ライフサイエンスコーパス: des-

1 enhanced phosphorylation of Erk1/2 in ASMCs(Des-/-).

2 days 1-5 with equivalent estrogenic doses of DES (0.001 mg/kg/day) or genistein (50 mg/kg/day).

3 umen loss in lesions treated with BVS versus DES (0.30+/-0.59 versus 0.22+/-0.48 mm; P=0.035).

4 ing addition of the dAdo reactant (4) to the DEs (1 or 2) in over 25 molar equiv of TFE occurred high

5 -5 could be overcome by exogenous IGFs, with des (1-3) IGF-I, an analogue with decreased affinity for

6 ith relatively shorter implant durations for DES (1.5 +/- 0.4 years) compared to BMS (6.1 +/- 1.5 yea

7 Treating cells with des-(1-3)-IGF-I (an active derivative of IGF-I that does

8 y differentiated chondrocytes, stimulated by des-(1-3)-IGF-I and longR(3)-IGF-I (IGF-I analogs with r

9 ect on cell growth stimulated by insulin, or des-(1-3)-IGF-I or longR(3)IGF-I.

10 ke growth factor-binding proteins (IGF-BPs), des-(1-3)-IGF-I, was not competitive with (125)I-IGF-I f

11 of strain on IGF-IR is mimicked by exogenous des-(1-3)IGF-I and is blocked by the IGF-IR inhibitor H1

12 r ICI 182,780 increases the concentration of des-(1-3)IGF-I necessary to activate this cascade, where

13 oth basal AKT activity and its activation by des-(1-3)IGF-I.

14 The Gln192-->Met mutants of des-(1-45)-factor Xa activated prethrombin 1.8-11-fold s

15 interactions, we prepared forms of thrombin, des-(1-45)-factor Xa and activated des-(1-45)-protein C

16 >Gln and Glu192-->Met mutations of activated des-(1-45)-protein C both inactivated factor Va 2-3-fold

17 92-->Met mutations of thrombin and activated des-(1-45)-protein C increased the second-order rate con

18 ->Met mutants of both thrombin and activated des-(1-45)-protein C were effectively inhibited by tissu

19 thrombin, des-(1-45)-factor Xa and activated des-(1-45)-protein C with Glu, Gln, or Met at position 1

20 bin, and 185-fold and 150-fold for activated des-(1-45)-protein C, respectively.

21 ted factor Va 2-3-fold faster than activated des-(1-45)-protein C.

22 Myoblast death was prevented by IGF-I, des [1-3] IGF-I, IGF-II, and insulin with a dose potency

23 lated molecules (IGF-I, IGF-II, insulin, and des-[1-3]-IGF-I) as competitive inhibitors of [125I]-IGF

24 includes a total of 406 lesions-197 BMS, 209 DES (103 sirolimus-eluting stents [SES] and 106 paclitax

25 dural myocardial infarction occurred only in DES (11 versus 0; P=0.05), of which 6 (55%) could be att

26 1), I(2), and I(3), previously identified as des-[19-68,30-75], des-[30-75], and des-[19-68], respect

27 ified as des-[19-68,30-75], des-[30-75], and des-[19-68], respectively, are discussed.

28 phaERKO females were treated with vehicle or DES (2 microg/pup/day for Days 1-5) and terminated after

29 ale mice were treated with either vehicle or DES (2 mug/day) on neonatal days 1-5.

30 pe I thin-cap neoatheroma was more common in DES (20% versus 3%; P=0.01) and in areas of the stented

31 period immediately preceding the approval of DES (2001 to 2002) who received at least 1 BMS.

32 oximately 0.5 microM), whereas intracellular DES (25 microM) has no effect.

33 acilitated the isolation of des [58-110] and des [26-84], the other two native-like structured des sp

34 and oxidation reactions in des [58-110] and des [26-84], two long-lived disulfide-insecure intermedi

35 ntified and shown by mass spectrometry to be des-(27-31)C-peptide (loss of 5 C-terminal amino acids).

36 Des-(27-31)C-peptide is a major beta cell secretory prod

37 Des-(27-31)C-peptide is also secreted in a glucose-sensi

38 ) in transformed (INS) rat beta cells, human des-(27-31)C-peptide was secreted along with the intact

39 lusion, a novel beta cell secretory product, des-(27-31)C-peptide, has been identified and should be

40 unfolding) indicate that the conformation of des [30-75] is considerably less stable than that of the

41 While des [30-75] is formed very quickly by a partial reductio

42 The nature of des [30-75] is similar to that of des [40-95] RNase A, i

43 ilar to that of des [40-95] RNase A, in that des [30-75] ONC is also a disulfide-secure species.

44 reductive unfolding of frog onconase (ONC), des [30-75], analogous to the des [40-95] intermediate f

45 previously identified as des-[19-68,30-75], des-[30-75], and des-[19-68], respectively, are discusse

46 d by PC2, in contrast to PC2 nulls, in which des- 31,32 proinsulin intermediates predominate.

47 ces in target-vessel failure between BRS and DES (4.6% versus 7.7%; P=0.21).

48 The roles of des [40-95] and des [65-72], the two native-like structu

49 nconase (ONC), des [30-75], analogous to the des [40-95] intermediate found in the reductive unfoldin

50 wt-RNase A indicated the predominance of the des [40-95] intermediate over des [65-72] after the rate

51 proceeds through a single intermediate, the des [40-95] P93A species, as in onconase.

52 nature of des [30-75] is similar to that of des [40-95] RNase A, in that des [30-75] ONC is also a d

53 in ONC than the formation of the structured des [40-95] species in RNase A.

54 of the mutant to form a single intermediate (des [40-95] Y92A), i.e. it resulted in an onconase-like

55 he major pathway leading to the formation of des-[40-95] (the major three-disulfide intermediate form

56 abilizing the oxidative folding intermediate des-[40-95] (with three native disulfide bonds but lacki

57 r oxidative regeneration pathway of RNase A (des-[40-95] --> N).

58 he native-like intermediates des-[65-72] and des-[40-95] are formed.

59 to stabilizing the global chain fold of the des-[40-95] disulfide-folding intermediate in the wild-t

60 Des-[40-95] has three of the four disulfide bonds of nat

61 e observations for understanding the role of des-[40-95] in the folding pathway of RNase A are discus

62 ative isomers of essential proline residues, des-[40-95] may reshuffle before completing the conforma

63 ional folding of the nativelike intermediate des-[40-95] on the major oxidative folding pathway of bo

64 That portion of the des-[40-95] population which has native isomers of essen

65 ic ribonuclease A (RNase A) proceeds through des-[40-95] RNase A, a three-disulfide intermediate lack

66 the two major three-disulfide intermediates (des-[40-95]) observed in the regeneration of wild-type R

67 disordered three-disulfide precursors (3S if des-[40-95]).

68 nd the other lacks the 40-95 disulfide bond (des-[40-95]).

69 As a result of this competition, 15-85% of des-[40-95], depending on the experimental conditions, u

70 ration process from isolated des-[65-72] and des-[40-95], it is shown that both intermediates lie dir

71 ike three-disulfide species, des-[65-72] and des-[40-95], that convert to the native structure during

72 A stable analogue of des-[40-95], viz., [C40A, C95A] RNase A, which contains

73 zing early folding intermediates, leading to des-[40-95].

74 Of these, 327 were treated with re-DES (58.1%), 132 underwent vascular brachytherapy (23.4%

75 Nase A; it also facilitated the isolation of des [58-110] and des [26-84], the other two native-like

76 tween reshuffling and oxidation reactions in des [58-110] and des [26-84], two long-lived disulfide-i

77 icantly greater with the BVS compared to the DES (6.7 +/- 12.6% vs. 2.9 +/- 11.5%; p = 0.003); the re

78 minance of the des [40-95] intermediate over des [65-72] after the rate-determining step in the regen

79 te of this mutant, compared to its analogue (des [65-72]) of wt-RNase A.

80 The roles of des [40-95] and des [65-72], the two native-like structured three-disulf

81 steps in which the native-like intermediates des-[65-72] and des-[40-95] are formed.

82 rting the regeneration process from isolated des-[65-72] and des-[40-95], it is shown that both inter

83 to two native-like three-disulfide species, des-[65-72] and des-[40-95], that convert to the native

84 These mutants are analogues of the des-[65-72] intermediate, which is one of the two major

85 A three-disulfide intermediate, des-[65-72] RNase A, lacking the disulfide bond between

86 oxidation pathway (2S --> 3S*, where 3S* is des-[65-72]) in the regeneration of the wild-type protei

87 airings, one lacks the 65-72 disulfide bond (des-[65-72]), and the other lacks the 40-95 disulfide bo

88 jor disulfide-rearrangement pathways (3S --> des-[65-72]).

89 , a key structured disulfide-bonded species, des-[65-72], involved in the oxidative folding pathway o

90 From a registry of 40 autopsies of DES (68 stents), 23 DES cases of >30 days duration were

91 ry restenosis was comparable between BVS and DES (7.8% versus 8.9%; P=0.90).

92 Variants of pK3 and eIF2alpha, des-(75-78)-K3L (pK3deltaGYID), and des-(80-83)-eIF2alph

93 Characterisation of des-[76-94] by 2D1H NMR shows that it has a highly nativ

94 g, largely by facilitating the conversion of des-[76-94] to the native state.

95 tive-like, kinetically trapped intermediate, des-[76-94], although a significant population (approxim

96 e dominant intermediate was identified to be des-[76-94].

97 e native-like three-disulphide intermediate, des-[77-95].

98 F2alpha, des-(75-78)-K3L (pK3deltaGYID), and des-(80-83)-eIF2alpha (eIF2alphadeltaGYID), from which t

99 (predefined margin, 3.80%) compared with DP-DES (absolute risk difference, 0.78%; -1.93% to 3.50%; P

100 1 year, cumulative death and MI was 7.6% in DES- and 8.7% in BMS-treated patients (adjusted hazard r

101 probability of treatment weighting to create DES- and BMS-treated groups whose observed baseline char

102 ADAPT-DES (Assessment of Dual Antiplatelet Therapy With Drug-E

103 The prospective ADAPT-DES (Assessment of Dual Antiplatelet Therapy With Drug-E

104 METHODS AND ADAPT-DES (Assessment of Dual Antiplatelet Therapy With Drug-E

105 ternal validation was performed in the ADAPT-DES (Assessment of Dual Antiplatelet Therapy With Drug-E

106 mined the binding of an insulin superanalog, des-(B25-30)-[His-A8, Asp-B10, Tyr-B25 alpha-carboxamide

107 In general des-(B25-30)-[His-A8, Asp-B10, Tyr-B25 alpha-carboxamide

108 the most profound decreases in affinity for des-(B25-30)-[His-A8, Asp-B10, Tyr-B25 alpha-carboxamide

109 tectable insulin binding but an affinity for des-(B25-30)-[His-A8, Asp-B10, Tyr-B25 alpha-carboxamide

110 In contrast the receptor binding potency of des-(B25-30)-[Tyr-B25 alpha-carboxamide]insulin was disp

111 ylated insulin analog Lys(B29)-tetradecanoyl des-(B30) human insulin, or NN304, as a marker for insul

112 acid acylated insulin [Lys(B29)-lithocholyl des-(B30) human insulin] has been crystallized and the s

113 lo Park, California) with those of the Taxus DES (Boston Scientific, Maple Grove, Minnesota) in de no

114 7 to 0.867 with BS imaging and to 0.916 with DES (both P < .001).

115 ificantly increased with each kilometer from DES [carbon, 0.2 Mgxha(-1); 0.1 species per sample area

116 k of death/MI was not significantly lower in DES- compared with BMS-treated patients (adjusted hazard

117 In RCTs, DES (compared with BMS) were associated with no detectab

118 y artery disease were randomized to PCI with DES (DES-PCI; n=953) or CABG (n=947).

119 riority margin of 5% uncovered struts versus DES (difference between treatment means, 0.71%; one-side

120 New-generation metallic DES (EES/BES) were not superior to BVS in terms of angio

121 ns of ANP and CNP, and low concentrations of des-[Gln(18),Ser(19),Gly(20),Leu(21),Gly(22)]-ANP(4-23)-

122 Of 23 patients with DES >30 days old, 14 had evidence of LST.

123 was higher following PCI with POBA than with DES (hazard ratio [HR], 2.79; 95% CI, 1.23-6.34; P=0.014

124 of early/late ST in patients treated with n-DES (hazard ratio [HR]: 0.65; 95% confidence interval [C

125 l no significant differences between BRS and DES (hazard ratio, 1.54; 95% confidence interval, 0.69-3

126 ed and adjusted Cox proportional models with DES (hazard ratio: 0.62, 95% confidence interval: 0.53 t

127 interval [CI]: 0.43 to 0.99; p = 0.04) and o-DES (HR: 0.60; 95% CI: 0.41 to 0.89; p = 0.01) compared

128 correlates included use of early generation DES (HR=1.75, P=0.02), no procedural intravascular ultra

129 Moreover, induction of ASMCs(Des-/-) hypertrophy by the Erk-1/2/Egr-1/miR-26a/GSK-3be

130 Knockdown of miR-26a in ASMCs(Des-/-) inhibits hypertrophy, whereas enforced expressio

131 - 0.9, and 35% of limbs received overlapping DES (length of 60 +/- 13 mm).

132 try enrolled in 2004 who received at least 1 DES (n = 1,460) were compared with 1,763 patients enroll

133 coronary intervention with BMS (n = 3165) or DES (n = 1501).

134 ere more frequent in BMS (n = 7, 4%) than in DES (n = 3, 1%; p = 0.17), with relatively shorter impla

135 of age) were randomized to BMS (n = 401) or DES (n = 399) for treatment of stable angina (32%) or ac

136 ere treated by PCI with n-DES (n = 4,811), o-DES (n = 4,271), or BMS (n = 25,065).

137 tients with STEMI were treated by PCI with n-DES (n = 4,811), o-DES (n = 4,271), or BMS (n = 25,065).

138 nt implantation with either BMS (n = 251) or DES (n = 498) from October 2002 to December 2004.

139 ts, who underwent secondary randomization to DES (n = 61) or BMS (n = 59) placement.

140 These complications included DES (n = 7 [14%]), (sub)retinal hemorrhage (n = 6 [12%])

141 ts with 239 lesions received BVS (n=112) and DES (n=127).

142 cessfully treated with the randomly assigned DES (n=257) or BMS (n=255).

143 : bare metal stent (n=388), first-generation DES (n=425), and second-generation DES (n=96), categoriz

144 0 patients were treated with either XIENCE V DES (n=51) or BMS postdilated with the SeQuent Please DE

145 eneration DES (n=425), and second-generation DES (n=96), categorized into acute coronary syndrome (AC

146 r in patients treated with second-generation DES (odds ratio, 0.51; 95% confidence interval, 0.38-0.6

147 113 g (4 oz)] was inversely associated with DES (OR: 0.81; 95% CI: 0.66, 0.99 for 2-4 servings/wk; O

148 attenuated with the use of second-generation DES (OR: 1.54 [95% CI: 0.96 to 2.47]) compared with the

149 iated with a significantly increased risk of DES (OR: 2.51; 95% CI: 1.13, 5.58) for >15:1 versus <4:1

150 ]) compared with the use of first-generation DES (OR: 3.94 [95% CI: 2.20 to 7.05]; p for interaction

151 by stent type was 5.1% for BMS and 4.3% for DES (P < .001).

152 worse treatment failure for PTA+/-BMS versus DES (P=0.041).

153 report that ASMCs of desmin null mice (ASMCs(Des-/-)) show hypertrophy and up-regulation microRNA-26a

154 istration-approved durable stent and polymer DES (sirolimus eluting stent, paclitaxel eluting stent,

155 istration-approved durable stent and polymer DES (sirolimus-eluting stent [SES], paclitaxel-eluting s

156 lar observational studies (PROMETHEUS, ADAPT-DES [the Assessment of Dual AntiPlatelet Therapy with Dr

157 Extracellular DES (up to 30 microM) inhibited only CRAC but did not af

158 tcomes, including stent thrombosis, with any DES (versus BMS).

159 hed cohort, no significant association among DES (vs BMS) use and outcomes was observed at 1 and 2 ye