ライフサイエンスコーパス: very late

1 to three temporal classes: early, late, and very late.

2 ity to some viral proteins was detected only very late.

3 th GVHD in that the onset of her disease was very late.

4 s, with the majority (92%) occurring late or very late.

5 The very late-acting factor CHMP1 is not recruited unless th

6 est whether natalizumab, an antibody against very late activating antigen (VLA)-4, interferes with ce

7 of eosinophils into the lung is dependent on very late activating antigen-4 (VLA-4) expression.

8 ar cell adhesion molecule-1, VCAM-1), CD49d (very late activating antigen-4, VLA-4), and/or MUC-1 on

9 artly dependent on the integrin alpha4beta1 (very late activation 4[VLA-4]) and major histocompatibil

10 a6 in the laminin-specific integrin receptor very late activation Ag (VLA)-6 (alpha6beta1).

11 of inflammatory cells, reduced expression of very late activation Ag-4, lymphocyte function-associate

12 Combined treatments of Ptx with anti-very late activation antigen (anti-VLA-4), uncovered pot

13 nce in the expression of the beta 1-integrin very late activation antigen (VLA)-4 and beta 2-integrin

14 ent study, we investigated the importance of very late activation antigen (VLA)-4 in the early phases

15 ne the effects of sVCAM-1 on and the role of very late activation antigen 4 (VLA-4) in peripheral blo

16 and integrins on Tck cells, including CXCR4, very late activation antigen 4 (VLA-4), and lymphocyte f

17 sing TNFalpha, interleukin-1beta (IL-1beta), very late activation antigen 4 (VLA-4), vascular cell ad

18 The VCAM-1/very late activation antigen 4 adhesive system criticall

19 Two adhesion receptors, very late activation antigen-4 (VLA-4) and CD36, are fou

20 In turn, inflammatory cells expressing very late activation antigen-4 (VLA-4), the leukocyte li

21 rovessel endothelium via interaction between very late activation antigen-4 (VLA4) expressed on sickl

22 revious studies have shown that alpha4beta1 (very late activation antigen-4 [VLA-4]) and vascular cel

23 Minimal levels of very late activation antigen-4(+) (VLA4(+)) erythrocytes

24 aive T-cell marker, and CD29, members of the very late activation family.

25 Mac-1 and very late Ag 5 and enhancement of very late Ag 3-mediated migration.

26 Projections formed independently of VCAM-1/very late Ag 4 interactions, shear, and proactive contri

27 ppression of migration mediated by Mac-1 and very late Ag 5 and enhancement of very late Ag 3-mediate

28 dendritic cells (DC), which recognize Hc via very late Ag 5.

29 and this molecule was identical with CD49b (very late Ag-2, alpha(2) integrin).

30 Engagement of very late Ag-4 (integrin alpha(4)beta(1)) by ligands suc

31 ndent rolling was blocked completely by anti-very late Ag-4 (VLA-4) Abs.

32 plaque, but the mechanism of CD11c/CD18 and very late Ag-4 (VLA-4) activation and cooperation in she

33 mediated, whereas beta2 integrin and VCAM-1/very late Ag-4 (VLA-4) interactions promoted static adhe

34 rming membrane ruffles and showing increased very late Ag-4 (VLA-4)-mediated adhesion to VCAM-1-expre

35 ), a high affinity peptidomimetic ligand for very late Ag-4 (VLA-4; also called integrin alpha4beta1)

36 e diseases because it binds to the integrins very late Ag-4 and alpha(4)beta(7) on lymphocytes and mo

37 eraction of VCAM-1 and its integrin receptor very late Ag-4 is believed to be critically involved in

38 rphostin AG490 are less adhesive on purified very late Ag-4 ligands compared with adhesion of leukocy

39 tometric analysis identified the presence of very late Ag-4 on mouse peripheral neutrophils.

40 retion was inhibited by the addition of anti-very late Ag-4 to plasma cell/stromal cell cocultures in

41 Furthermore, cross-linking of CD49d/CD29 (very late Ag-4) on the surface of B cells rescued them f

42 Anti-VLA-4 (very late Ag-4) treatment prevented lung eosinophilia an

43 Neutrophils were able to use very late Ag-4/VCAM-1 interactions to transmigrate into

44 ized Hc yeasts via the fibronectin receptor, very late Ag-5, and not via CD18 receptors.

45 with manifestation from as early as birth to very late age of onset in life.

46 However, recent studies have found that at very late ages, the genetic variance components decline.

47 mRNA followed a slower time course, peaking very late and continuing expression even after the AOM w

48 r processes insinuate between glomeruli only very late and then form only a sparse, open network arou

49 bnAbs appear very late, and patients are typically not protected by t

50 otif that has homology to the alpha-chain of very late antigen (a known ligand for VCAM-1), was shown

51 The human integrin very late antigen (VLA)-2 (CD49b/CD29) mediates interact

52 Despite the higher level of very late antigen (VLA)-2, VLA-4, and VLA-5 on Sca-1(+)c

53 eceptors on Tc1 and Tc2 cells, we found that very late antigen (VLA)-4 (a heterodimer of CD49d and CD

54 tinct kinetic patterns for the regulation of very late antigen (VLA)-4 (alpha 4 beta 1) and VLA-5 (al

55 sp (RGD) sensitive and partially mediated by very late antigen (VLA)-4 and VLA-5 but not alpha(v) or

56 The transient regulation of very late antigen (VLA)-4 avidity by CC chemokines may p

57 This study tested the hypothesis that very late antigen (VLA)-4 mediates CD18-independent neut

58 n to be important in hematopoiesis, CD44 and very late antigen (VLA)-4.

59 s subset depends on the alpha4beta1 integrin very late antigen (VLA)-4.

60 lar endothelial growth factor (VEGF)-induced very late antigen (VLA)-4.

61 Cross-linking of adherent PMN very late antigen (VLA)-5 and VLA-6 receptors resulted i

62 adhesion/transmigration, upregulates preDC2 very late antigen (VLA)-5, and protects preDC2s from tum

63 ing that stem cells may express the integrin very late antigen (VLA)-5.

64 vious study showed that the cross-linking of very late antigen (VLA)/beta1 with anti-CD29 monoclonal

65 In this study, we investigated whether very late antigen (VLA)4 and VLA-6 integrins, which play

66 These findings establish human very late antigen 2 transgenic mice as a model for echov

67 Production of human integrin very late antigen 2, a receptor for echovirus type 1, in

68 Very late antigen 4 (VLA-4) and CD11/CD18 integrins medi

69 tes matrix metalloproteinase-9 secretion and very late antigen 4 (VLA-4)-mediated adhesion to vascula

70 s mediated by a single integrin heterodimer, very late antigen 4 (VLA-4).

71 e function-associated antigen 1 (LFA-1), and very late antigen 4 (VLA-4).

72 Anti-very late antigen 4 (VLA-4; on neutrophils) inhibited ad

73 To provide further insights into the anti-very late antigen 4 (VLA4)/anti-vascular cell adhesion m

74 e detected the active conformational form of very late antigen 4 after stimulation with a peptide mim

75 s of beta1 phosphorylation and a decrease in very late antigen 4 binding to its ligand vascular cell

76 r by chemokines leads to the inactivation of very late antigen 4.

77 investigated the role of adhesion molecules (very late antigen [VLA]-4 [ alpha 4 beta 1 integrin] and

78 odies (MoAbs) enhanced integrin alpha4beta1 (very late antigen [VLA]-4) and alpha5 beta1 (VLA-5)-depe

79 The alpha1beta1 integrin, very late antigen-1 (VLA-1), is a collagen receptor expr

80 thelial growth factor receptor-3) and VLA-1 (very late antigen-1) promotes high-risk transplant survi

81 AQC2 to the alpha1 chain of human and sheep very late antigen-1, given 30 minutes before challenge,

82 on, but an increase in p150,95 (CD11c/CD18), very late antigen-1, or ICAM-1 expression was not observ

83 The integrin alpha1beta1 (very late antigen-1; CD49a/CD29) is a major adhesion rec

84 eater glycoprotein (GP) IIb/IIIa (p = 0.04), very late antigen-2 (p = 0.04) and platelet/endothelial

85 The leukocyte integrin very late antigen-4 (alpha(4)beta(1), CD49d/CD29) is an

86 The leukocyte integrin very late antigen-4 (VLA-4) (alpha 4 beta 1, CD49d/CD29)

87 hocytes that expressed low or high levels of very late antigen-4 (VLA-4) and non-antigen-specific act

88 rs to stromal cells is primarily mediated by very late antigen-4 (VLA-4) and vascular cell adhesion m

89 Extremely potent very late antigen-4 (VLA-4) antagonists with picomolar,

90 nction-associated antigen (LFA-1) and VCAM-1/very late antigen-4 (VLA-4) at select time points compar

91 rsor cells were transiently transfected with very late antigen-4 (VLA-4) binding to vascular cell adh

92 As very late antigen-4 (VLA-4) can exist in different funct

93 later, GVHD-associated increase in CD25 and very late antigen-4 (VLA-4) expression on donor T cells

94 lar endothelial growth factor receptor-1 and very late antigen-4 (VLA-4) have been shown to arrive at

95 ell adhesion molecule-1 (VCAM-1), LFA-1, and very late antigen-4 (VLA-4) have relatively little effec

96 esent study was to determine the role of the very late antigen-4 (VLA-4) integrin/ligand interaction

97 te function-associated antigen-1 (LFA-1) and very late antigen-4 (VLA-4) on adhesion of influenza hem

98 The expression of very late antigen-4 (VLA-4) on the surface of MBP-primed

99 scular cell adhesion molecule 1 (VCAM-1) and very late antigen-4 (VLA-4) played an integral role in t

100 Interaction of very late antigen-4 (VLA-4) with its ligand vascular cel

101 ion, we show that MBP-primed T cells express very late antigen-4 (VLA-4), and functional blocking ant

102 the adhesion molecules CD11a, CD11b, CD11c, very late antigen-4 (VLA-4), and L-selectin, as assessed

103 The alpha(4)beta(1)-integrin (very late antigen-4 (VLA-4), CD49d/CD29) is an adhesion

104 portance of VCAM-1, and its leukocyte ligand very late antigen-4 (VLA-4), in such leukocyte migration

105 Natalizumab, which binds very late antigen-4 (VLA-4), is a potent therapy for mul

106 he affinity of the alpha(4)beta(1) integrin, very late antigen-4 (VLA-4), measured with an LDV-contai

107 lasts within the bone marrow is adhesion via very late antigen-4 (VLA-4), the alpha(4)beta(1) integri

108 D49d), in complex with integrin beta1, forms very late antigen-4 (VLA-4), which interacts with vascul

109 cular cell adhesion molecule-1 (VCAM-1)- and very late antigen-4 (VLA-4)-mediated localization of CXC

110 and human monoblastoid U937 cells expressing Very Late Antigen-4 (VLA-4).

111 ascular cell adhesion molecule-1 (VCAM-1) or very late antigen-4 (VLA-4).

112 une cells from patients under long-term anti-very late antigen-4 (VLA-4)/natalizumab therapy (LTNT) a

113 skin fibroblasts, making it unlikely that a very late antigen-4 (VLA-4)/VCAM-1 interaction is requir

114 ion of one of the major leukocyte integrins, very late antigen-4 (VLA-4, CD49d/CD29).

115 duced by IL-3 in a dose-dependent manner via very late antigen-4 (VLA-4; alpha4beta1 integrins) and V

116 Very late antigen-4 (VLA-4; also called integrin alpha4b

117 ascular cell adhesion molecule-1 (VCAM1) and very late antigen-4 (VLA4) using monoclonal antibodies.

118 cule antagonist, compound A, to nonactivated very late antigen-4 (VLA4) was examined in lung inflamma

119 BL1(+) progenitors had similar expression of very late antigen-4 (VLA4), VLA5, leukocyte functional a

120 elated protein ligand, resulting in enhanced very late antigen-4 [VLA-4] directed adhesion and motili

121 lymphocyte adhesion but partially conserved very late antigen-4 adhesiveness.

122 irway inflammation and was prevented by anti-very late antigen-4 and anti-interleukin-5 treatments, w

123 Very late antigen-4 and CD11/CD18 integrins mediated pas

124 and natalizumab (Tysabri/Antegren) targeting very late antigen-4 for the treatment of relapsing-remit

125 ncrease expression of VCAM-1, a receptor for very late antigen-4 found on many hematopoietic progenit

126 dent mechanism to increase CD11c expression, very late antigen-4 function, and integrin coclustering

127 for the integrin alpha4beta1 (also known as very late antigen-4 or VLA-4).

128 ction by 50%, whereas blocking L-selectin or very late antigen-4 showed significant but smaller effec

129 te function-associated antigen-1) and VLA-4 (very late antigen-4) is essential for T-cell trafficking

130 lymphocyte function-associated antigen-1 and very late antigen-4) on splenocytes.

131 tide affinity ligand, VHPKQHR, homologous to very late antigen-4, a known ligand for VCAM-1.

132 The antigen alpha4beta1 (very late antigen-4, VLA-4) plays an important role in t

133 al cells, and mild expression of its ligand, very late antigen-4, was apparent in perivascular lympho

134 imilar to, but more restricted than, current very late antigen-4-directed approaches that have signif

135 Activated T cells use very late antigen-4/alpha4beta1 integrin for capture, ro

136 The optimization and validation of the very late antigen-4/vascular cell adhesion molecule-1 as

137 nocyte chemoattractant protein-1) and VLA-4 (very-late antigen-4).

138 , a ligand for the alpha(4)beta(1) integrin, very-late-antigen-4 (VLA-4 or CD49d).

139 Very-late-antigen-4 (VLA-4, alpha4beta1 integrin, CD49d/

140 ve been associated with an increased risk of very late (beyond 1 year) stent thrombosis.

141 tality was markedly increased after late and very late BMS thrombosis, particularly during the first

142 tructure and function, potentially improving very late clinical outcomes.

143 n beta2 expression in bipolar cells occurred very late, coinciding with synaptogenesis in the inner p

144 The C. elegans nuclear envelope disassembles very late compared with vertebrates and Drosophila.

145 lopidogrel treatment >12 months may decrease very late death or MI only in patients with DM receiving

146 Very late definite or probable stent thrombosis occurred

147 The risks of early/late (up to 1 year) and very late definite ST (after 1 year) were estimated.

148 95% CI: 0.07 to 0.46), with a lower risk of very late definite stent thrombosis in the EES group (0.

149 patients, due largely due to a lower risk of very late definite stent thrombosis.

150 The threshold excess risk of very late DES thrombosis compared with BMS, above which

151 ly ascribed to G2, overlaps extensively with very late DNA replication.

152 e enzyme-bound DNA substrate, and then, only very late during the reaction trajectory do strong speci

153 The p7/p1 mutation appeared very late during the selection process and was strongly

154 lones containing protease mutations observed very late during the selection process were constructed

155 duced during erythropoiesis, and abundant in very late erythroblasts.

156 events (1.6%), 32 late events (1.0%), and 33 very late events (1.1%).

157 The pathogenesis of these very late events is likely related to the permanent pres

158 zinc finger domain contributed primarily to very late events.

159 Very late expression factor 1 (VLF-1) of Autographa cali

160 Very late factor 1 (VLF-1) of Autographa californica mul

161 The product of the vlf-1 (very late factor 1) gene is required for expression of v

162 Along with very late flowering, these transgenic plants produced a

163 rring Arabidopsis (Arabidopsis thaliana) are very late flowering, unless flowering is promoted by a p

164 ngly up-regulated by FRI-Sf2, resulting in a very late-flowering phenotype.

165 ed by cAMP indicate that the block occurs in very late G1.

166 yrosine recombinase and is required for both very late gene expression and budded virus production.

167 factor 1) gene is required for expression of very late genes during the final phase of infection.

168 f transcripts from selected early, late, and very late genes showed that late and very late transcrip

169 KO/GUS showed that transcription of late and very late genes was lower at later times posttransfectio

170 tailbud contains multipotent cells that make very late germ-layer decisions.

171 tion of children starting the primary series very late (> or =12 months old) fell from 14% to 6%, and

172 Risk of late (30 days to 1 year) and very late (>1 year) BMS thrombosis was increased among p

173 ly (<30 days), late (30 days to 1 year), and very late (>1 year) periods (pinteraction = 0.49).

174 In late (>1 month) and very late (>1 year) ScT (respectively, 5 and 2 cases), 5

175 Very late IA (> 6 months after transplantation) was asso

176 unctional abnormality (ataxia) develops only very late in alpha-TTP-KO mice in spite of the severe al

177 ot show any enrichment of Mi-2/NuRD proteins very late in culture.

178 e when breaks were made either very early or very late in development, but was much more frequent in

179 sequentially, with some being expressed only very late in development.

180 creatic islets; it is usually diagnosed only very late in disease progression, after the critical aut

181 rski images); and finally, we analyze clones very late in embryonic development, which reveals novel

182 dependent antiviral gene expression occurred very late in infection.

183 r as T prolymphocytic leukemias, which occur very late in life, or as T chronic lymphocytic leukemias

184 r as T prolymphocytic leukemias, which occur very late in life, or as T chronic lymphocytic leukemias

185 e CBA/CaJ mouse maintains good hearing until very late in life, whereas the C57Bl/6 strain exhibits s

186 novel including S/D10, a cDNA only expressed very late in pollen development and highly up-regulated

187 ing the IS1112C male-sterile cytoplasm occur very late in pollen maturation.

188 ctions in (5me)C content in the genome occur very late in prostate cancer progression, appearing at a

189 trations of LINE-1 elements to be replicated very late in S phase.

190 The centromere-proximal zone replicates very late in S, whereas the distal zone normally replica

191 In P. falciparum, MyoB is synthesized very late in schizogony/merogony, and its location in me

192 Q into high-molecular-mass forms occurs only very late in sporulation, after mother cell lysis.

193 ospice, and those who enroll generally do so very late in the course of their illness.

194 und compartments in the larval brain, appear very late in the embryonic neuropile, clearly after the

195 Finally, Sec2p is dephosphorylated very late in the exocytic reaction to facilitate recycli

196 species damage, a feature not observed until very late in the pathology of the CIV model.

197 Separation of the sites of chemistry until very late in the splicing pathway may be crucial for pre

198 A1, also protected glycogen stores, but only very late in the stationary phase.

199 ed that the side-chain epoxide be introduced very late in the synthesis, owing to the ease with which

200 integrin (CD103) expression is up-regulated very late in thymic development on a subset of CD8(+)/CD

201 thrombosis, which is relevant to reports of very late in-stent thrombosis at altitude.

202 on traverse of G1 or S, but stalled cells in very late interphase.

203 Very late LAVA (>100 ms after QRS complex) were almost e

204 the domain has generally been restricted to very late Mesoproterozoic and Neoproterozoic successions

205 ifornica nuclear polyhedrosis virus late and very late mRNAs are transcribed by an RNA polymerase con

206 , in part, responsible for resistance to the very late onset disease.

207 That allele may contribute to very late onset form of Alzheimer disease when we are ag

208 lated to demographic data (non-white origin, very late onset), clinical features (limited recovery fr

209 GS differs notably from CVID and B(-) CVID: very late onset, no familial cases, and absence of lymph

210 e familial characteristics of high-incidence very late-onset AD (VLOAD, defined here as AD with onset

211 Very late-onset AD may be a good target for investigatin

212 llele-bearing genes that are associated with very late-onset AD should target the families of nonagen

213 4 and 15q22 are linked to early-onset AD and very-late-onset AD, respectively.

214 proteins that increases susceptibility to a very-late-onset form of AD.

215 ia (illness onset after 40 years of age) and very-late-onset schizophrenia-like psychosis (onset afte

216 he positions of late-onset schizophrenia and very-late-onset schizophrenia-like psychosis.

217 izophrenia into early-onset, late-onset, and very-late-onset subtypes now should be tempered by the r

218 >12 months versus </=12 months after PCI on very late outcomes in patients with diabetes mellitus (D

219 or, implicating cAMP signaling by PDE4B in a very late phase of consolidation.

220 s a 10-kDa auxiliary protein produced in the very late phase of gene transcription by Autographa cali

221 ntial for the burst of expression during the very late phase.

222 en though the infection proceeds through the very late phase.

223 ls, indicating progression into the late and very late phases of viral infection.

224 A polymerase stimulated transcription of the very late polyhedrin promoter but not the late 39k promo

225 Very late potentials (vLP) were defined as electrograms

226 Of all the fractionated, late, and very late potentials located in scar, only 21%, 26%, and

227 provide evidence that Rio1 associates with a very late pre-40S via its conserved C-terminal domain.

228 in-air capture motions were aborted, even at very late prey removals (<20 ms = 6 cm before expected c

229 ate and specific transcription from late and very late promoters but was not active on viral early pr

230 the burst sequences of both the polh and p10 very-late promoters.

231 In contrast, very late reactivities may signify chemotactic propertie

232 Reliable prediction of very late recurrence of atrial fibrillation (VLRAF) occu

233 Under these conditions, dormant origins fire very late relative to other active origins.

234 /M cyclin fusion was functional for MMR at a very late-replicating region of the genome.

235 and appears to merge with the normal zone of very late replication in proximal Xq27.

236 sition states for C-H oxidative addition are very late, resembling the aryl iridium hydride intermedi

237 Although only a few origins that fire in very late S phase have been identified in fission yeast,

238 This study examined whether very late scaffold thrombosis (VLScT) occurs when resorp

239 splantation experiments indicating that even very late sclerotome tissue fragments are multipotential

240 The predominant finding in late and very late ScT is peristrut low-intensity area.

241 caffold collapse was found in 1 patient with very late ScT.

242 1 days to 1 year), cumulative 1-year ST, and very late ST (1-2 years).

243 The risk of very late ST is low and comparable between n-DES and BMS

244 and larger studies will have to show whether very late ST rates will also be improved in newer DES.

245 to 2.98; p = 0.21), whereas a higher risk of very late ST was observed with o-DES compared with BMS (

246 The risk of very late ST was similar between the n-DES and BMS group

247 nd 155 (71.4%) presented with early and late/very late ST, respectively.

248 3.3%) and severe restenosis (19.1%); and for very late ST, the most common dominant finding was neoat

249 In patients presenting very late ST, uncovered stent struts were a common domin

250 BVS had a higher risk of subacute, late, and very late ST, whereas the risk of acute ST was similar.

251 BVS had a higher risk of subacute, late, and very late ST, whereas the risk of TLF and TLR was higher

252 atherosclerosis and uncovered struts in late/very late ST.

253 ment is associated with an increased risk of very late ST.

254 ificantly reduced ARC definite ST, including very late ST.

255 ronic inflammation, predisposing to late and very late ST.

256 or pancreatic cancer is often diagnosed at a very late stage at which point treatment options are min

257 -CD8 cells can block HSV-1 reactivation at a very late stage in the viral life cycle.

258 We conclude that L40 is assembled at a very late stage into pre-60 S ribosomal subunits and tha

259 ecific needs, such as water solubility, on a very late stage of the multistep synthesis are described

260 evere, sustained pulmonary hypertension in a very late stage of the Sugen 5416/hypoxia/normoxia-expos

261 entified a new function of IFITMs during the very late stage of virus replication, i.e., virion assem

262 ides a first glimpse into the structure of a very late-stage intermediate in the lesion-extrusion pat

263 Instead, SAP is necessary for very late stages of differentiation or, most likely, for

264 in complex that can regulate EGFR traffic at very late stages of the endocytic pathway.

265 to HCC, while Ctnnb1 mutations occur only at very late stages.

266 d similar risks of late definite or probable very late stent thrombosis (RR, 1.06; 95% CI, 0.53-2.11;

267 n AMI are still feared for possible late and very late stent thrombosis (ST).

268 The pathomechanisms underlying very late stent thrombosis (VLST) after implantation of

269 indings regarding the prevalence of late and very late stent thrombosis (VLST) and the mechanisms tha

270 Thus, very late stent thrombosis (VLST) attributable to durabl

271 We sought to define what incremental risk of very late stent thrombosis (VLST) in drug-eluting stents

272 Furthermore, the contribution of very late stent thrombosis (VLST) to these events remain

273 dies on the pathophysiological mechanisms of very late stent thrombosis (VLST).

274 as been observed frequently in patients with very late stent thrombosis after drug eluting stent impl

275 arly (0-30 days), late (31 days-1 year), and very late stent thrombosis amounted to 0.6, 0.1, and 0.6

276 with EES is associated with a lower risk of very late stent thrombosis compared with early-generatio

277 n, less fibrin deposition, and less late and very late stent thrombosis compared with SES and PES in

278 Observational studies suggest higher very late stent thrombosis incidence, but the relative r

279 (PES) are associated with increased risk of very late stent thrombosis occurring >1 year after stent

280 It is unknown whether the risk of very late stent thrombosis persists with newer-generatio

281 The incidence of very late stent thrombosis was also similar between the

282 The observed frequency of late and very late stent thrombosis was less in CoCr-EES (4%) ver

283 There was no increase in very late stent thrombosis with EES versus BMS (RR, 0.89

284 ue to a metal cage, and the risk of late and very late stent thrombosis.

285 t-generation DES and BMS with no increase in very late stent thrombosis.

286 herapy due to the increased risk of late and very late stent thrombosis.

287 Furthermore, the risk of very late stent, although substantially reduced with new

288 thrombosis (RR, 3.22; 95% CI, 1.89-5.49) and very late stent/scaffold thrombosis (>1 year; RR, 4.78;

289 te or probable stent/scaffold thrombosis and very late stent/scaffold thrombosis seems to be higher w

290 able protocol for postharvest storage of the very-late Tarocco "Sant'Alfio" orange to prolong the ava

291 s, ICP27 was confined to the nucleus even at very late times after infection.

292 dentified multicistronic RNAs, from early to very late times of infection, that potentially encode th

293 Interestingly, even at very late times postinfection, a mixture of multiple sma

294 te, and very late genes showed that late and very late transcription was absent in cells transfected

295 ion was apparently unaffected, both late and very late transcription were delayed in cells infected w

296 refore, we hypothesize that KN-93 prevents a very late, uncharacterized step in cyclin D/cdk4 activat

297 during virus DNA synthesis and impaired both very late viral gene expression and production of infect

298 5 increased transcription from both late and very late viral promoters.

299 , whereas its caspase (ORF073) was expressed very late, which correlated with apoptotic events leadin

300 People with glaucoma frequently present very late with advanced disease, and acceptance of and a