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1 ysplasias characterized by carpal/tarsal and epiphyseal abnormalities, are caused by mutations in v-m
2 ximal tibial physes were similar to those of epiphyseal and articular cartilage but had a different p
3 he physis of the tibia and femur, and in the epiphyseal and articular cartilage of these bones.
4        Femoral non-weight-bearing unossified epiphyseal and articular cartilage showed spatial variat
5  femoral weight-bearing cartilage (including epiphyseal and articular cartilage) was mapped for each
6 similar to that of weight-bearing unossified epiphyseal and articular cartilage, but with increased T
7 al weight- and non-weight-bearing unossified epiphyseal and articular hyaline cartilage and for the d
8 wth plate chondrocytes were similar to fetal epiphyseal and growth plate chondrocytes, with respect t
9 component, neurovascular bundle involvement, epiphyseal and joint involvement, and the presence or ab
10 tures, epiphyseal and physeal cartilage, and epiphyseal and metaphyseal marrow were compared (Mann-Wh
11 o independent readers qualitatively analyzed epiphyseal and metaphyseal shape, secondary ossification
12 rmal proximal and distal femoral structures, epiphyseal and physeal cartilage, and epiphyseal and met
13            MR imaging findings differentiate epiphyseal and physeal regions and correlate with histol
14 latyspondyly, midface retrusion, progressive epiphyseal anomalies and brachytelephalangism.
15 icrotrauma may interrupt the already tenuous epiphyseal blood supply in the growing child and contrib
16                                    Injury of epiphyseal blood vessels in immature joints leads to sub
17 enuated arthritis characterized by preserved epiphyseal bone and cartilage.
18 -14 have integral roles in carpal/tarsal and epiphyseal bone development.
19  performances (mean F1-score of 0.96 for the epiphyseal bone, 0.95 for the growth plate, 0.92 for the
20 ernal dataset (mean F1-score of 0.99 for the epiphyseal bone, 0.97 for the growth plate, 0.92 for the
21 lassified into four anatomical compartments, epiphyseal bone, growth plate, primary spongiosa, and se
22  we segmented the trabecular bone within the epiphyseal bone, primary spongiosa, and secondary spongi
23 a prominent 240-kDa component in extracts of epiphyseal but not tracheal tissue.
24 n young mice, but not in adult mice, whereas epiphyseal cancellous bone mass decreased with loading i
25                           ADC was greater in epiphyseal cartilage (mean +/- 1 SD, 1.62 x 10(-3) mm2/s
26 axation time were greater in physeal than in epiphyseal cartilage (P < .01).
27 gressive signal intensity changes within the epiphyseal cartilage along the weight-bearing region and
28 ominent in equimolar amounts in fetal bovine epiphyseal cartilage and absent from adult articular car
29 ly, primary cartilaginous lesions within the epiphyseal cartilage developed a rim calcification that
30  matrix degradation during SOC formation and epiphyseal cartilage development and that its actions ar
31                    To understand its role in epiphyseal cartilage development, we generated transgeni
32    By electron microscopy, chondrocytes from epiphyseal cartilage exhibited dilated rough endoplasmic
33  (IS) versus deep layer (ID) chondrocytes of epiphyseal cartilage in infant rats.
34 g protocol allowed for identification of the epiphyseal cartilage origin and subsequent stages of oss
35        Histologic findings revealed abnormal epiphyseal cartilage thickening, cartilaginous islands w
36                            In early infancy, epiphyseal cartilage was homogeneous.
37 is of the secondary ossification center, (c) epiphyseal cartilage, (d) physis, and (e) zone of provis
38 for gadopentetate dimeglumine in the physis, epiphyseal cartilage, and secondary ossification center
39 sing dissociative extraction of bovine fetal epiphyseal cartilage, followed by sequential ion-exchang
40              T2 is slower in physeal than in epiphyseal cartilage, probably reflecting differences in
41       The relative visibility of the physis, epiphyseal cartilage, secondary ossification center, and
42  directing chondrogenesis into articular- or epiphyseal cartilage-like tissue.
43 es as reported for collagen calcification in epiphyseal cartilages.
44     Bulk RNA-Sequencing (RNA-Seq) of primary epiphyseal cells from both gain-of-function models estab
45       There was no significant difference in epiphyseal changes between boys and girls or between med
46 ctivate prehypertrophic chondrocyte markers, epiphyseal chondroblasts ectopically activate hypertroph
47                                  Human fetal epiphyseal chondrocytes (HFCs) were cultured either on p
48  of pathways associated with inflammation in epiphyseal chondrocytes and disrupts the transcriptome p
49 sion of the VEGFA receptors Npr1 and Npr2 in epiphyseal chondrocytes and lack of blood vessel reducti
50 the deficient VEGFA production in Hif1a null epiphyseal chondrocytes demonstrate that HIF1 alpha and
51 -trans-retinoic acid (RA) treatment of mouse epiphyseal chondrocytes in culture did increase Wnt/beta
52 ction of small interfering RNA-GADD45beta in epiphyseal chondrocytes in vitro blocked terminal differ
53 6-27 was stably transfected into human fetal epiphyseal chondrocytes in vitro.
54 GFR downstream signaling pathways in primary epiphyseal chondrocytes revealed that up-regulation of M
55 on of extracellular PGE2, PTHrP, and ATP (by epiphyseal chondrocytes), which together engage both PKA
56 becular surfaces and in cortical osteocytes, epiphyseal chondrocytes, marrow adipocytes and mesenchym
57 nction in multiple signaling pathways in the epiphyseal chondrocytes, such as those derived by WNT, B
58 at were distinct from tendon fibroblasts and epiphyseal chondrocytes.
59 s lacked tooth eruption and showed premature epiphyseal closure, indicating that both processes invol
60 arization by 4 weeks, culminating in chronic epiphyseal compromise with articular surface collapse at
61                                      Physeal-epiphyseal demarcation, visibility of the secondary ossi
62                                      Physeal-epiphyseal demarcation, visibility of the secondary ossi
63 n long bones, precipitating limb shortening, epiphyseal distortion, and widespread chondrodysplasia.
64 om pseudoachondroplasia (PSACH) and multiple epiphyseal dysplasia (EDM1) patients display an enlarged
65 s, pseudoachondroplasia (PSACH) and multiple epiphyseal dysplasia (EDM1).
66  contains the genes responsible for multiple epiphyseal dysplasia (MED) and pseudoachondroplasia (PSA
67    Pseudoachondroplasia (PSACH) and multiple epiphyseal dysplasia (MED) are autosomal dominant osteoc
68    Pseudoachondroplasia (PSACH) and multiple epiphyseal dysplasia (MED) are relatively common skeleta
69    Pseudoachondroplasia (PSACH) and multiple epiphyseal dysplasia (MED) are two human autosomal domin
70                                     Multiple epiphyseal dysplasia (MED) is a degenerative cartilage c
71                                     Multiple epiphyseal dysplasia (MED) is a relatively mild and clin
72 tations in matrilin 3 can result in multiple epiphyseal dysplasia (MED), a disease characterized by d
73                  One such disorder, multiple epiphyseal dysplasia (MED), is characterized by mild dwa
74 s, pseudoachondroplasia (PSACH) and multiple epiphyseal dysplasia (MED/EDM1).
75 tion mutations in DDR2 develop spondylo-meta-epiphyseal dysplasia (SMED), a rare, autosomal recessive
76 iology of MED we generated a murine model of epiphyseal dysplasia by knocking-in a matn3 mutation.
77 n, which ultimately, causes growth plate and epiphyseal dysplasia in mice.
78  defect in pseudoachondroplasia and multiple epiphyseal dysplasia is not specific for chondrocytes, n
79  DTD, whereas the milder, recessive multiple epiphyseal dysplasia phenotype is homozygous for partial
80 esult in pseudoachondrodysplasia or multiple epiphyseal dysplasia when found in the homologous wire a
81 that include diastrophic dysplasia, multiple epiphyseal dysplasia, atelosteogenesis type 2 and achond
82 ysplasias, pseudoachondroplasia and multiple epiphyseal dysplasia, disturb COMP secretion leading to
83 Col9a3, Comp, and Matn3 genes cause multiple epiphyseal dysplasia, in which patients develop early on
84 uding spondyloepiphyseal dysplasia, multiple epiphyseal dysplasia, Legg-Calve-Perthes disease, and Os
85 rder that included a severe form of spondylo-epiphyseal dysplasia, sensorineural hearing loss, intell
86 ntified in pseudoachondroplasia and multiple epiphyseal dysplasia, two human autosomal dominant osteo
87 ysplasias, pseudoachondroplasia and multiple epiphyseal dysplasia.
88 elated chondrodysplasias, PSACH and multiple epiphyseal dysplasia.
89 gene cause pseudoachondroplasia and multiple epiphyseal dysplasia.
90  inherited pseudoachondroplasia and multiple epiphyseal dysplasia.
91 lopment of pseudoachondroplasia and multiple epiphyseal dysplasia.
92 tiology of pseudoachondroplasia and multiple epiphyseal dysplasia.
93 ysplasias, pseudoachondroplasia and multiple epiphyseal dysplasia; both show a characteristic growth
94 lopment of pseudoachondroplasia and multiple epiphyseal dysplasia; however, the functions of both wil
95 vasculature and underscore the importance of epiphyseal ECs during bone and haematopoietic developmen
96 a fully articulated with an enlarged femoral epiphyseal end that accommodated both elements, and the
97 and body stature, yet the systems regulating epiphyseal fusion are poorly understood.
98                     Estrogen is critical for epiphyseal fusion in both young men and women.
99                    Our data suggest that (i) epiphyseal fusion is triggered when the proliferative po
100                  In senescent growth plates, epiphyseal fusion was observed to be an abrupt event in
101                              The increase in epiphyseal grade correlated with age for both the medial
102 h (as an indication of gestational age) with epiphyseal growth in multiple dimensions by using Pearso
103  influence chondrogenesis in the neighboring epiphyseal growth plate (GP).
104 displayed chondrocyte disorganization in the epiphyseal growth plate associated with decreased prolif
105 ed to deficits in the hypothalamic-pituitary epiphyseal growth plate axis.
106  To address this hypothesis, we used primary epiphyseal growth plate chondrocytes isolated from newbo
107                                Maturation of epiphyseal growth plate chondrocytes plays an important
108         Enhanced terminal differentiation of epiphyseal growth plate chondrocytes was also observed i
109 ncluded older adolescents, potentially after epiphyseal growth plate closure.
110             Hypertrophic chondrocytes in the epiphyseal growth plate express the angiogenic protein v
111 ene expression analysis of the cartilaginous epiphyseal growth plate of normal newborn mice.
112 ncy and by the local SMPD3 deficiency in the epiphyseal growth plate to the skeletal phenotype, we in
113 understanding of bone development within the epiphyseal growth plate, factors that regulate periostea
114 egulator of chondrogenesis; in the long bone epiphyseal growth plate, PTHrP expressed by resting zone
115 t tissue and bone changes, such as increased epiphyseal growth plate, synovial hyperplasia, and incre
116  stem cell niche develops postnatally in the epiphyseal growth plate, which provides a continuous sup
117 lar matrix calcification in arteries and the epiphyseal growth plate.
118 rative or prehypertrophic compartment of the epiphyseal growth plate.
119 inkage to chondrocyte differentiation in the epiphyseal growth plate.
120 velopment and enchondral ossification in the epiphyseal growth plate.
121 emoral metaphysis and atrophy of the femoral epiphyseal growth plate.
122 ation of cell growth that is specific to the epiphyseal growth plate.
123  is thought to be regulated solely by genes, epiphyseal growth plates are known to respond to mechani
124 d binucleated chondrocytes were prominent in epiphyseal growth plates of bones in Spg20-/- mice, perh
125 on imaging revealed widened and disorganized epiphyseal growth plates with delayed mineralization of
126                          Chondrocytes of the epiphyseal growth zone are regulated by the Indian hedge
127 lgi secretory pathway of chondrocytes of the epiphyseal growth zone leads to dysproteostasis, skeleta
128 nt while T1 and STIR were the best to assess epiphyseal involvement.
129  were 0.897 for diaphyseal length, 0.738 for epiphyseal length, and 0.801 for epiphyseal width with r
130 age-estimation techniques based on dry bone, epiphyseal lines, and tooth analysis gave very wide age
131 ) mm2/sec +/- 0.31) (P <.007) and greater in epiphyseal marrow (1.26 x 10(-3) mm2/sec +/- 0.38) than
132 plasia in 11 (37%) of 30 knees, and abnormal epiphyseal marrow in eight (27%) of 30 knees.
133    This may be related to weight bearing and epiphyseal maturation and should not be confused with di
134 from micro-CT scans (5 um voxel size) of the epiphyseal-metaphyseal region in the mouse tibia.
135                                          The epiphyseal-metaphyseal region is classified into four an
136 e that develops postnatally, concurrent with epiphyseal mineralization.
137                               Diaphyseal and epiphyseal morphometric measurements were correlated wit
138 4-fold more hypertrophic chondrocytes in the epiphyseal plate (P<0.01).
139 ciency in chondrocytes impeded the fusion of epiphyseal plate and promoted chondrogenesis in joint ca
140 in childhood, Pb in the skeleton can disrupt epiphyseal plate function, constrain the growth of long
141  most prominent accumulation occurred in the epiphyseal plates of trabecular bones.
142 ith a defect in endochondral ossification at epiphyseal plates similar to human hypochondroplasia.
143                            In the peripheral epiphyseal portion, significant bone loss (by 0.32 +/- 0
144 ndrium and lateral chondrocytes flanking the epiphyseal region of mouse embryo long bone anlagen - a
145 nce massive cell death was seen in joint and epiphyseal regions of Vegfa CKO endochondral bones.
146                       With advancing GA, the epiphyseal shape changed from spherical (r(2) = 0.664) t
147 he articular cartilage typically produces an epiphyseal skeletal dysplasia phenotype.
148 stature, rhizomelic shortening of the limbs, epiphyseal stippling and craniofacial defects (MIM 30296
149 ever, gelsolin-null mice had mildly abnormal epiphyseal structure, retained cartilage proteoglycans i
150     When extensive (affecting >/= 30% of the epiphyseal surface), 80% of joints collapse within 2 yea
151 one phenotype characterized by osteopenia of epiphyseal trabecular bone and subchondral cortical plat
152 ale mice, there was significant reduction in epiphyseal trabecular bone volume fraction (BV/TV), Tb.T
153                                              Epiphyseal type was compared with age, sex, and distribu
154 , 0.738 for epiphyseal length, and 0.801 for epiphyseal width with respect to GA.

 
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