ライフサイエンスコーパス: cartilage

1 nsversally-oriented clones into pre-existing cartilage.

2 ive potential residing within osteoarthritic cartilage.

3 or exceed those of prototype tissues, e.g., cartilage.

4 surrounding the rostral process of Meckel's cartilage.

5 pplication of miRNAs to regenerate articular cartilage.

6 devices and structural biomaterials such as cartilage.

7 full-length CHADL transcript is expressed in cartilage.

8 ssociated with the degeneration of articular cartilage.

9 partially rescued abnormalities in Meckel's cartilage.

10 inkage between these processes in chick limb cartilage.

11 uld provide a solution for replacing damaged cartilage.

12 at are morphologically reminiscent of native cartilage.

13 f the nasal septum or defects in vomeronasal cartilage.

14 osteoarthritis (OA) promote gradual loss of cartilage.

15 an OA knee cartilage compared to normal knee cartilage.

16 and LCN2 in the pathophysiology of articular cartilage.

17 ng in the tissue of the joint, including the cartilage.

18 e sGAG and collagen content of the articular cartilage.

19 s involved in the degradation of aggrecan in cartilage.

20 ive rise to an activation of chondrocytes or cartilage.

21 n, the major structural protein of articular cartilage.

22 ty to inhibit TIMP-3 endocytosis and protect cartilage.

23 nd MMP13 protein levels, similar to human OA cartilage.

24 WIST1 expression is a feature of OA-affected cartilage.

25 ute to the growth and reshaping of articular cartilage.

26 loading of histologically intact human knee cartilage.

27 ), the major boundary lubricant of articular cartilage.

28 ed cartilage resembling the native articular cartilage.

29 ed the maintenance of functional and hyaline cartilage.

30 nt (CA4+) is described for imaging articular cartilage.

31 e ceratohyal, and all of the ceratobranchial cartilages.

32 ession is reduced in T2DM versus non-T2DM OA cartilage (0.57-fold Nrf-2 and 0.34-fold HO-1), and pros

33 to manage osteoarthritis (OA) and articular cartilage (AC) injuries.

34 hin ECM actively enhance RASF attraction and cartilage adhesion.

35 proliferating, and hypertrophic growth-plate cartilage and assembles into an extended extracellular n

36 -2 in tissues of the skeletal system such as cartilage and bone as well as in in vitro cultures of os

37 kine secreted by activated T cells, protects cartilage and bone damage in murine models of inflammato

38 In rheumatoid arthritis (RA), cartilage and bone matrix are degraded, and extracellula

39 scular scar, aberrant differentiation toward cartilage and bone, with persistently impaired function.

40 ce for a critical function of fibronectin in cartilage and bone.

41 ised by progressive destruction of articular cartilage and chondrocyte cell death.

42 Since the majority of the bones, cartilage and connective tissues that comprise the head

43 tigate the levels of TWIST1 in normal and OA cartilage and examine its role in regulating gene expres

44 d that a single FCSC colony formed transient cartilage and host endothelial cells may participate in

45 Two radiologists assessed cartilage and meniscus defects on right knee 3-T MR imag

46 h as aggrecan, leading to the destruction of cartilage and osteoarthritis.

47 synovitis but might have adverse effects on cartilage and periarticular bone.

48 aggressive behavior, invading the articular cartilage and promoting inflammation.

49 aspects of post-natal maturation in immature cartilage and provides the basis to evaluate a new biolo

50 al region that are predominantly involved in cartilage and skeletal development as well as proteoglyc

51 by fabricating mandible and calvarial bone, cartilage and skeletal muscle.

52 Both the cartilage and skin sulfated GAG polysaccharides showed g

53 des were successfully extracted from chicken cartilage and skin.

54 This study investigates how age affects cartilage and subchondral bone changes in mouse joints f

55 gender-dependent structural changes in joint cartilage and subchondral bone post-DMM, facilitating mo

56 ar joints that leads to degeneration of both cartilage and subchondral bone.

57 found that SnCs accumulated in the articular cartilage and synovium after ACLT, and selective elimina

58 revents the proper formation of craniofacial cartilage and the heart in developing zebrafish.

59 autophagy flux, restored collagen levels in cartilage, and ameliorated the bone phenotype.

60 al cells; however, the majority of the bone, cartilage, and connective tissue is derived from the neu

61 ADAMTS-5 is the major aggrecanase in mouse cartilage, and is also likely to be the major aggrecanas

62 ctive tissues, such as cardiac, nerve, bone, cartilage, and skeletal muscle.

63 protein with those of CLEC3A extracted from cartilage; and investigated its tissue distribution and

64 as absent in the subarticular regions of the cartilage anlagen and entheses at a time point most rele

65 oint (TMJ) mandibular condyle that generates cartilage anlagen, which is subsequently remodeled into

66 Here, by using self-assembled articular cartilage as a model to examine the effects of intermitt

67 IFT proteins in the development of bone and cartilage, as well as the differentiation and mechanotra

68 Loss of Islet1 caused a lack of cartilage at the distal tip, leading the fusion of two g

69 level of ADAM12 protein in the KBD articular cartilage (average positive chondrocyte rate = 47.59 +/-

70 .59 +/- 7.79%) compared to healthy articular cartilage (average positive chondrocyte rate = 64.73 +/-

71 that anisotropic proliferation might explain cartilage bending and groove formation at the macro-scal

72 c MR imaging mapping can be used to evaluate cartilage beyond mere static analysis and may provide th

73 beta-signaling proteins involved in bone and cartilage biology.

74 Twenty macroscopically intact cartilage-bone samples were obtained from the central la

75 factor alpha expression, and was induced in cartilage by a pro-inflammatory stimulus.

76 (LWIs) on the stresses in the medial tibial cartilage by combining musculoskeletal (MS) modelling wi

77 le therapeutic strategies to prevent ectopic cartilage calcification and some forms of congenital cra

78 The digital flexor tendons passed through cartilages, cartilaginous cristae and ridges on the plan

79 Purpose To assess the incidence of costal cartilage (CC) fractures in whole-body computed tomograp

80 signs of cartilage injury, it is likely that cartilage cell apoptosis can be used to predict the exte

81 Normal cartilage cells are susceptible to lysis by NK cells.

82 s deleted using Aggrecan-Cre (ERT2) in early cartilage cells with a one-time tamoxifen injection.

83 ave begun to precociously differentiate into cartilage cells.

84 sociation of weight loss with progression of cartilage changes at magnetic resonance (MR) imaging ove

85 [CI] = 0.60, 0.83) and weak correlation with cartilage collagen content (r = 0.40; 95% CI: 0.18, 0.58

86 T1 expression was increased in human OA knee cartilage compared to normal knee cartilage.

87 ly greater agent uptake of CA4+ in articular cartilage compared to that of similar anionic or nonioni

88 position, as assessed by T2 mapping, whereas cartilage composition was observed to differ between kne

89 association of early ROA (osteophytes) with cartilage composition, as assessed by T2 mapping, wherea

90 s (ROA) and ROA risk factors on femorotibial cartilage composition, we studied baseline values and on

91 The joints of mammals are lined with cartilage, comprised of individual chondrocytes embedded

92 to engineer anatomically shaped, functional cartilage constructs capable of tunable and inducible ex

93 tion obtained from imaging ex vivo human hip cartilage correlates with the glycosaminoglycan content,

94 including arthritis indices, paw thickness, cartilage damage and neutrophil infiltration in both CIA

95 CM-MSC treatment reduces cartilage damage and suppresses immune responses by redu

96 Intra-articular corticosteroids could reduce cartilage damage associated with synovitis but might hav

97 to stimulate the repair of acute and chronic cartilage damage even though there is no definitive evid

98 ntiviral Wnt7a strongly attenuated articular cartilage damage induced by destabilization of the media

99 and gene expression patterns associated with cartilage damage were also evaluated.

100 eral immune cell populations are involved in cartilage damage, bone erosion, and resorption processes

101 To follow osteoarthritis progression, cartilage damage, synovial thickening, and osteophyte fo

102 els of distinct mechanisms, without inducing cartilage damage.

103 t is poorly known about their selectivity in cartilage damage.

104 of these cells reconstitute adult articular cartilage de novo, entirely substituting fetal chondrocy

105 PCP/CE-related phenotypes as well, including cartilage defects in Xenopus and misalignment of inner e

106 is (OA) is a common disease characterized by cartilage degeneration and joint remodeling.

107 ondylar cartilage of UAC rats, together with cartilage degeneration and subchondral bone loss.

108 ht over 48 months showed significantly lower cartilage degeneration, as assessed with MR imaging; rat

109 is for more refined graduation strategies of cartilage degeneration.

110 trong up-regulation of genes associated with cartilage degradation and cell death.

111 ndrocyte-specific deletion of BMAL1 leads to cartilage degradation and disruption of key pathways, sh

112 r cartilage, the lack of which protects from cartilage degradation and osteoarthritis (OA) in mice.

113 e-negative control mice, including articular cartilage degradation and subchondral sclerosis, while t

114 actively mitigate local joint inflammation, cartilage degradation and systemic neutrophil activity v

115 We aimed to inhibit cartilage degradation by augmenting levels of the endoge

116 xtracellular levels of TIMP-3 and inhibiting cartilage degradation by the TIMP-3 target enzyme, adama

117 roteinase (MMP)-13 is a major contributor to cartilage degradation in osteoarthritis (OA).

118 eutics to increase TIMP-3 levels and inhibit cartilage degradation in osteoarthritis.

119 In an in vitro model of cartilage degradation treatment with F4 inhibited s-GAG

120 ages, gene expression of enzymes involved in cartilage degradation was up-regulated in chGRKO but not

121 Inflammation, cartilage degradation, and local bone erosion were asses

122 ed milder OA than males as indicated by less cartilage degradation, less subchondral bone plate scler

123 resulted in chronic arthritis with excessive cartilage destruction and bone loss.

124 Osteoarthritis (OA) is characterized by cartilage destruction and chondrocytes have a central ro

125 rsor which is found in broccoli, can prevent cartilage destruction in cells, in in vitro and in vivo

126 TSP) matriptase acts as a novel initiator of cartilage destruction via the induction and activation o

127 Unlike SzV-1287, LJP-1207 induced cartilage destruction, which was confirmed in vitro.

128 This phenomenon may play a role in immune cartilage destruction; however, the mechanisms of chondr

129 cartilaginous lesions within the epiphyseal cartilage developed a rim calcification that originated

130 Methods to better match cartilage developed in vitro to characteristic in vivo f

131 sh, ddrgk1 deficiency disrupted craniofacial cartilage development and led to decreased levels of the

132 This work links glucose metabolism with cartilage development and provides insight into the fund

133 sources and signaling account for divergent cartilage development between proximal and distal CT reg

134 de that Phd2 is a key regulator of articular cartilage development that acts by inhibiting the differ

135 n vitro recapitulated some aspects of native cartilage development, and potentiated the maturation of

136 (SEMD) is a skeletal dysplasia that affects cartilage development.

137 ost-traumatic OA, reduced pain and increased cartilage development.

138 Self-assembling hMSCs formed cartilage discs in Transwell inserts following isotropic

139 o a hypertrophic regimen with thyroxine, the cartilage discs underwent progressive deep-zone hypertro

140 ilia and IFT proteins in the pathogenesis of cartilage diseases, including osteoarthritis, osteosarco

141 t implications for the treatment of bone and cartilage diseases.

142 rocyte repertoire of lncRNAs from normal hip cartilage donated by neck of femur fracture patients.

143 mJ/mm(3), where W = work done, Q = volume of cartilage) during 10 symmetrical jaw-closing cycles with

144 disease, including systemic inflammation and cartilage dysplasia, but the mechanisms of skeletal mani

145 nic phenotype in bovine nucleus pulposus and cartilage endplate cells at the gene level.

146 The 12 M and 19 M+ male mice developed more cartilage erosions and thicker subchondral bone plates a

147 e targeted to the mitochondria (MCAT) and in cartilage explants from MCAT transgenic mice.

148 Ex-vivo FRET imaging of mouse cartilage explants showed that intermediate level of int

149 erapeutically active dose of KAFAK to bovine cartilage explants, suppressing pro-inflammatory interle

150 ed s-GAG release from IL-1beta-treated human cartilage explants.

151 Irreversible breakdown of cartilage extracellular matrix (ECM) by the collagenase

152 These features included cartilage extracellular matrix loss without proteoglycan

153 ecrete collagens, the main components of the cartilage extracellular matrix.

154 Cartilage fatigue may be a factor in the precocious deve

155 ross-sectional study estimated potential for cartilage fatigue via TMJ energy densities (ED) and jaw

156 mbination sites and efficiency in mandibular cartilage for Cre-driver strains.

157 r and may determine RUNX2 availability in OA cartilage for transactivation of genes such as MMP13.

158 inhibit angiogenesis to allow for avascular cartilage formation.

159 Cartilage formed from hMSCs remained stable and organize

160 We assessed the in vivo stability of the cartilage formed under different induction regimens.

161 Cartilage formed under spatiotemporal regulation in vitr

162 Moreover, OA cartilage from patients with T2DM exhibits a greater res

163 Finally, mouse articular cartilage from Sirt1(-/-) presented increased LEF1 and M

164 (HO-1), one of its main target genes, in OA cartilage from T2DM and non-T2DM patients as well as in

165 he greater inflammatory responsiveness of OA cartilage from T2DM patients and may inform treatments o

166 ent of friction, which are key indicators of cartilage functional performance and osteoarthritis stag

167 py analysis of PRP and growth factor treated cartilage gave a 5-fold increase in stiffness correlatin

168 Cartilage grown from human mesenchymal stem cells (hMSCs

169 calization, increased cilia length, aberrant cartilage growth plate structure, defective Hedgehog and

170 focused on FlnA and FlnB interactions in the cartilage growth plate, since mutations in both molecule

171 re we report a novel principle of vertebrate cartilage growth that is based on introducing transversa

172 cause pleiotropic human diseases, including cartilage hair hypoplasia (CHH).

173 ve rise to the autosomal recessive condition cartilage-hair hypoplasia (CHH).

174 has become increasingly clear that articular cartilage harbours a viable pool of progenitor cells and

175 Articular cartilage has little regenerative capacity.

176 ral knees were harvested and evaluated using cartilage histology scores and muCT quantification of su

177 portant role of SHP2 in bone development and cartilage homeostasis by influencing the osteogenic diff

178 ion and disruption of key pathways, shifting cartilage homeostasis toward a catabolic state.

179 However, its effect on cartilage homeostasis under pathological conditions is n

180 Cartilage homeostasis, chondrocyte maturation, and termi

181 anging mechanical loads in order to maintain cartilage homeostasis.

182 e and maintain ATP, a molecule important for cartilage homeostasis.

183 ostin sustains the FCSC pool and regenerates cartilage in a TMJ injury model.

184 tially regulated between intact and degraded cartilage in at least two -omics levels, 16 of which hav

185 organized and thicker while the growth plate cartilage in cKO mice was disorganized and wider compare

186 we demonstrate that addition of hepsin to OA cartilage in explant culture induced significant collage

187 rocyte progenitors, which form the articular cartilage in juvenile mice.

188 estruction of extracellular matrices such as cartilage in osteoarthritis (OA).

189 s a key process in the formation of bone and cartilage in vertebrates, involving the deposition of ca

190 l cell (BMSC) and CB-BF pellet cultures make cartilage in vitro Furthermore, upon in vivo transplanta

191 e defect but transdifferentiate into ectopic cartilage; in the absence of tenogenic cells, extrinsic

192 Articular cartilage injury can result in chondrocyte loss and dimi

193 nitor the extent of mechanical force-induced cartilage injury in vivo.

194 Cartilage injury induced by acute excessive contact stre

195 Although early detection of cartilage injury may prevent serious and lifelong arthri

196 Following cartilage injury, Gdf5-lineage cells underpin synovial h

197 subsequent cell death are the early signs of cartilage injury, it is likely that cartilage cell apopt

198 interventions in the course of pathological cartilage injury.

199 -articular injection of AAT or GSN protected cartilage integrity in mice with inflammatory arthritis.

200 o attenuate MMP activities and promote joint cartilage integrity in mouse experimental OA, demonstrat

201 an in vivo model of inflammatory arthritis, cartilage integrity was determined histologically 48 h a

202 By immunoblotting, CD36 but not cartilage intermediate layer protein decreased steadily

203 n vivo, GF(-) matrix decreased RASF-mediated cartilage invasion compared with GF(+) matrix.

204 other ECM components on human RASF-mediated cartilage invasion were examined in the SCID mouse model

205 Cartilage is a structural tissue with unique mechanical

206 oduction of the charged environment found in cartilage is achieved using polyelectrolyte hydrogels ba

207 s, although their relationship to vertebrate cartilage is enigmatic.

208 Articular cartilage is exposed to a gradient of oxygen levels rang

209 e characterized by degeneration of articular cartilage leading to pain and physical disability.

210 Load-bearing soft tissues, e.g., cartilage, ligaments, and blood vessels, are made predom

211 This cartilage-like mechanical behavior displayed by responsi

212 ed down the chondrogenic lineage to generate cartilage-like structures containing type II collagen.

213 Cartilage-like tissues also exist outside the vertebrate

214 t cellular-level preservation of tendon- and cartilage-like tissues from the lower hindlimb of Early

215 e acetonide every 3 months on progression of cartilage loss and knee pain.

216 nt swelling, histopathological signs of AIA, cartilage loss and suppressed TNFalpha induction.

217 Disease severity and cartilage loss were evaluated by histopathological analy

218 nknown exactly how glycosylation facilitates cartilage lubrication.

219 known to play a role in bone remodeling and cartilage maintenance.

220 ral ossification, retained the expression of cartilage markers, and remained organized following s.c.

221 here it promotes chondrocyte hypertrophy and cartilage matrix catabolism.

222 mapping has been shown to be associated with cartilage matrix composition (hydration, collagen conten

223 However, elastic stresses may restrict cartilage matrix formation and alter the chondrocyte phe

224 ing increase in the volume of interconnected cartilage matrix formed by chondrocytes.

225 s of the metalloproteinases that degrade the cartilage matrix have been hampered by a lack of specifi

226 Loss of cartilage matrix is accompanied by an increase in matrix

227 oteoglycan aggrecan, a main component of the cartilage matrix, were associated with idiopathic short

228 is rescued the mutant phenotype of premature cartilage maturation, thereby indicating that IGF2 contr

229 The formation of the mandibular condylar cartilage (MCC) and its subchondral bone is an important

230 ndrogenic lineage of the mandibular condylar cartilage (MCC) are not well understood.

231 , we demonstrate that loss of TRPV4-mediated cartilage mechanotransduction in adulthood reduces the s

232 Chondrocytes were isolated from articular cartilage obtained during talonavicular joint surgery.

233 Cartilage of rib 7 (21.3%, 47 of 221) was most commonly

234 vels of hypertrophy markers in the articular cartilage of the cKO mice.

235 al nervous system, melanocytes, and bone and cartilage of the face.

236 m expression of SMAD3 in intact and degraded cartilage of the knee and hip.

237 J fibrocartilage and not seen in the hyaline cartilage of the knee.

238 receptor expression was observed in condylar cartilage of UAC rats, together with cartilage degenerat

239 o seven in the exonic region of the gene for cartilage oligomeric matrix protein (COMP) leads to pseu

240 allowed for identification of the epiphyseal cartilage origin and subsequent stages of ossification i

241 ably assess indicators of mandibular condyle cartilage pathology in mice.

242 e Phd2 gene in chondrocytes on the articular cartilage phenotype in mice.

243 eletal elements-a proximal bone and a distal cartilage portion.

244 e sulfated GAG oligosaccharides derived from cartilage possessed the greatest DPPH scavenging and fer

245 inhibiting the differentiation of articular cartilage progenitors via modulating HIF-1alpha signalin

246 erged as a favourable approach for articular cartilage regeneration.

247 Furthermore, we found that cartilage renewal occurs as the progeny of superficial c

248 ) perivascular population, and contribute to cartilage repair.

249 reases contribution of Gdf5-lineage cells to cartilage repair.

250 While most cartilage research is performed in supraphysiological ox

251 f-assembling hMSCs into stable and organized cartilage resembling the native articular cartilage.

252 single and multiple donors of osteoarthritic cartilage revealed the presence of a divergent progenito

253 from paired intact versus degraded articular cartilage samples across 38 patients undergoing joint re

254 es at dGEMRIC showed strong correlation with cartilage sGAG content (r = 0.73; 95% credibility interv

255 We were able to alter cartilage shape by experimentally manipulating clonal ge

256 the apoptosis probes at the injured xiphoid cartilage site.

257 re-express phenotypic biomarkers of immature cartilage so tissue maturation is a potential pathway fo

258 MSC chondrogenesis, concomitant with reduced cartilage-specific gene expression and incomplete matrix

259 distribution, and molecular function of the cartilage-specific lectin CLEC3A and show that CLEC3A bi

260 Articular cartilage specimens from 8 subjects were collected for i

261 t of MMP and IL-1beta in individual human OA cartilage specimens.

262 hell) to endoskeletal materials (bone, shark cartilage, sponge spicules) to attachment devices (musse

263 ression of type X collagen which, in hyaline cartilage structure is not characteristic of the mid-zon

264 In rod-shaped cartilage structures (Meckel, ribs and skeletal elements

265 Hepsin is another TTSP expressed in OA cartilage such that we hypothesized this proteinase may

266 PRP increased cartilage surface cell density 1.5-fold (P < 0.05), conf

267 and one-year change in superficial and deep cartilage T2 layers in 60 subjects (age 60.6 +/- 9.6 y;

268 hondral ossification depends on an avascular cartilage template that completely remodels into vascula

269 naling functions early to pattern the stapes cartilage template, with stapes malformations correlatin

270 ties including the complete loss of Meckel's cartilage, the ceratohyal, and all of the ceratobranchia

271 h chondrocyte hypertrophy in adult articular cartilage, the lack of which protects from cartilage deg

272 aline for a mean change in index compartment cartilage thickness of -0.21 mm vs -0.10 mm (between-gro

273 ved cartilaginous sheets from the control of cartilage thickness, a process which might be the evolut

274 creased proteoglycan distribution, increased cartilage thickness, increased TRAP activity, and minera

275 freedom in joint rotation or gliding of two cartilages (thyroid and cricoid), so that vocal fold len

276 ess relaxation as a key design parameter for cartilage tissue engineering.

277 Cartilage tissue equivalents formed from hydrogels conta

278 markers while also increasing expression of cartilage tissue extracellular matrix proteins.

279 Senescent chondrocytes are found in cartilage tissue isolated from patients undergoing joint

280 Human cartilage tissues and chondrocytes were obtained at auto

281 fracture callus and a delay in conversion of cartilage to bone.

282 fter fracture and are required for effective cartilage-to-bone transformation in the fracture callus

283 ng, disturbed osteoclastogenesis and delayed cartilage-to-bone transformation.

284 adipokine that negatively impacts articular cartilage, triggering catabolic and inflammatory respons

285 rthermore, the treatment technique preserves cartilage under harsh articulation conditions, showing p

286 tivation of PDGFRalpha leads to expansion of cartilage underlying the coronal sutures, which contribu

287 nance imaging for quantitative evaluation of cartilage volume (minimal clinically important differenc

288 ar saline, resulted in significantly greater cartilage volume loss and no significant difference in k

289 amcinolone resulted in significantly greater cartilage volume loss than did saline for a mean change

290 differences in change in MRI-measured tibial cartilage volume or WOMAC knee pain score over 2 years.

291 icant differences in annual change of tibial cartilage volume or WOMAC pain score.

292 ermore, DDR2-dependent MT1-MMP activation by cartilage was found to be more efficient when the tissue

293 omised in vitro chondrogenesis, and Meckel's cartilage was underdeveloped in vivo.

294 genitor numbers in normal and osteoarthritic cartilage where we observed a 2-fold increase in disease

295 otic chondrocytes within the injured xiphoid cartilage, which was confirmed by TUNEL assay.

296 We report that human cartilage with physiologic organization and in vivo stab

297 for maturation were mimicked in PRP treated cartilage, with chondromodulin, collagen types II/X down

298 as significantly associated with increase in cartilage WORMS (beta = 0.2; 95% CI: 0.02, 0.4; P = .007

299 ts Over 48 months, adjusted mean increase of cartilage WORMS was significantly smaller in the 5%-10%

300 The entire sample and specific cartilage zones (superficial zone [SZ], transitional zon