ライフサイエンスコーパス: cartilage

1 al properties of this important component of cartilage.

2 iation of MF-activated SSCs toward articular cartilage.

3 lage that was also found in undamaged DDH-OA cartilage.

4 s essential to help stem cells create stable cartilage.

5 rtrophic chondrocytes in articular calcified cartilage.

6 ter was measured from the mid-portion of the cartilage.

7 stem are strikingly similar to that of human cartilage.

8 esent in many other tissues such as skin and cartilage.

9 ex vivo cartilage explants and in vivo joint cartilage.

10 tion-driven degradation in tissue-engineered cartilage.

11 nal properties and biomechanical behavior of cartilage.

12 tion (ACI) in order to heal the damaged knee cartilage.

13 ificantly lower AFL compared to normal human cartilage.

14 ine the viscoelastic properties of articular cartilage.

15 , and the medial laminal thickness of the ET cartilage.

16 t composition and collagen disruption in AKU cartilage.

17 he low intrinsic repair potential of hyaline cartilage.

18 related to the proteoglycan concentration in cartilage.

19 plasty, 21 facial feminization, and 31 voice/cartilage.

20 an be used to infer the biochemical state of cartilage.

21 ss, and volume of the femoral head articular cartilage.

22 it low friction and low wear against natural cartilages.

23 les, a robust tympanum and several accessory cartilages.

24 rsible, progressive destruction of articular cartilage(1).

25 Cartilage abnormalities seen in this HGPS model resemble

26 Articular cartilage (AC) and intervertebral discs are cartilaginou

27 D exhibits a protective effect in engineered cartilage against interferon type II.

28 nsion in the molecular mechanisms underlying cartilage ageing and osteoarthritis through the dysregul

29 emonstrate that snoRNA expression changes in cartilage ageing, and osteoarthritis and in osteoarthrit

30 ss of Tbx4(+) tracheal mesoderm and tracheal cartilage agenesis.

31 t of synthetic composite gel-based articular cartilage analog suggests new avenues to explore materia

32 to SOX9's dual role as a master regulator of cartilage and an important regulator of crypt stem cell

33 ch promotes FCSC differentiation toward both cartilage and bone lineages, but inhibits adipogenesis.

34 c invasive tissue that causes destruction of cartilage and bone.

35 ceptor interactions, and MPC trajectories to cartilage and bone.

36 cell-derived mesenchyme surrounding Meckel's cartilage and in the palatal shelves in Med23(fx/fx);Wnt

37 F injections which resulted in a decrease in cartilage and increase of bone volume.

38 3T MRI provides an evaluation of the ET cartilage and isthmus level, which are small but importa

39 tendons, and bones led to hypoplasia of the cartilage and its attachment to tendons and muscle.

40 s is stronger than an unfused one spanned by cartilage and ligaments.

41 ns, sox10(+) perichondrial cells surrounding cartilage and nkx2.5(+) cells surrounding muscle.

42 with decreased expression in osteoarthritic cartilage and osteoarthritic chondrocytes.

43 ound in a nasal septal biopsy, i.e., hyaline cartilage and perichondrium, for a novel tissue identity

44 fiber orientation more similar to the normal cartilage and protects the subchondral bone plate from e

45 ndyle superficial zone niche that regenerate cartilage and repair joint injury.

46 The periodic cartilage and smooth muscle structures in mammalian trac

47 sion to control mesenchymal specification to cartilage and smooth muscle, coupling epithelial identit

48 nchi and on upper airways in 2 compartments, cartilage and submucosal glands, but they were surprisin

49 elucidated the molecular cross-talk between cartilage and synovium in osteoarthritis, the most wides

50 suggest that Gdf5 upregulation in articular cartilage and synovium is a generic response to knee inj

51 Layered structure of bone, cartilage and the bone-cartilage interface must be taken

52 y progressive structural changes in both the cartilage and the underlying subchondral bone.

53 defects contain damage to both the articular cartilage and underlying subchon- dral bone, which remai

54 uctured interfaces between tendons/ligaments/cartilages and bones, we report that bonding ordered nan

55 for diverse applications such as artificial cartilages and tendons, robust antifouling coatings, and

56 collagen triple helix in pigmented AKU human cartilage, and in cartilage from patients with osteoarth

57 tations were not identified in the overgrown cartilage, and thus local cartilage overgrowth likely re

58 drocyte death, lower chondrocyte numbers per cartilage area, and thickening of subchondral bone.

59 lage post-DMM, and was increased in human OA cartilage as determined by immunohistochemistry and micr

60 ect development and homeostasis of articular cartilage, as evidenced by the fact that aberrant FGF si

61 Advances in quantitative morphologic cartilage assessment and semiquantitative whole-organ as

62 al microRNAs including upregulation of known cartilage associated microRNAs and those transcribed fro

63 age can be detected in chondrocytes from DDH cartilage before histological manifestations of degenera

64 provide a promising strategy for iPSC-based cartilage bioengineering for study of disease mechanisms

65 s placebo and substantially reduced bone and cartilage biomarker levels.

66 applications, with a focus on how 3D-printed cartilage, bone and skin can be designed for individual

67 kness, suprapatellar effusion, and irregular cartilage-bone margin, were similar between hemiplegic a

68 tion of the lubricating superficial layer of cartilage by mediating interaction between lubricin and

69 and its hallmark is degradation of articular cartilage by proteolytic enzymes leading to loss of join

70 e development of the extracellular matrix in cartilage by regulating both anabolic and catabolic cell

71 ene expression data from beta-NGF stimulated cartilage callus explants show a promotion in markers as

72 mature nasal chondrocyte-derived engineered cartilage can be assessed with Raman spectroscopy for th

73 her cellular changes in chondrocytes from OA cartilage can be detected in chondrocytes from DDH carti

74 (FCD) for delivering small molecule drugs to cartilage cell and matrix sites.

75 aracterizing running-induced changes in knee cartilage composition.

76 and the proteoglycan aggrecan contribute to cartilage compression resistance and are necessary for h

77 Our work shows that muscle and cartilage connective tissues harbor progenitor cells cap

78 Growth plate and articular cartilage constitute a single anatomical entity early in

79 aims to develop transplantable hyaline-like cartilage constructs by stimulating MSC chondrogenic dif

80 s for developing composite tissue-engineered cartilage constructs for regenerative medicine applicati

81 for fabricating scaffold-free, hyaline-like cartilage constructs from MSCs for future transplantable

82 This approach is applied to engineer cartilage constructs with a depth-dependent cellularity

83 e studied ear AVMs to determine if overgrown cartilage contained AVM-causing mutations.

84 Human osteoarthritis cartilage contains chondrocytes (OAC) and mesenchymal st

85 body weight, tissue source, and the type of cartilage damage as critical properties that significant

86 agonist, CGS21680, significantly reduced OA cartilage damage in a murine model of obesity-induced OA

87 urther, critical thresholds at 6% and 64% of cartilage damage in area, and 22% and 56% in depth were

88 ector in an orthotopic large animal model of cartilage damage is reported here.

89 ACVR1 in both cell types, LDN193189 inhibits cartilage degeneration through suppressing hypertrophy a

90 Low grade cartilage degeneration, predominantly loss of proteoglyc

91 ammation leads to chondrocyte senescence and cartilage degeneration, resulting in osteoarthritis (OA)

92 tory phenotype (SASP) has been implicated in cartilage degradation and OA.

93 mation following joint trauma contributes to cartilage degradation and progression of post traumatic

94 s to provide a label-free optical readout of cartilage degradation that could enable earlier detectio

95 After knee loading, however, cartilage degradation was effectively prevented, and the

96 tic osteoarthritis (PTOA) is associated with cartilage degradation, ultimately leading to disability

97 reciprocally modulate each other to regulate cartilage degradation.

98 is still not known, nor how it induces joint cartilage degradation.

99 ng cartilage lesions, leading to accelerated cartilage degradation.

100 ying TIMP3 to specifically target a class of cartilage-degrading proteinases and to minimize adverse

101 h translational potential for enabling intra-cartilage delivery of a broad array of small molecule OA

102 As a result, this study suggests articular cartilage derived-CPSC can be used as a novel tool for c

103 accumulation of leukocytes in the synovium, cartilage destruction and bone erosion.

104 The primary cause of cartilage destruction is considered to be the presence o

105 erexpression proved to be less protective in cartilage destruction than [-1A]TIMP3 at late stages of

106 -/-) mice, whereas the inflammation area and cartilage destruction was comparable to wild-type mice.

107 t osteoarthritis (TMJ OA) leads to permanent cartilage destruction, jaw dysfunction, and compromises

108 injury to investigate inflammatory response, cartilage development, bone deposition, and mechanical i

109 MicroRNAs have been shown to play a role in cartilage development, homeostasis and breakdown during

110 nown to play an important role in regulating cartilage development.

111 is allows tumor, muscle, tendon, ligament or cartilage disease monitoring for therapy and general lab

112 context for observed methylation changes in cartilage diseases such as osteoarthritis.

113 Because cartilage does not have blood vessels, we studied ear AV

114 relative proteoglycan concentration of knee cartilage due to water flow are mitigated within 24 hour

115 ichondral progenitor cells that generate new cartilage during adult growth, and we show that persiste

116 ound presence of cilia on growth plate (GP), cartilage endplate (EP) annulus fibrosus (AF), and nucle

117 ur data suggest that AFL can detect areas of cartilage erosion and may potentially be utilised as a m

118 nd decreased with applied load; GAG depleted cartilage exhibited higher hydraulic permeability than e

119 y better than unmodified Dex over 2 weeks in cartilage explant culture models of OA.

120 Cytokine-induced biochemical cartilage explant degradation occurs near the sides, top

121 n creep and recovery tests were conducted on cartilage explants (N = 10), and the resulting mechanica

122 miRs were mechanically-regulated in ex vivo cartilage explants and in vivo joint cartilage.

123 a-5p were significantly increased in ex vivo cartilage explants subjected to increasing load magnitud

124 Bovine full-depth articular cartilage explants were loaded to 2.5 MPa (physiological

125 creasing load magnitude and in in vivo joint cartilage exposed to abnormal loading.

126 hanical forces act on these complexes in the cartilage extracellular matrix, motivating the need for

127 ion-driven degradation, and also predisposes cartilage for further biomechanical degradation.

128 ination of frequency-dependent properties of cartilage for more comprehensive and impactful results f

129 m-cell population can be induced to generate cartilage for treatment of localized chondral disease in

130 s from MaR1-treated mice displayed decreased cartilage formation and increased bone deposition which

131 d myocardial fibrosis presented with bone or cartilage formation, and increased collagen levels in ti

132 in injured synovium in prospective areas of cartilage formation, where it inversely correlated with

133 ical behaviour of bone tumours, particularly cartilage-forming tumours, and tumours are now further s

134 haracterized undamaged and damaged articular cartilage from 22 participants having hip replacement su

135 In one model, clinical TMJ-OA cartilage from 5 different samples in TMJ-OA cartilage p

136 Further, human cartilage from OA patients presents a significantly lowe

137 lix in pigmented AKU human cartilage, and in cartilage from patients with osteoarthritis.

138 Articular cartilage from young, old and OA knees was used in a mic

139 ifferentiation including changes at many key cartilage gene loci.

140 nsequences of which has potential to improve cartilage generation for tissue engineering purposes and

141 d for protein secretion in chondrocytes, and cartilage growth and bone mineralization in medaka fish.

142 AP5SA or knockout of Lats1/2 do not increase cartilage growth, but instead lead to catastrophic malfo

143 ncreasing frequency and applied load; mature cartilage had generally the highest moduli and GAG deple

144 Nasal chondrocyte-derived engineered cartilage has been demonstrated to be safe and feasible

145 Snorc (Small NOvel Rich in Cartilage) has been identified as a chondrocyte-specific

146 ually, yet how this exercise influences knee cartilage health is poorly understood.

147 0.001) but did not alter ligament structure, cartilage health, or chondrocyte homeostasis.

148 critical autocrine factor for maintenance of cartilage homeostasis and here we report that injection

149 A charge-based cartilage homing drug delivery platform like this can el

150 issues, including healthy and diseased adult cartilage, identified chondrocyte-specific regions of hy

151 XL2 has beneficial functions in human TMJ-OA cartilage implants and promotes gender-specific anabolic

152 rks and extracellular matrix in human TMJ-OA cartilage implants in vivo.

153 response for mechanical characterization of cartilage in a controlled, ex vivo environment.

154 idly penetrate through the full thickness of cartilage in high concentration and have long intra-cart

155 nhibitor with beneficial effects on bone and cartilage in preclinical osteoarthritis models.

156 al stem-cell (SSC) populations to regenerate cartilage in relation to age, a possible contributor to

157 on of the transcriptome of tissue-engineered cartilage in response to IL-1beta and TNF-alpha using an

158 eatment also improved swelling and preserved cartilage in the affected knees in a rat model of establ

159 Here, we show that embryonic development of cartilage in the skate (Leucoraja erinacea) mirrors that

160 ets' chondrogenic differentiation to hyaline cartilage in vitro via post-contraction cytoskeletal reo

161 is anabolic to human and mouse TMJ condylar cartilage in vivo and evaluate the protective and anabol

162 It is challenging to monitor the status of cartilage in vivo and this study explores the use of aut

163 Physiological YAP target genes in cartilage include Ctgf, Cyr61 and several matrix remodel

164 Mechanical loading on articular cartilage induces various mechanical stresses and strain

165 pain resulting from degradation of articular cartilage, inflammation of the synovial lining, and chan

166 relates with ability to spontaneously repair cartilage injuries.

167 of the medial meniscus (DMM) and after acute cartilage injury and repair.

168 ed structure of bone, cartilage and the bone-cartilage interface must be taken into account in the ca

169 Articular cartilage is a load-bearing tissue found in animal and h

170 Mammalian articular cartilage is an avascular tissue with poor capacity for

171 dark brown pigmentation, especially of joint cartilage, leading to severe early osteoarthropathy.

172 safe and feasible for the treatment of focal cartilage lesions with promising preliminary evidences o

173 chondrogenic precursor cells from repairing cartilage lesions, leading to accelerated cartilage degr

174 of GRASLND resulted in lower accumulation of cartilage-like extracellular matrix in a pellet assay, w

175 ing HMP deviation in order to minimize joint cartilage loading in sub-areas of the knee.

176 -21-5p and miR-27a-5p in ex vivo and in vivo cartilage loading models.

177 The avascular nature of cartilage makes it a unique tissue(1-4), but whether and

178 usive transport through the dense, avascular cartilage matrix comprised of negatively charged glycosa

179 a CRISPR-dCas9-VP64 - significantly enhanced cartilage matrix production.

180 Cartilage matrix-related proteins were assessed by enzym

181 oading, the unloading (recovery) response of cartilage may also enable determination of mechanical re

182 ginate at the chondrocyte level and that DDH cartilage may provide a novel opportunity to study these

183 mAv's intra-cartilage mean uptake was found to be 112x and 33x the e

184 Despite the well-established dependence of cartilage mechanical properties on the frequency of the

185 Thus, measurement of the in vivo cartilage mechanical response may serve as an earlier in

186 mation and producing molecules essential for cartilage metabolism.

187 on in vivo, and instead functions to control cartilage morphogenesis via regulation of the extracellu

188 ments in MRI techniques capable of assessing cartilage morphologic features and the methods for evalu

189 orphome to robustly predict changes in bone, cartilage, muscle and fibrous gene expression induced by

190 s were present in the tissue adjacent to the cartilage [mutant allele frequency (MAF) 6-8%], and were

191 The scaffold mimics the cartilage niche, allowing both cell populations to maint

192 e that changes in the mechanical function of cartilage occur as degeneration progresses during OA.

193 ain tissues and elastic fibers in developing cartilage of mice.

194 d sheath and in close contact with the basal cartilage of the pectoral fins; cells of this epithelium

195 attenuates pro-inflammatory signaling in OA cartilage of the TMJ and knee joint, induces chondroprot

196 The gene for cartilage oligomeric matrix protein (COMP) was the most

197 Both exhibited increased cartilage oligomeric protein, COMP mRNA expression.

198 connective tissues (tendons, ligaments, and cartilages) on bones in many animals can maintain high t

199 drocytes has potential for repairing damaged cartilage or to generate disease models via gene editing

200 se findings suggest that early events in DDH cartilage originate at the chondrocyte level and that DD

201 d in the overgrown cartilage, and thus local cartilage overgrowth likely results from the effects of

202 nafarnib monotherapy did not improve bone or cartilage parameters, but treatment combinations with pr

203 kate, transcriptional features of developing cartilage persist into adulthood, both in peripheral cho

204 n of our work is direct visualization of the cartilage phenotype defining predictive ability as our t

205 cartilage from 5 different samples in TMJ-OA cartilage plugs were implanted subcutaneously in nude mi

206 The plug also comprises a Cartilage Portion (component 2) which is a 3D printed ge

207 Cartilage Portion is secured on top of the Bone Portion

208 ting of polycaprolactone (PCL) on top of the Cartilage Portion to facilitate sliding of the knee join

209 modified to have specific affinity with the Cartilage Portion.

210 ace while allowing nutrients delivery to the Cartilage Portion.

211 fic knobs in the 3D printed construct of the Cartilage Portion.

212 Gdf5 expression was upregulated in articular cartilage post-DMM, and was increased in human OA cartil

213 different intervertebral soft tissue types (cartilage, probable notochord) seen in extant reptiles.

214 In this study we propose articular cartilage progenitor/stem cells (CPSC) as a valid altern

215 pain, but it significantly reduced bone and cartilage progression with a reassuring safety profile.

216 analyses provide a limited representation of cartilage properties thus greatly reducing the impact of

217 ion of senescence in the synovial tissue and cartilage protection.

218 sms have been suggested to result in loss of cartilage proteoglycans, the source of tissue fixed char

219 the rotating frame (T(1rho)) mapping of knee cartilage, reducing the usual long scan time.

220 tissue engineering approaches for articular cartilage regeneration increasingly focus on mesenchymal

221 Effective engineering approaches for cartilage regeneration involve a combination of cells an

222 rom MSCs for future transplantable articular cartilage regeneration therapies.

223 stem cells (MSCs) are important sources for cartilage regeneration.

224 ng tissue engineered constructs for bone and cartilage regeneration.

225 erentiation and are a potential approach for cartilage regeneration.

226 ts therapeutic potential in the treatment of cartilage-related diseases, such as osteoarthritis.

227 Targeted drug delivery to joint tissues like cartilage remains a challenge that has prevented clinica

228 a unique model for adult chondrogenesis and cartilage repair and may serve as inspiration for novel

229 ng-based treatment of osteoarthritis and for cartilage repair in animal models and clinical trials ar

230 Gdf5 expression was also upregulated during cartilage repair in mice and was switched on in injured

231 Cartilage repair in osteoarthritic patients remains a ch

232 enabled precise prediction of post-treatment cartilage repair scores with coefficient of determinatio

233 w-derived mesenchymal stem cells (BMMSC) for cartilage repair strategies after trauma.

234 rformed a meta-analysis on MSC therapies for cartilage repair using machine learning.

235 gmented microfracture significantly improves cartilage repair with a collagen fiber orientation more

236 therapeutic solution for targeted articular cartilage repair, allowing for a controlled and minimall

237 critical properties involved in MSC-induced cartilage repair, and adapted for other clinical indicat

238 25 million MSCs was found to achieve optimal cartilage repair.

239 critical properties that significant impact cartilage repair.

240 r investigative methods, but their uptake in cartilage research is limited by the highly specialised

241 ge in high concentration and have long intra-cartilage residence time in both healthy and arthritic c

242 cing tissue specificity and prolonging intra-cartilage residence time of OA drugs.

243 in healthy and arthritic (50% GAG depleted) cartilage, respectively.

244 and trypsinased (as model of osteoarthritis) cartilage samples to determine the dynamic shear moduli

245 in SAMP8 at 6 weeks than SAMR1, while OARSI cartilage scores became higher only at 14 weeks.

246 Cartilage-specific expression of nls-YAP5SA or knockout

247 aluate the protective and anabolic effect on cartilage-specific factors.

248 However, in vivo, cartilage-specific knockout of Yap/Taz does not prevent

249 joints and to explore the role of calcified-cartilage stiffness on the biomechanics of healthy and p

250 bone structure and mechanical properties and cartilage structural parameters, which ameliorate the mu

251 Ex vivo cartilage studies indicate that changes in the mechanica

252 ated mechano-regulation of miRs in articular cartilage subjected to 'physiological' and 'non-physiolo

253 ifferentiated cell sheets adhere directly to cartilage surfaces via retention of adhesion molecules w

254 (mean +/- SEM) patellar, tibial, and femoral cartilage T1rho relaxation times significantly decreased

255 d for alternative experimental approaches to cartilage testing to be deployed in research and clinica

256 e progressors and nonprogressors on baseline cartilage texture maps, which achieved a robust test acc

257 e early biochemical patterns of fissuring in cartilage that define future onset of OA.

258 staining revealed changes in damaged OA-only cartilage that was also found in undamaged DDH-OA cartil

259 Unlike appendicular articular cartilage, the TMJ has two distinct functions as the syn

260 e no bone contact with the ossified Meckel's cartilage; the latter is loosely lodged on the medial re

261 ly loss of glycosaminoglycans, and decreased cartilage thickness and volume.

262 Other secondary end points included cartilage thickness on quantitative MRI and type I and I

263 atellar effusion and reduced lateral femoral cartilage thickness were more prevalent in the hemiplegi

264 included reduced lateral and medial femoral cartilage thickness, suprapatellar effusion, and irregul

265 d and 0.004 for 200 mg/d) and medial femoral cartilage thinning (P = 0.023 for 100 mg/d and 0.125 for

266 Synthetic pigment and pigmented human cartilage tissue both showed hydroquinone-resembling NMR

267 ged in engineering MSC behavior for bone and cartilage tissue engineering, including gene delivery, g

268 be a viable alternative to growth factors in cartilage tissue engineering.

269 There have been no reports of cartilage to bone transdifferentiation or vasculature in

270 ght to characterize putative vasculature and cartilage to bone transdifferentiation using healthy and

271 pregulated and coupled with cells undergoing cartilage to bone transdifferentiation, which may contri

272 drugs that target angiogenesis or block the cartilage to bone transformation.

273 and the molecular switches that occur during cartilage to bone transformation.

274 ss, inflammation, oxidative stress, bone and cartilage turnover, blood pressure, and blood lipids.

275 blood pressure, markers of inflammation, or cartilage turnover.

276 rospectively assess the Eustachian tube (ET) cartilage using 3 Tesla (3T) magnetic resonance imaging

277 d temporal changes of FCD content in injured cartilage using a novel finite element model that incorp

278 In contrast, tracheal cartilage, vasculature, and neural innervation patterns

279 residence time in both healthy and arthritic cartilage via weak-reversible binding with negatively ch

280 ow higher reductions of knee joint articular cartilage volume after 75 minutes of running.

281 outcome was absolute change in tibiofemoral cartilage volume assessed using MRI over 24 months (the

282 d with placebo, did not significantly reduce cartilage volume loss over 24 months.

283 We found significantly more cartilage volume reductions in the medial knee compartme

284 We also found higher cartilage volume reductions on the medial tibia when run

285 Change in tibiofemoral cartilage volume was not significantly different between

286 We quantified knee joint articular cartilage volumes before and after the run using a 3.0-T

287 In the OA and OPOA groups, articular cartilage was degenerated and Osteoarthritis Research So

288 Intact cartilage was enriched for homeostatic and hypertrophic

289 and hypertrophic chondrocytes, while damaged cartilage was enriched for prefibro- and fibro-, regulat

290 Cartilage was separated from its surrounding tissue and

291 In the patient group, the diameter of the ET cartilage was significantly smaller than in the control

292 poptosis rates in articular and growth plate cartilage were similar between groups, homozygous mitoch

293 the Hippo pathway during the development of cartilage, which forms the majority of the skeleton.

294 lagen levels in tissues adjacent to the bone/cartilage, while unaffected hearts did not present with

295 lvic cartilaginous symphysis-a noncapsulated cartilage with a naturally high endogenous expression of

296 ng vasculature with osteoprogenitors replace cartilage with bone.

297 s able to produce 3D-T(1rho) mapping of knee cartilage with lower error than CS.

298 y reported that treatment of ex vivo porcine cartilage with proteolytic enzymes resulted in decreased

299 collagen II immunostaining in undamaged DDH cartilage, with no evidence of augmented cell death by a

300 l bone turnover and hypertrophy in calcified cartilage, yet additional mechanical or metabolic stimul