          To determine if the perichondrium and periosteum regulate growth through the
39 irement for regulatory factors from both the perichondrium and periosteum suggests a novel mechanism
40  the inhibition of chondrocyte maturation by perichondrium and reveals that Runx2 fulfills antagonist
41 nding that VEGF is expressed robustly in the perichondrium and surrounding tissue of cartilage templa
42 spatially adjacent tissues such as cartilage/perichondrium and tendon/muscle connective tissue.
43  Here we show that Fgf18 is expressed in the perichondrium and that mice homozygous for a targeted di
44  is required for blood vessel recruitment in perichondrium and the differentiation of osteoblast prec
45 ll cultures of the region bordering both the perichondrium and the periosteum, (2) co-cultures of per
46 d, elongated cells called, respectively, the perichondrium and the periosteum.
47 into the hypertrophic cartilage and both the perichondrium and the vasculature are essential for endo
48 anization and morphogenesis of chondrocytes, perichondrium, and bone in uxs1 mutants.
49 esenchymal condensations of limbs, vertebral perichondrium, and mesenchymal cells of the intervertebr
50 h is expressed in chondrocytes, cells of the perichondrium, and the primary spongiosa in fetal growth
51  implicate three tissues, the cartilage, the perichondrium, and the vascular endothelium.
52  further the contributions of the cartilage, perichondrium, and vascular endothelium to long bone dev
53 cytes and in the outermost cell layer of the perichondrium, and Wnt-4 is expressed in cells of the jo
54 uggests that both types of regulation by the perichondrium are local effects.
55        Endothelial cells residing within the perichondrium are the first cells to participate in the
56  P38 was detected in articular cartilage and perichondrium; articular and sternal chondrocytes expres
57 res, here we identify the outer layer of the perichondrium as the tissue responsible for long bone ov
58                                      Because perichondrium becomes deranged and interrupted by cartil
59 elayed recruitment of blood vessels into the perichondrium but also show delayed invasion of vessels
60 llagen in superficial layer cells in the MCC perichondrium but is present at high levels in the cytos
61                            We found that the perichondrium, but not the host vasculature, is the sour
62 normal initiation of cartilage canals at the perichondrium, but the excavation of these canals into t
63 , changes in BMP5 and BMP7 expression in the perichondrium correspond to altered differentiation stat
64  premature osteoblast differentiation in the perichondrium, coupled with impaired proliferation, surv
65                                          The perichondrium decreased (r(2) = 0.684) from 20 weeks onw
66 s caused by dysregulation of chondrocyte and perichondrium development partially due to loss of Trps1
67 lization of fibrillin and fibulin-2 in skin, perichondrium, elastic intima of blood vessels, and kidn
68 ose expression in cartilage is restricted to perichondrium, favors chondrocyte maturation in a Runx2-
69 l septal biopsy, i.e., hyaline cartilage and perichondrium, for a novel tissue identity assay.
70 the important roles of TGF-beta signaling in perichondrium formation and differentiation, as well as
71 ition of bovine parathyroid hormone (PTH) to perichondrium-free cultures reversed the expansion of th
72                           Partial removal of perichondrium from one side of the tibiotarsus led to ex
73 in chondrocyte layer located adjacent to the perichondrium in the peripheral cartilage.
74                      We examined the role of perichondrium in this process using an organ culture sys
75 monstrated accelerated mineralization of the perichondrium in Trps1 mutant mice and impaired dentin m
76 rentiation and accelerated mineralization of perichondrium in Trps1 mutant mice.
77                                   Removal of perichondrium, in addition, resulted in an extended zone
78                    We show that although the perichondrium influences the rate of chondrocytes matura
79 sion are also observed in endothelial cells, perichondrium, intestine, and mesenchyme of the face and
80 dothelial cells and osteoclasts migrate from perichondrium into primary ossification centers of carti
81 led that fibrillin-1 deficiency in the outer perichondrium is associated with decreased accumulation
82                               The absence of perichondrium is correlated with an extended zone of car
83                                          The perichondrium is crucial for the proper invasion of bloo
84 n cultures and that TGFbeta signaling in the perichondrium is required for inhibition of differentiat
85 ten into a definitive, endothelial cell-rich perichondrium like their wild-type counterparts.
86 sing chondrocytes and fibronectin-expressing perichondrium-like cells surrounding chondrocyte nodules
87                         These defects in the perichondrium likely caused the short bones and ectopic
88 P-2 colocalized with tropoelastin within the perichondrium, lung, dermis, large arterial vessels, epi
89 es expression of Tgfb2 and Tgfb3 mRNA in the perichondrium of embryonic mouse metatarsal bones grown
90 rsely, Bmp4 expression is upregulated in the perichondrium of Fgfr3-/- mice.
91 A transcripts were strongly expressed in the perichondrium of Meckel's cartilage and mesenchymal area
92 is process is specifically restricted to the perichondrium of synovial joints.
93 ensive expression of Preb is observed in the perichondrium of the craniofacial, axial, and appendicul
94 pression of human WNT11 is restricted to the perichondrium of the developing skeleton, lung mesenchym
95 and this together with its expression in the perichondrium of the developing skeleton, makes it a pla
96 yseal shape, secondary ossification, and the perichondrium on 1.5-T echo-planar MR images and correla
97 le of Smad3 independently of its role in the perichondrium or other tissues.
98 ipulations to address how the absence of the perichondrium or the vascular endothelium affected skele
99 ilage and bone are surrounded by the fibrous perichondrium (PC) and periosteum (PO), respectively, wh
100 expressed genes in the fibrillin-1-deficient perichondrium predicted that loss of TGFbeta signaling m
101 essing osteoblast precursors, labeled in the perichondrium prior to vascular invasion of the cartilag
102 model in which overexpression of Wdr5 in the perichondrium promotes chondrocyte differentiation by mo
103 se results are consistent with a model where perichondrium regulates both the exit of chondrocytes fr
104 anism by which overexpression of Wdr5 in the perichondrium regulates chondrocyte differentiation, stu
105 ressing collagen type X, suggesting that the perichondrium regulates chondrocyte hypertrophy in a neg
106 one at the site of removal but not where the perichondrium remained intact.
107  and HS are needed to establish and maintain perichondrium's phenotype and border function, restrain
108  in mutants, reflecting improper chondrocyte/perichondrium signaling.
109 s, increases tendon progenitor number in the perichondrium, suggesting a mechanism to regulate attach
110 , the first osteoblasts differentiate in the perichondrium surrounding avascular cartilaginous rudime
111 A expression was localized to the periosteum/perichondrium, syno-vium, and articular cartilage.
112 l plate mesoderm-derived tissues (cartilage, perichondrium, tendon, muscle connective tissue, and der
113 e connective tissue fibroblasts of the outer perichondrium, tendons and muscle connective tissue of t
114 ral chondrocytes and in cells of the fibrous perichondrium that ensheaths the skeleton.
115 e, which is derived from the Dlx5-expressing perichondrium that surrounds the diaphyses of the cartil
116 nonendothelial Nes(+) cells in the embryonic perichondrium; the latter were early cells of the osteob
117 ck loop that signals through the periosteum/ perichondrium to inhibit cartilage differentiation.
118                                              Perichondrium was quite rich in atRA (about 4.9 nM).
119    The direct target of Ihh signaling is the perichondrium, where Gli and Ptc flank the expression do
120  that resemble chondrocytes derived from the perichondrium, which is not typical of Indian hedgehog m
121 he fibrillin-1-deficient matrix of the outer perichondrium, which results in less TGFbeta signaling l
122  and their growth plates become delimited by perichondrium with which they interact functionally.
123 n with ADAMTS10 led to excess fibrillin-2 in perichondrium, with impaired skeletal development define
124 the chicken limb: Wnt-5a is expressed in the perichondrium, Wnt-5b is expressed in a subpopulation of

 
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