ライフサイエンスコーパス: epiphyseal

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 component, neurovascular bundle involvement, epiphyseal and joint involvement, and the presence or ab

9 tures, epiphyseal and physeal cartilage, and epiphyseal and metaphyseal marrow were compared (Mann-Wh

10 o independent readers qualitatively analyzed epiphyseal and metaphyseal shape, secondary ossification

11 rmal proximal and distal femoral structures, epiphyseal and physeal cartilage, and epiphyseal and met

12 MR imaging findings differentiate epiphyseal and physeal regions and correlate with histol

13 icrotrauma may interrupt the already tenuous epiphyseal blood supply in the growing child and contrib

14 -14 have integral roles in carpal/tarsal and epiphyseal bone development.

15 a prominent 240-kDa component in extracts of epiphyseal but not tracheal tissue.

16 n young mice, but not in adult mice, whereas epiphyseal cancellous bone mass decreased with loading i

17 ADC was greater in epiphyseal cartilage (mean +/- 1 SD, 1.62 x 10(-3) mm2/s

18 axation time were greater in physeal than in epiphyseal cartilage (P < .01).

19 gressive signal intensity changes within the epiphyseal cartilage along the weight-bearing region and

20 ominent in equimolar amounts in fetal bovine epiphyseal cartilage and absent from adult articular car

21 ly, primary cartilaginous lesions within the epiphyseal cartilage developed a rim calcification that

22 matrix degradation during SOC formation and epiphyseal cartilage development and that its actions ar

23 To understand its role in epiphyseal cartilage development, we generated transgeni

24 By electron microscopy, chondrocytes from epiphyseal cartilage exhibited dilated rough endoplasmic

25 (IS) versus deep layer (ID) chondrocytes of epiphyseal cartilage in infant rats.

26 g protocol allowed for identification of the epiphyseal cartilage origin and subsequent stages of oss

27 Histologic findings revealed abnormal epiphyseal cartilage thickening, cartilaginous islands w

28 In early infancy, epiphyseal cartilage was homogeneous.

29 is of the secondary ossification center, (c) epiphyseal cartilage, (d) physis, and (e) zone of provis

30 for gadopentetate dimeglumine in the physis, epiphyseal cartilage, and secondary ossification center

31 sing dissociative extraction of bovine fetal epiphyseal cartilage, followed by sequential ion-exchang

32 T2 is slower in physeal than in epiphyseal cartilage, probably reflecting differences in

33 The relative visibility of the physis, epiphyseal cartilage, secondary ossification center, and

34 directing chondrogenesis into articular- or epiphyseal cartilage-like tissue.

35 es as reported for collagen calcification in epiphyseal cartilages.

36 There was no significant difference in epiphyseal changes between boys and girls or between med

37 ctivate prehypertrophic chondrocyte markers, epiphyseal chondroblasts ectopically activate hypertroph

38 Human fetal epiphyseal chondrocytes (HFCs) were cultured either on p

39 sion of the VEGFA receptors Npr1 and Npr2 in epiphyseal chondrocytes and lack of blood vessel reducti

40 the deficient VEGFA production in Hif1a null epiphyseal chondrocytes demonstrate that HIF1 alpha and

41 -trans-retinoic acid (RA) treatment of mouse epiphyseal chondrocytes in culture did increase Wnt/beta

42 ction of small interfering RNA-GADD45beta in epiphyseal chondrocytes in vitro blocked terminal differ

43 6-27 was stably transfected into human fetal epiphyseal chondrocytes in vitro.

44 GFR downstream signaling pathways in primary epiphyseal chondrocytes revealed that up-regulation of M

45 on of extracellular PGE2, PTHrP, and ATP (by epiphyseal chondrocytes), which together engage both PKA

46 becular surfaces and in cortical osteocytes, epiphyseal chondrocytes, marrow adipocytes and mesenchym

47 nction in multiple signaling pathways in the epiphyseal chondrocytes, such as those derived by WNT, B

48 at were distinct from tendon fibroblasts and epiphyseal chondrocytes.

49 s lacked tooth eruption and showed premature epiphyseal closure, indicating that both processes invol

50 Physeal-epiphyseal demarcation, visibility of the secondary ossi

51 Physeal-epiphyseal demarcation, visibility of the secondary ossi

52 om pseudoachondroplasia (PSACH) and multiple epiphyseal dysplasia (EDM1) patients display an enlarged

53 s, pseudoachondroplasia (PSACH) and multiple epiphyseal dysplasia (EDM1).

54 contains the genes responsible for multiple epiphyseal dysplasia (MED) and pseudoachondroplasia (PSA

55 Pseudoachondroplasia (PSACH) and multiple epiphyseal dysplasia (MED) are autosomal dominant osteoc

56 Pseudoachondroplasia (PSACH) and multiple epiphyseal dysplasia (MED) are relatively common skeleta

57 Pseudoachondroplasia (PSACH) and multiple epiphyseal dysplasia (MED) are two human autosomal domin

58 Multiple epiphyseal dysplasia (MED) is a degenerative cartilage c

59 Multiple epiphyseal dysplasia (MED) is a relatively mild and clin

60 tations in matrilin 3 can result in multiple epiphyseal dysplasia (MED), a disease characterized by d

61 One such disorder, multiple epiphyseal dysplasia (MED), is characterized by mild dwa

62 s, pseudoachondroplasia (PSACH) and multiple epiphyseal dysplasia (MED/EDM1).

63 iology of MED we generated a murine model of epiphyseal dysplasia by knocking-in a matn3 mutation.

64 n, which ultimately, causes growth plate and epiphyseal dysplasia in mice.

65 defect in pseudoachondroplasia and multiple epiphyseal dysplasia is not specific for chondrocytes, n

66 DTD, whereas the milder, recessive multiple epiphyseal dysplasia phenotype is homozygous for partial

67 esult in pseudoachondrodysplasia or multiple epiphyseal dysplasia when found in the homologous wire a

68 that include diastrophic dysplasia, multiple epiphyseal dysplasia, atelosteogenesis type 2 and achond

69 ysplasias, pseudoachondroplasia and multiple epiphyseal dysplasia, disturb COMP secretion leading to

70 Col9a3, Comp, and Matn3 genes cause multiple epiphyseal dysplasia, in which patients develop early on

71 uding spondyloepiphyseal dysplasia, multiple epiphyseal dysplasia, Legg-Calve-Perthes disease, and Os

72 ntified in pseudoachondroplasia and multiple epiphyseal dysplasia, two human autosomal dominant osteo

73 ysplasias, pseudoachondroplasia and multiple epiphyseal dysplasia.

74 elated chondrodysplasias, PSACH and multiple epiphyseal dysplasia.

75 gene cause pseudoachondroplasia and multiple epiphyseal dysplasia.

76 inherited pseudoachondroplasia and multiple epiphyseal dysplasia.

77 lopment of pseudoachondroplasia and multiple epiphyseal dysplasia.

78 tiology of pseudoachondroplasia and multiple epiphyseal dysplasia.

79 ysplasias, pseudoachondroplasia and multiple epiphyseal dysplasia; both show a characteristic growth

80 lopment of pseudoachondroplasia and multiple epiphyseal dysplasia; however, the functions of both wil

81 a fully articulated with an enlarged femoral epiphyseal end that accommodated both elements, and the

82 Estrogen is critical for epiphyseal fusion in both young men and women.

83 Our data suggest that (i) epiphyseal fusion is triggered when the proliferative po

84 In senescent growth plates, epiphyseal fusion was observed to be an abrupt event in

85 The increase in epiphyseal grade correlated with age for both the medial

86 h (as an indication of gestational age) with epiphyseal growth in multiple dimensions by using Pearso

87 displayed chondrocyte disorganization in the epiphyseal growth plate associated with decreased prolif

88 ed to deficits in the hypothalamic-pituitary epiphyseal growth plate axis.

89 To address this hypothesis, we used primary epiphyseal growth plate chondrocytes isolated from newbo

90 Maturation of epiphyseal growth plate chondrocytes plays an important

91 Enhanced terminal differentiation of epiphyseal growth plate chondrocytes was also observed i

92 ncluded older adolescents, potentially after epiphyseal growth plate closure.

93 Hypertrophic chondrocytes in the epiphyseal growth plate express the angiogenic protein v

94 ene expression analysis of the cartilaginous epiphyseal growth plate of normal newborn mice.

95 ncy and by the local SMPD3 deficiency in the epiphyseal growth plate to the skeletal phenotype, we in

96 understanding of bone development within the epiphyseal growth plate, factors that regulate periostea

97 t tissue and bone changes, such as increased epiphyseal growth plate, synovial hyperplasia, and incre

98 rative or prehypertrophic compartment of the epiphyseal growth plate.

99 inkage to chondrocyte differentiation in the epiphyseal growth plate.

100 velopment and enchondral ossification in the epiphyseal growth plate.

101 emoral metaphysis and atrophy of the femoral epiphyseal growth plate.

102 ation of cell growth that is specific to the epiphyseal growth plate.

103 lar matrix calcification in arteries and the epiphyseal growth plate.

104 is thought to be regulated solely by genes, epiphyseal growth plates are known to respond to mechani

105 d binucleated chondrocytes were prominent in epiphyseal growth plates of bones in Spg20-/- mice, perh

106 on imaging revealed widened and disorganized epiphyseal growth plates with delayed mineralization of

107 Chondrocytes of the epiphyseal growth zone are regulated by the Indian hedge

108 nt while T1 and STIR were the best to assess epiphyseal involvement.

109 were 0.897 for diaphyseal length, 0.738 for epiphyseal length, and 0.801 for epiphyseal width with r

110 age-estimation techniques based on dry bone, epiphyseal lines, and tooth analysis gave very wide age

111 ) mm2/sec +/- 0.31) (P <.007) and greater in epiphyseal marrow (1.26 x 10(-3) mm2/sec +/- 0.38) than

112 plasia in 11 (37%) of 30 knees, and abnormal epiphyseal marrow in eight (27%) of 30 knees.

113 This may be related to weight bearing and epiphyseal maturation and should not be confused with di

114 e that develops postnatally, concurrent with epiphyseal mineralization.

115 Diaphyseal and epiphyseal morphometric measurements were correlated wit

116 4-fold more hypertrophic chondrocytes in the epiphyseal plate (P<0.01).

117 in childhood, Pb in the skeleton can disrupt epiphyseal plate function, constrain the growth of long

118 most prominent accumulation occurred in the epiphyseal plates of trabecular bones.

119 ith a defect in endochondral ossification at epiphyseal plates similar to human hypochondroplasia.

120 In the peripheral epiphyseal portion, significant bone loss (by 0.32 +/- 0

121 ndrium and lateral chondrocytes flanking the epiphyseal region of mouse embryo long bone anlagen - a

122 nce massive cell death was seen in joint and epiphyseal regions of Vegfa CKO endochondral bones.

123 With advancing GA, the epiphyseal shape changed from spherical (r(2) = 0.664) t

124 he articular cartilage typically produces an epiphyseal skeletal dysplasia phenotype.

125 stature, rhizomelic shortening of the limbs, epiphyseal stippling and craniofacial defects (MIM 30296

126 ever, gelsolin-null mice had mildly abnormal epiphyseal structure, retained cartilage proteoglycans i

127 When extensive (affecting >/= 30% of the epiphyseal surface), 80% of joints collapse within 2 yea

128 Epiphyseal type was compared with age, sex, and distribu

129 , 0.738 for epiphyseal length, and 0.801 for epiphyseal width with respect to GA.