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 asthma-protective fraction of Amish cowshed DEs (~0.5% of the total carbon content of unfractionated

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

6 -5 could be overcome by exogenous IGFs, with des (1-3) IGF-I, an analogue with decreased affinity for

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

8 low but tended to be lower after DCB versus DES (1.6% versus 3.7%; P=0.064), were similar in patient

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

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

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

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

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

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

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

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

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

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

19 92-->Met mutations of thrombin and activated des-(1-45)-protein C increased the second-order rate con

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

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

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

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

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

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

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

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

28 hagia (65% vs 51%, P < .01) and diagnosis of DES (11% vs 5%, P < .01) and HE (9% vs 3%, P < .01).

29 ce in the primary endpoint between TiNOS and DES (12.6% vs. 16.2%; hazard ratio [HR] .82, 95% confide

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

56 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

96 aring clinical outcomes with ultrathin-strut DES ( 70 um strut thickness) with conventional 2nd-gener

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

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

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

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

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

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

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

104 1,057 lesions) or control second-generation DES (860 patients, 1,084 lesions).

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

106 1 year, cumulative death and MI was 7.6% in DES- and 8.7% in BMS-treated patients (adjusted hazard r

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

108 cts of temperature and water addition during DES- and ethanol-based extractions were analyzed using r

109 only optimised the antimicrobial activity of des-(Asp(20)-Cys(37))-E2P but also exhibited lower toxic

110 hese results suggest that [hArg(7,11,15,19)]-des-(Asp20-Cys37)-E2P held great promise as a novel anti

111 showed that the derivate, [hArg(7,11,15,19)]-des-(Asp20-Cys37)-E2P, not only optimised the antimicrob

112 Building on the best derivative, des-(Asp20-Cys37)-E2P, which demonstrated considerable a

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

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

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

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

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

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

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

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

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

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

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

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

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

126 signed to evaluate the patency of the Eluvia DES (Boston Scientific, Marlborough, MA), a polymer-coat

127 7 to 0.867 with BS imaging and to 0.916 with DES (both P < .001).

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

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

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

131 Pablo Picasso's Femme (Epoque des "Demoiselles d'Avignon") (1907) includes two commerc

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

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

134 The final myco-DES (dried extract spots) protocol allows quantification

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

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

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

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

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

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

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

142 ated with a lower risk of MACE compared with DES [hazard ratio (HR) 0.67, 95% confidence interval (CI

143 farction in the first 30 days after PCI with DES (HR(adj), 1.65 [95% CI, 1.24-2.19]) but a comparable

144 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

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

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

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

148 erformed in 20% (w/v) aqueous glycerol or in DES (lactic acid: glucose) instead of water.

149 - 0.9, and 35% of limbs received overlapping DES (length of 60 +/- 13 mm).

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

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

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

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

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

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

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

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

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

159 signed to receive the bioadaptor (n=1201) or DES (n=1198; ITT population).

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

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

162 ndomized to DCB (n=382) or second-generation DES (n=376).

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

164 nts were randomly assigned to treatment with DES (n=508) or commercially available BMSs (n=267).

165 0 patients were treated with either XIENCE V DES (n=51) or BMS postdilated with the SeQuent Please DE

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

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

168 113 g (4 oz)] was inversely associated with DES (OR: 0.81; 95% CI: 0.66, 0.99 for 2-4 servings/wk; O

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

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

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

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

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

174 ation Polymer-Free vs- Biodegradable-Polymer DES [PARTHENOPE]; NCT04135989).

175 with conventional 2nd-generation thin-strut DES [relative risk (RR) 0.85, 95% confidence interval (C

176 Milpitas, CA, USA) or a zotarolimus-eluting DES (Resolute Onyx and Onyx Trustar, Medtronic, Minneapo

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

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

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

180 The thymol:oleic acid DES (TAO) could preserve astaxanthin content after prolo

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

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

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

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