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-derived cells were used to study regulation of MKX e

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

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

7 ACLs were also evaluated with accepted criteria for the

8 ACLs were mechanically tested, and the intercondylar not

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

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

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

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

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

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

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

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

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

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

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

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

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

22 en posteromedial tibial plateau injuries and ACL tears.

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

24 ine their relationship to cartilage loss and ACL tears.

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

26 3-year survival, as assessed by both Op and ACL (P<0.0001).

27 Op and ACL assessment of angiographic markers of reperfusion in

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

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

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

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

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

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

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

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

36 A correlation between ACL degeneration and cartilage degeneration was observed

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

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

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

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

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

42 415 patients with final TIMI flow 0 to 2 by ACL, Op scoring was TIMI flow 3 in 267 (64.3%).

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

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

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

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

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

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

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

50 ad arthroscopically or surgically documented ACL tears.

51 erived from hamstring tendon obtained during ACL reconstruction.

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

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

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

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

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

57 < 0.001) reduced at an early stage following ACL injury when compared with those in the contralateral

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

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

60 both the Arabidopsis genes are required for ACL activity.

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

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

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

64 All 10 patients had ACL tears at MR imaging.

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

66 Histologic ACL substance scores and ligament sheath inflammation sc

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

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

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

70 most stable structure of reconstituted holo-ACL.

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

72 However, ACL knockdown significantly impairs Akt-mediated tumorig

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

74 be appropriate for replacing ruptured human ACL.

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

76 -1-mediated pro-survival function in hypoxic ACL tumor microenvironment.

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

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

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

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

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

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

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

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

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

86 albeit unproductive, phosphoryl transfer in ACL.

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

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

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

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

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

92 ents with typical bone contusions had intact ACLs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

110 placing ruptured anterior cruciate ligament (ACL).

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

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

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

114 re prepared and encapsulated into liposomes (ACL).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

131 r their suspected role as reservoir hosts of ACL.

132 Inactivation of ACL by treatment with diethylpyrocarbonate suggested the

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

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

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

136 tonated for the catalytic phosphorylation of ACL to occur.

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

138 tibial plateau injuries may be predictive of ACL status.

139 0 degrees of knee flexion in the presence of ACL deficiency.

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

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

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

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

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

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

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

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

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

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

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

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

152 hat of previously prepared native C. tepidum ACL.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

174 Inflammation surrounding the ACL was assessed separately.

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

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

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

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

179 Op tended to favorably grade unfavorable ACL results.

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

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

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

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

184 Whether ACL regulates nuclear targets in addition to histones du

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

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

187 Cells with ACL knockdown display decreased cytokine-stimulated cell

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

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

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

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

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

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

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

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