ライフサイエンスコーパス: ACL

1 ACL activity and the ACLA and ACLB polypeptides are loca

2 ACL catalyzes the coenzyme A (CoA)-dependent and MgATP-d

3 ACL deficiency alters the in vivo cartilage contact biom

4 ACL forces were high in extension and decreased with fle

5 ACL induction is associated with increased ectopic lipid

6 ACL structural property estimates via MRI may provide a

7 ACL-derived cells were used to study regulation of MKX e

8 ACL-mediated suppression of DNMT1 occurs at least in par

9 ACL-tibial angles became significantly larger (P < .001)

10 ACLs from a minimum of 44 nm to the maximum of 3.5 mum w

11 ACLs were also evaluated with accepted criteria for the

12 ACLs were mechanically tested, and the intercondylar not

13 TN 84752559), 119 participants with an acute ACL injury were evaluated.

14 agement strategy for patients with non-acute ACL injury with persistent symptoms of instability was c

15 Twelve patients with acute ACL injuries were imaged with 3.0-T MR imaging at baseli

16 sion and muscle fibrosis were observed after ACL injury in TG mice compared to WT mice.

17 maintain their muscle function 4 weeks after ACL rupture with the muscle function of female TG mice d

18 However, 32 weeks after ACL transection, the mean proteoglycan concentration and

19 creased clinical outcome scores 1 year after ACL reconstruction surgery.

20 rior to ACL reconstruction) and 1 year after ACL reconstruction.

21 reconstructed knees as early as 1 year after ACL reconstruction.

22 Cholesterol Lowering via Bempedoic Acid, an ACL-Inhibiting Regimen (CLEAR) Outcomes trial were patie

23 Cholesterol Lowering via Bempedoic Acid, an ACL-Inhibiting Regimen (CLEAR) program was a series of p

24 (Cholesterol Lowering via Bempedoic Acid, an ACL-Inhibiting Regimen Outcomes Trial) randomly allocate

25 (Cholesterol Lowering via Bempedoic Acid, an ACL-Inhibiting Regimen) Outcomes trial, treatment of sta

26 traarticular lubricin injection following an ACL injury may be beneficial in retarding the degenerati

27 ecoup impaction injury directly following an ACL tear, as the knee reduces.

28 from patients who recently suffered from an ACL injury, along with matched controls, were subjected

29 ability can affect histone acetylation in an ACL-dependent manner.

30 differentiation, DNMT1 levels decline in an ACL-dependent manner.

31 are completely blocked in the presence of an ACL inhibitor.

32 ee problems (instability) consistent with an ACL injury were eligible.

33 eater than that of MMRTs in patients with an ACL tear.

34 rupture who received individualized anatomic ACL reconstruction surgery at our center.

35 determined by various methods (DPPH, ACW and ACL), red gooseberry Black Negus and black currant Otelo

36 PBDE input (>99% in mole fraction in AED and ACL, and 94.7% in AMW).

37 nd in all three water bodies (<1% in AED and ACL; and 1.1% and 4.1% in AMW, respectively).

38 nderwent magnetic resonance (MR) imaging and ACL reconstruction surgery and who filled out Internatio

39 en posteromedial tibial plateau injuries and ACL tears.

40 deformation were compared between intact and ACL-deficient knees.

41 ine their relationship to cartilage loss and ACL tears.

42 The presence of meniscal and ACL tears was associated with more rapid cartilage loss.

43 3-year survival, as assessed by both Op and ACL (P<0.0001).

44 Op and ACL assessment of angiographic markers of reperfusion in

45 Nonetheless, both Op and ACL assessment of reperfusion strongly inform prediction

46 Discordance between Op and ACL for final TIMI flow (0 to 2 versus 3) occurred in 12

47 Baseline and final Op and ACL TIMI flow and MBG assessment were compared from the

48 were trained using MRI T(2)* relaxometry and ACL tensile testing data from minipigs (n = 65).

49 rs ages 23-92) were obtained at autopsy, and ACLs and cartilage were graded macroscopically and histo

50 In contrast, all known animal ACL enzymes have a homomeric structure, indicating that

51 Arabidopsis ACL is a heteromeric enzyme composed of two distinct sub

52 All of the patients underwent arthroscopic ACL reconstruction with autologous hamstring tendons.

53 ch, in patients undergoing knee arthroscopy (ACL injury) or arthroplasty (late-stage primary OA) or i

54 At baseline, we assessed ACL tears and central BMLs located at or between the tib

55 A correlation between ACL degeneration and cartilage degeneration was observed

56 ly; however, this dependence differs between ACL and MCL fibroblasts in many ways, especially in the

57 significant differences in T2 values between ACL-injured and control knees were found.

58 al translation of a functional bioengineered ACL matrix.

59 ntegration, making it an ideal bioengineered ACL matrix.

60 phthalate (PET), into the PLLA bioengineered ACL matrix to fabricate a "tiger graft." The tiger graft

61 , a poly(l-lactic) acid (PLLA) bioengineered ACL matrix, and demonstrated its feasibility to regenera

62 rate of regeneration using the bioengineered ACL matrix by supplementation with bone marrow aspirate

63 In conclusion, both ACL and MCL fibroblast adhesion depends on cytoskeletal

64 significantly decreased the adhesion of both ACL and MCL cells with increasing concentrations of anti

65 idualized anatomic single- and double-bundle ACL reconstruction techniques.

66 among 706 patients with final MBG 0 to 1 by ACL, 563 (79.7%) were classified as MBG 2 to 3 by Op.

67 415 patients with final TIMI flow 0 to 2 by ACL, Op scoring was TIMI flow 3 in 267 (64.3%).

68 vels in adipocytes are controlled in part by ACL and that silencing of DNMT1 can accelerate adipocyte

69 In mesangial cells, ACL is synergistically induced by high glucose, palmitat

70 wo had no bone abnormalities but had chronic ACL tears.

71 Fifteen other patients had complete ACL disruptions: 13 of these patients had typical bone c

72 By raising acetyl-CoA concentration ACL promotes H3K9/14 and H3K27 hyperacetylation leading

73 in yeast (Saccharomyces cerevisiae) confers ACL activity, indicating that both the Arabidopsis genes

74 The sagittal and coronal ACL-tibial angles, Blumensaat line-ACL angle, angle of i

75 ify and characterize the N-acyl-cyclolysine (ACL) system-a cell-density-dependent chemical signalling

76 xpression of MKX is a feature of degenerated ACL in OA-affected joints, and this may be mediated in p

77 Researchers have developed ACL scaffolds with collagen fibers, silk, biodegradable

78 roidota strains produce structurally diverse ACLs and encode transcription factors with varying ligan

79 ad arthroscopically or surgically documented ACL tears.

80 erived from hamstring tendon obtained during ACL reconstruction.

81 ACL insertion site is a response to elevated ACL laxity.

82 The lowest MAE model was used to estimate ACL failure load for surgical patients at 9 months post-

83 stained expression of lipogenic enzymes FAS, ACL, and SCD1.

84 ay, loss of PERK inhibits expression of FAS, ACL, and SCD1 in immortalized murine embryonic fibroblas

85 These findings may explain higher female ACL failure rates as greater matrix damage combined with

86 Female ACLs showed significantly greater collagen denaturation

87 Here, we test the hypothesis that female ACLs would accumulate more extracellular matrix (ECM) da

88 ease in SF lubricin concentrations following ACL injury may place the joint at an increased risk of w

89 is of musculoskeletal degeneration following ACL injury.

90 CII degradation is an early event following ACL injury and is unlikely to be a direct result of mech

91 < 0.001) reduced at an early stage following ACL injury when compared with those in the contralateral

92 The overall accuracies for ACL injury classification using the 3D CNN and 2D CNN we

93 developing potential therapeutic agents for ACL-related diseases with strong links to traditional me

94 However, for ACL fibroblasts, Tmod significantly reduced adhesion, wh

95 at may synergize with Notch-1 inhibition for ACL treatment.

96 both the Arabidopsis genes are required for ACL activity.

97 s preliminary in vivo rabbit model study for ACL reconstruction, the histological and mechanical eval

98 works could be used to help nonexperts grade ACL injuries.

99 In mice deficient in BNIP-H, ACL fails to interact with KLC1, and formation of the AC

100 There, BNIP-H/ACL complex synergistically recruits another enzyme chol

101 All 10 patients had ACL tears at MR imaging.

102 Hence, ACL deficiencies may not only be important in posttrauma

103 Histologic ACL substance scores and ligament sheath inflammation sc

104 istinct polypeptide chains, recombinant holo-ACL as well as its two individual subunit polypeptides w

105 levels approaching that of recombinant holo-ACL prepared from coexpressed genes.

106 Purified recombinant holo-ACL was isolated at high specific activity, and its k(ca

107 most stable structure of reconstituted holo-ACL.

108 ypeptides were able to reconstitute the holo-ACL in vitro, with activity levels approaching that of r

109 However, ACL knockdown significantly impairs Akt-mediated tumorig

110 tudies were performed with recombinant human ACL to ascertain the nature of the catalytic phosphoryla

111 be appropriate for replacing ruptured human ACL.

112 Experiments in which human ACL cells were injected in mice confirmed elevated and s

113 -1-mediated pro-survival function in hypoxic ACL tumor microenvironment.

114 In ACL-derived cells, IL-1beta strongly suppressed MKX expr

115 vely, also significantly reduced adhesion in ACL and MCL cells.

116 genitor cells and chondrocytes as well as in ACL progenitor cells in which POSTN activity was altered

117 ght-bearing medial femorotibial cartilage in ACL-injured knees were significantly elevated at 1-year

118 es of the posterolateral tibial cartilage in ACL-injured knees were significantly elevated at baselin

119 ession of MKX was significantly decreased in ACL-derived cells from OA knees compared with normal kne

120 stic implications of periostin deficiency in ACL biology, utilizing ligament fibroblasts derived from

121 Sex differences in ACL structure and function are primary factors for incre

122 trix (ECM) production and differentiation in ACL-derived cells.

123 n with siRNA up-regulated SOX9 expression in ACL-derived cells, whereas the expression of COL1A1 and

124 positive cells were significantly reduced in ACL tissue from OA donors, in particular in cells locate

125 a subset of candidate genes was revealed in ACL progenitor cells and chondrocytes as well as in ACL

126 not be used for mass screening of samples in ACL epidemiological studies.

127 albeit unproductive, phosphoryl transfer in ACL.

128 subcompartments at baseline and follow-up in ACL-injured knees and were compared with measures acquir

129 iated abnormalities were analyzed, including ACL tears, medial meniscal tears, and other lateral femo

130 Furthermore, injured ACL with silenced periostin expression, achieved through

131 suffer an anterior cruciate ligament injury (ACL) relative to males when participating in the same, o

132 During the acute phase of injury, ACL tissues express elevated periostin levels that decli

133 patients with bone contusions had an intact ACL at MR imaging.

134 of knee laxity in the presence of an intact ACL graft have a high specificity, the low PPV means tha

135 tusions as adults but may maintain an intact ACL owing to increased ligamentous laxity.

136 apoptosis and senescence compared to intact ACL in C57BL/6 mice.

137 NN performed similarly in classifying intact ACLs (2D CNN, sensitivity of 93% [188 of 203] and specif

138 ents with typical bone contusions had intact ACLs.

139 Eight patients with an isolated ACL injury in 1 knee, with the contralateral side intact

140 tor (Op) versus angiography core laboratory (ACL) assessed TIMI flow and MBG are unknown.

141 f West Lake of El Dorado (AED), Calion Lake (ACL), and the lagoon of Magnolia Wastewater Treatment Fa

142 In DH guinea pigs, laxer ACLs, which are associated with increased collagen turno

143 DH guinea pigs had significantly laxer ACLs than did BS2 guinea pigs, at 12, 16, and 24 weeks.

144 nsport layer (PTL) and anode catalyst layer (ACL), which can lead to a reduction in performance at ty

145 reened for American cutaneous leishmaniasis (ACL) infection by established PCR-based and enzyme-linke

146 site between the anterior cruciate ligament (ACL) and bone, the objectives of this study are: (i) to

147 d changes in the anterior cruciate ligament (ACL) and their relationship to articular cartilage degen

148 Anterior Cruciate Ligament (ACL) injuries are a major concern in sports, especially

149 Although anterior cruciate ligament (ACL) injuries are not gender specific, they do occur at

150 Anterior cruciate ligament (ACL) injuries lead to an increased risk of osteoarthriti

151 Anterior cruciate ligament (ACL) injuries pose a significant challenge due to their

152 Anterior cruciate ligament (ACL) injury adversely affects skeletal muscle, leading t

153 nt changes after anterior cruciate ligament (ACL) injury, but no long-term data are available for com

154 ration following anterior cruciate ligament (ACL) injury.

155 narrowing at the anterior cruciate ligament (ACL) insertion site is associated with disease severity,

156 prescribed after anterior cruciate ligament (ACL) reconstruction and postoperative opioid consumption

157 rd treatment for anterior cruciate ligament (ACL) reconstruction is the use of tendon autografts and

158 ualized anatomic anterior cruciate ligament (ACL) reconstruction, we retrospectively analyzed the dat

159 hly expressed in anterior cruciate ligament (ACL) remnants compared with articular cartilage at the c

160 may be useful in Anterior Cruciate Ligament (ACL) repair and provide a novel, alternative treatment t

161 Anterior cruciate ligament (ACL) rupture is a common debilitating injury that can ca

162 ere are >200,000 anterior cruciate ligament (ACL) ruptures each year in the United States, and, due t

163 document healing anterior cruciate ligament (ACL) structural properties could potentially identify pa

164 jects who had an anterior cruciate ligament (ACL) tear.

165 Anterior cruciate ligament (ACL) tears had a borderline significant influence (P <or

166 Anterior cruciate ligament (ACL) tears result in unresolved muscle weakness and post

167 Associated anterior cruciate ligament (ACL) tears were found in 25 of the 25 (100%) examination

168 ed in rabbits by anterior cruciate ligament (ACL) transection.

169 A) and an intact anterior cruciate ligament (ACL) underwent magnetic resonance imaging and single-pla

170 lls from a human anterior cruciate ligament (ACL) were used to engineer ligament constructs in vitro.

171 ng ligament, the anterior cruciate ligament (ACL), than in the flexor digitorum longus tendon.

172 The anterior cruciate ligament (ACL), which lacks a functional healing response, and the

173 healthy limb and anterior cruciate ligament (ACL)-deficient limb of 27 subjects.

174 placing ruptured anterior cruciate ligament (ACL).

175 injury to their anterior cruciate ligament (ACL).

176 struction of the anterior cruciate ligament (ACL).

177 anatomically to anterior cruciate ligament [ACL]/posterior cruciate ligament [PCL] insertions, and t

178 The Blumensaat line-ACL angle was constant after age 2 years.

179 d coronal ACL-tibial angles, Blumensaat line-ACL angle, angle of inclination of the intercondylar roo

180 re prepared and encapsulated into liposomes (ACL).

181 Compared to ANE-loaded liposomes, ACL-90H, ACL2-90H and ACL2-S100 displayed significantly

182 h-1 signaling in adenocarcinoma of the lung (ACL) cells causes apoptosis specifically under hypoxia.

183 ly shown to modulate both ATP-citrate lyase (ACL) and AMP-activated protein kinase (AMPK) activity in

184 ATP citrate lyase (ACL) catalyzes an ATP-dependent biosynthetic reaction wh

185 The ATP citrate lyase (ACL) inhibitor, bempedoic acid, reduces low-density lipo

186 ATP-citrate lyase (ACL) is an essential enzyme of the reductive tricarboxyl

187 links kinesin-1 (KLC1) to ATP citrate lyase (ACL), a key enzyme for ACh synthesis, and transports it

188 ities (IC(50) s <5 uM) of ATP-citrate lyase (ACL), a new drug target for the treatment of glycolipid

189 Here we showed that ATP-citrate lyase (ACL), an enzyme converting citrate to acetyl-CoA, is hig

190 adenosine triphosphate (ATP)-citrate lyase (ACL), the enzyme that converts glucose-derived citrate i

191 and nuclear functions of ATP-citrate lyase (ACL).

192 ate through the action of ATP citrate lyase (ACL).

193 carboxy portions of human ATP-citrate lyase (ACL).

194 production by the enzyme ATP-citrate lyase (ACL).

195 All the mice received a mechanical ACL rupture and were euthanized at 4- and 8-week post-in

196 Here, we show that the female mouse ACL accrues more collagen matrix damage than males under

197 otope exchange rate observed in H760A mutant ACL (~150 fold less than wild type), collectively sugges

198 ormation and tensile strength of the natural ACL but is decellularized for a decreased immunogenic re

199 ming of differentiation and describe a novel ACL-miR-148a-dependent mechanism for regulating DNMT1 du

200 The collagen V-null ACL and flexor digitorum longus tendon both had signific

201 The ATPase activity of ACL, along with the small yet significant positional iso

202 associated operons and the autoinduction of ACL biosynthesis.

203 Classification of ACL injuries using deep learning involved use of two typ

204 roduced by both wild type and H760A forms of ACL, with rates at three magnitudes lower than that of k

205 r their suspected role as reservoir hosts of ACL.

206 Inactivation of ACL by treatment with diethylpyrocarbonate suggested the

207 odulate both targets, and that inhibition of ACL leads to LDL receptor upregulation, decreased LDL-C

208 Stable knockdown of ACL leads to a significant impairment of glucose-depende

209 ection of changes in the cartilage matrix of ACL-reconstructed knees as early as 1 year after ACL rec

210 derived from patients and a murine model of ACL rupture.

211 tonated for the catalytic phosphorylation of ACL to occur.

212 e of the pre-steady-state phosphorylation of ACL with [gamma-(33)P]-ATP revealed an ionizable group w

213 tibial plateau injuries may be predictive of ACL status.

214 0 degrees of knee flexion in the presence of ACL deficiency.

215 inactivation of the biosynthetic reaction of ACL, in good agreement with the involvement of a catalyt

216 he presence of cuboidal cells reminiscent of ACL fibroblasts and chondrocytes surrounded by an extrac

217 e excess acetyl-CoA generated as a result of ACL induction provides the substrate for these lipogenic

218 active factors and PET incorporation have on ACL regeneration and signal a promising step toward the

219 change significantly in patients with OA or ACL injury compared with controls.

220 The nature of the formation of the phospho-ACL was further investigated by positional isotope excha

221 uently ameliorated muscle function loss post-ACL rupture.

222 evaluate machine learning models to predict ACL failure load from magnetic resonance images (MRI) an

223 Preoperatively, ACL forces correlated with anteroposterior translation o

224 nversely, overexpression of IGF-1R protected ACL cells from GSI toxicity.

225 naling affects Akt-1 activation in PTEN(-/-) ACL cells.

226 y torn, 77 fully torn, and 140 reconstructed ACLs) from 224 patients (mean age, 47 years +/- 14 [stan

227 The 2D CNN classified all reconstructed ACLs correctly.

228 d demonstrated its feasibility to regenerate ACL tissue.

229 e mice demonstrated a slower, more regulated ACL reparative response, while male mice exhibited a mor

230 e types and temporal sequence of age-related ACL changes and to determine their correlation with cart

231 le of inclination of the intercondylar roof, ACL-tibial insertion site, and PCL angle and horizontal

232 d pig PTs were implanted to replace ruptured ACL in patients.

233 Furthermore, we find that secreted ACLs are sensed by a dedicated transcription factor, Acl

234 S-1) and dominant-negative IGF-1R sensitized ACL cells to gamma-secretase inhibitor (GSI)-induced apo

235 d to determine the forces needed to separate ACL and MCL cells from a fibronectin-coated surface.

236 e, prepared from coexpressed large and small ACL genes, and the individual large and small subunit po

237 undergo anterior cruciate ligament surgery (ACL; n = 42), (3) non-surgical subjects with knee osteoa

238 icular bone loss 6 months following surgical ACL reconstruction.

239 e-associated BNIP-H mutation fails to target ACL for neurite outgrowth.

240 hat of previously prepared native C. tepidum ACL.

241 contribute to the active site of C. tepidum ACL.

242 We found that ACL is required for increases in histone acetylation in

243 Our findings indicate that ACL degeneration is highly prevalent in knees with carti

244 Taken together, these results indicate that ACL, encoded by the ACLA and ACLB genes of Arabidopsis,

245 Notably, in vivo data revealed that ACL in Postn(-/-) mice exhibited a higher tearing freque

246 Together, these findings suggest that ACL activity is required to link growth factor-induced i

247 Collectively, these data suggest that ACL is an epigenetic regulator that promotes renal ELA a

248 The ACL also had a higher collagen V content than did the fl

249 The ACL and PCL forces of the knees post-UKA were larger tha

250 The ACL-tibial insertion site was constant at the junction o

251 The ACL-transected and contralateral joints of these rats we

252 of which 129 had type 1 BMLs (96 abutted the ACL and had no coexistent type 2 features) and 25 had ty

253 Central BMLs that abutted the ACL were highly prevalent and strongly related to ACL pa

254 Additionally, the ACL-deficient and healthy limb were compared to determin

255 utaneously at a dose of 0.5 mg/kg around the ACL-transected joints, using different dosing strategies

256 nimals indicates that bone remodeling at the ACL insertion site is a response to elevated ACL laxity.

257 clinical differences in healing between the ACL and the MCL.

258 he absence of serum TNF-a alterations in the ACL group.

259 degeneration and chondroid metaplasia in the ACL increased with the development of cartilage lesions.

260 with collagen abundance and unfolding in the ACL-deficient limb, and T1p relaxation time was strongly

261 axation time was significantly longer in the ACL-deficient limb, coinciding with significant increase

262 s of collagen content and remodelling in the ACL-deficient limb.

263 catalytic phosphorylation that initiates the ACL reaction and the identity of the active site residue

264 s underwent a capsulotomy alone, leaving the ACL intact (n = 11).

265 Rupture of the ACL changed the cartilage contact biomechanics between 0

266 During growth, angulation of the ACL is age dependent.

267 d, due to the poor healing properties of the ACL, surgical reconstruction with autograft or allograft

268 to interact with KLC1, and formation of the ACL/ChAT complex is prevented, whereas the disease-assoc

269 To regenerate the ACL, the ideal matrix should be biodegradable, porous, a

270 Inflammation surrounding the ACL was assessed separately.

271 or CSF1-R from patients with injury to their ACL.

272 Two-dimensional and 3D CNNs applied to ACL lesion classification had high sensitivity and speci

273 and neuromuscular factors that contribute to ACL injuries in females, and provide a foundation from w

274 e been documented as factors contributing to ACL injuries, however little research has been conducted

275 aging at baseline (after injury and prior to ACL reconstruction) and 1 year after ACL reconstruction.

276 ere highly prevalent and strongly related to ACL pathology, suggesting a role of enthesopathy in OA.

277 ticular cartilage transcriptomic response to ACL injury and attenuated PTOA severity and deficits in

278 ized musculoskeletal deficits in response to ACL injury.

279 Op tended to favorably grade unfavorable ACL results.

280 Unilateral ACL transection (ACLT) of the right hind limb was perfor

281 Unilateral ACL transection (ACLT) was performed in Lewis rats (n =

282 orted outcomes at six months post unilateral ACL reconstruction.

283 5 participants at six-months post unilateral ACL reconstruction.

284 om both knees of 30 patients with unilateral ACL insufficiency, 32-364 days postinjury.

285 Three patients with visible ACL graft tears at MR imaging were excluded.

286 to this disparity are less stiff and weaker ACLs, and greater knee laxity than males.

287 Whether ACL regulates nuclear targets in addition to histones du

288 rtality was intermediate in patients in whom ACL and Op were discordant, without marked prognostic di

289 s in biomechanical variables associated with ACL injury risk during SL-DJ tasks, suggesting enhanced

290 Type 1 lesions were associated with ACL tears (odds ratio [OR] 5.9, 95% confidence interval

291 Cells with ACL knockdown display decreased cytokine-stimulated cell

292 All menisci from joints with ACL transection demonstrated degenerative changes.

293 on, was prominent in menisci from knees with ACL transection.

294 Most of the patients with ACL injury had no clinical signs of OA or macroscopic ca

295 In addition, the cartilage of patients with ACL injury was assessed at arthroscopy, and the knee fun

296 Fifty-two patients with ACL reconstruction and no injury to the contralateral kn

297 zed the data and charts of 920 patients with ACL rupture who received individualized anatomic ACL rec

298 rtical depression fractures in patients with ACL tear are associated with decreased clinical outcome

299 t alterations in mechanical properties, with ACL exhibiting more severe changes.

300 e of 26.1 and 25.1 years, respectively) with ACL tear who underwent magnetic resonance (MR) imaging a