ライフサイエンスコーパス: plaque formation

1 (EC) dysfunction, leading to atherosclerotic plaque formation.

2 nhibition of Abeta deposition and to reduced plaque formation.

3 smooth muscle cell (VSMC) proliferation and plaque formation.

4 ich suggests effective inhibition of de novo plaque formation.

5 ch are highly susceptible to atherosclerotic plaque formation.

6 rbed flow contributes to the atherosclerotic plaque formation.

7 idomide significantly reduces Abeta load and plaque formation.

8 K5-EKO-LDLR(-/-) mice and observed increased plaque formation.

9 idation is known to initiate atherosclerotic plaque formation.

10 elop strategies to prevent dental caries and plaque formation.

11 a42 peptide is sufficient to promote amyloid plaque formation.

12 logical changes closely resembling psoriatic plaque formation.

13 model that closely resembles human psoriatic plaque formation.

14 thelial changes conducive to atherosclerotic plaque formation.

15 to both neurofibrillary tangles and amyloid plaque formation.

16 ral behaviors independent of visible amyloid plaque formation.

17 haracteristics of the biofilm during de novo plaque formation.

18 renal fibrosis and increased atherosclerotic plaque formation.

19 following 1, 2, 4, and 7 days of undisturbed plaque formation.

20 nd play important roles in the initiation of plaque formation.

21 n cell bodies, neurites, and synapses before plaque formation.

22 in normal arteries, could be induced during plaque formation.

23 to support production of infectious virus or plaque formation.

24 ularization; and corneal opacity, leading to plaque formation.

25 Both mutants were defective in plaque formation.

26 influence steps in S. flexneri invasion and plaque formation.

27 the PSAPP mouse model of AD as a function of plaque formation.

28 ficial in lowering the incidence of coronary plaque formation.

29 ction are critical events in atherosclerotic plaque formation.

30 r distances and times important for adhesive plaque formation.

31 iferase reporter gene, virus production, and plaque formation.

32 onfirmed by studies of heparin inhibition of plaque formation.

33 ion of drug required to inhibit 90% of viral plaque formation.

34 nes are associated with Abeta deposition and plaque formation.

35 + and Zn2+) play critical roles in the Abeta plaque formation.

36 isrupt synaptic activity or act as seeds for plaque formation.

37 t it is involved in APP processing and Abeta plaque formation.

38 beta42-induced neurodegeneration and amyloid plaque formation.

39 rtension, increased vascular resistance, and plaque formation.

40 sease with a higher risk for atherosclerotic plaque formation.

41 ys a central role in arterial thrombosis and plaque formation.

42 the disease, either before or after amyloid plaque formation.

43 s and apoptosis, designed to reduce unstable plaque formation.

44 rmation had strongly reduced atherosclerosis plaque formation.

45 tions that abolished viability as assayed by plaque formation.

46 y contribute to elevated levels of Abeta and plaque formation.

47 nd expand the degenerative zone resulting in plaque formation.

48 ndent on inducer for single-cycle growth and plaque formation.

49 oM only had a relatively minor effect on MDV plaque formation.

50 pressing cell line restored v3480 growth and plaque formation.

51 have been implicated in AD pathogenesis and plaque formation.

52 ow progressed at a rapid rate with expanding plaque formation.

53 ggregation and toxicity, and inhibits senile plaque formation.

54 ersity of cellular processes involved in the plaque formation.

55 ion in culture, causing cell destruction and plaque formation.

56 pressing hypothalamic arcuate neurons before plaque formation.

57 whereas cross-sectional OCT reveals Paques' plaque formation.

58 and consequently alleviated atherosclerosis plaque formation.

59 PKCbeta initially diminished APP and delayed plaque formation.

60 lementation and calcium intakes in Randall's plaque formation.

61 uronal dysfunction that can be active before plaque formation.

62 y oxidative stress promoting atherosclerotic plaque formation.

63 rastically impairs viral RNA replication and plaque formation.

64 osclerotic lesion development and vulnerable plaque formation.

65 e model of shear stress-modulated vulnerable plaque formation.

66 s important for efficient HSV-1 assembly and plaque formation.

67 a model of shear stress-modulated vulnerable plaque formation.

68 hematopoietic EphA2 deletion does not affect plaque formation.

69 a hallmark of all stages of atherosclerotic plaque formation.

70 ng that these interactions trigger the Abeta plaque formation.

71 h play a key role in atherogenesis, inhibits plaque formation.

72 G, implicating ceramide-enriched exosomes in plaque formation.

73 M2 macrophages together with a reduction in plaque formation.

74 therogenic phenotypes and reduce the rate of plaque formation.

75 coronary arteries and LAD predisposition to plaque formation.

76 role against neointimal and atherosclerotic plaque formations.

77 mice before and during the process of Abeta plaque formation (age 3-28 months).

78 fied high-risk locations for atherosclerotic plaque formation along the entire aorta, which was valid

79 from 5XFAD or APP/PS1 mice decreases senile plaque formation, ameliorates synapse loss, elevates lon

80 ve been recognized as key factors in amyloid plaque formation and aggravation of AD.

81 ormin attenuated Ang-II-induced atheromatous plaque formation and aortic aneurysm in ApoE(-/-) mice p

82 their aortic infiltration, delaying atheroma plaque formation and aortic valve calcification.

83 wever, their contribution to atherosclerotic plaque formation and arterial thrombosis remains unclear

84 causative role in triggering atherosclerotic plaque formation and arterial thrombosis.

85 production of Abeta peptide leads to amyloid plaque formation and associated neuritic dystrophy.

86 ice harboring Mir155-/- macrophages enhanced plaque formation and CCL2 expression.

87 marrow to p53-/-/ApoE-/- mice reduced aortic plaque formation and cell proliferation in brachiocephal

88 ts highlight the role of 3-OS HS during HCMV plaque formation and cell-to-cell fusion and identify a

89 pp71 mutant HCMV while IE1 increased wt HCMV plaque formation and completely complemented the IE1 mut

90 K-null phenotype characterized by very small plaque formation and drastic reduction in infectious vir

91 t to inflamed arterial endothelium initiates plaque formation and drives progression of atheroscleros

92 ts were able to inhibit wild-type (WT) virus plaque formation and filament formation, whereas a doubl

93 fide bonds plays an important role in dental plaque formation and fitness for the bacteria.

94 ome with the TR, is sufficient for efficient plaque formation and generation of infectious virus.

95 ctors that influence the dynamics of amyloid plaque formation and growth in vivo are largely unknown.

96 eral vibrissal deprivation decreased amyloid plaque formation and growth.

97 % was associated with a dramatic decrease in plaque formation and growth.

98 Hypercalciuria may promote Randall's plaque formation and growth.

99 Enhancement of atherosclerotic plaque formation and increase in macrophage content by n

100 V proteins complement ICP0-null mutant HSV-1 plaque formation and induce derepression of quiescent HS

101 ught to precede and underlie atherosclerotic plaque formation and instability.

102 erleukin 18 (IL-18) promotes atherosclerotic plaque formation and is increased in patients with acute

103 (APP23/TNFRII(-/-)), AD-like pathology, i.e. plaque formation and microglial activation, occurs as ea

104 cells (SMCs) contributes to atherosclerotic plaque formation and neointimal thickening in other occl

105 sease, but the temporal relationship between plaque formation and neuronal dysfunction is poorly unde

106 t that the pathological process of calcified plaque formation and progression is the same in men and

107 mic factors on the arterial wall response to plaque formation and progression.

108 , as part of the pst operon, restored normal plaque formation and regulation of phoA expression.

109 mutant, had a conditional-lethal phenotype: plaque formation and replication of infectious virus wer

110 e rendered them less able to support 22/n199 plaque formation and replication.

111 n, cartilage degradation, or atherosclerotic plaque formation and rupture.

112 that exert a broad effect on atherosclerotic plaque formation and stability in the carotid artery.

113 significantly contribute to atherosclerotic plaque formation and stability.

114 alcification, which are crucial processes in plaque formation and stability.

115 Consistent with this, both plaque formation and tachyzoite invasion were broadly si

116 that this downregulation is due to to Abeta-plaque formation and tau hyper-phosphorylation.

117 ke F13L in VACV, EVM036 is required for ECTV plaque formation and that EVM036 and EV are important fo

118 To investigate the temporal relation between plaque formation and the changes in local neuritic archi

119 SMCs undergo in atherosclerosis in regard to plaque formation and the structure of advanced lesions.

120 y, eosinophils contribute to atherosclerotic plaque formation and thrombosis through an interplay wit

121 In cell culture, ST-246 inhibited plaque formation and virus-induced cytopathic effects.

122 lasmic accumulation and lack of gap junction plaque formation and was not altered by coexpression of

123 owth in vitro in the HeLa cell assay and for plaque formation and were safe in the Sereny test and im

124 xpression of hfq in the dksA mutant restored plaque formation, and an hfq mutant failed to form plaqu

125 aired HSV-induced Ca2+ release, viral entry, plaque formation, and cell-to-cell spread of HSV-1 and H

126 phology to secA2 mutants, restored wild-type plaque formation, and increased virulence in mice.

127 The mutant defects in virus production, plaque formation, and pUL31 interaction can be suppresse

128 rkedly reduced Abeta deposition and neuritic plaque formation, and rescued memory deficits in the dou

129 ant phenotypes in assays for cell fusion and plaque formation, and time-course studies showed that pl

130 ssing human MxA protein did not support ASFV plaque formation, and virus replication in these cells w

131 ine; after 7, 14, and 21 days of undisturbed plaque formation; and 21 days after reinstitution of bru

132 treatments that can reverse atherosclerotic plaque formation are actively being sought.

133 mechanisms underlying early atherosclerotic plaque formation are not completely understood.

134 ns, but the specific contributions of KCs to plaque formation are not fully understood.

135 ces colonization and contributions to dental plaque formation, as well as their potential roles in th

136 y reduced early diet-induced atherosclerotic plaque formation associated with both diminished inflamm

137 fed Ldlr(-/-) mice decreased atherosclerotic plaque formation, associated with decreased macrophage a

138 dsorption, there was no inhibitory effect on plaque formation at any concentration.

139 is 7 muM, with complete inhibition of viral plaque formation at approximately 20 muM, and its antivi

140 eased PDGFRbeta signalling promotes advanced plaque formation at novel sites in the thoracic aorta an

141 s a lipoprotein-driven disease that leads to plaque formation at specific sites of the arterial tree

142 yte adhesion and accelerated atherosclerotic plaque formation at the carotid sinus of Adamts13(-/-)/A

143 coupling even in the presence of significant plaque formation between paired cells.

144 for its role in Alzheimer's disease amyloid plaque formation but also contributes to neurodegenerati

145 ied to have AD-type dementia without amyloid plaque formation but with extensive intraneuronal Abeta

146 oth IE1 and pp71 stimulated ICP0-null mutant plaque formation, but neither to the extent achieved by

147 hat aberrant proliferation of VSMCs promotes plaque formation, but that VSMCs in advanced plaques are

148 esponses, blocked viral entry, and inhibited plaque formation by 90% compared to control siRNA.

149 ck and Fgr led to attenuated atherosclerotic plaque formation by abrogating endothelial adhesion and

150 on of PML increases both gene expression and plaque formation by an ICP0-negative HSV-1 mutant, while

151 Plaque formation by both pathogens was dependent on the

152 aggregation occurs in the earliest stages of plaque formation by bringing bacteria together to create

153 ICP0-null mutant HSV-1, while ICP0 increases plaque formation by pp71-deficient HCMV.

154 ic flux under high SS limits atherosclerotic plaque formation by preventing endothelial apoptosis, se

155 were all required for IcsA localization and plaque formation by S. flexneri.

156 istic pathogen, is thought to promote dental plaque formation by serving as a bridge bacterium betwee

157 Surprisingly, plaque formation by the mutant virus was not improved in

158 rthermore, the marked exacerbation of aortic plaque formation caused by TTP deficiency in the APOE(-/

159 nockout mice show diminished atherosclerotic plaque formation, characterized by reduced proinflammato

160 arin (6 to 50 micro g/ml) as an inhibitor of plaque formation compared to the E2-G pseudotype virus.

161 mutants showed no significant differences in plaque formation compared to wild-type bacteria.

162 Western-type diet had a marked reduction in plaque formation compared with apoE(-/-) controls.

163 also caused a 10- or 4-fold decrease of Cx43 plaque formation compared with control cells.

164 individuals had 1.6-fold greater risk of new plaque formation compared with HIV-uninfected individual

165 ontribution of antibodies to atherosclerosis plaque formation, composition, and stability in vivo (1)

166 isolated extragenic suppressors of the Y68A plaque formation defect and mapped them by a combination

167 Tcad/ApoE-DKO mice increased atherosclerotic plaque formation, despite a 5-fold increase in plasma ad

168 of local ESS and the remodeling response to plaque formation determine the natural history of indivi

169 that target the key processes implicated in plaque formation, development, and disruption and highli

170 se aggregates may seed extracellular amyloid plaque formation during AD pathogenesis.

171 reducing excessive vascular inflammation and plaque formation during early atherosclerosis.

172 he C-terminal quarter of the protein reduced plaque formation efficiency by up to two orders of magni

173 Depletion of all PML isoforms increases the plaque formation efficiency of ICP0-null mutant HSV-1, a

174 latory factor 3 (IRF3) does not increase the plaque formation efficiency of ICP0-null mutant HSV-1, w

175 that 3-month-old Tg2576 mice, before amyloid plaque formation, exhibit decreased weight with markedly

176 Gal-3 binding protein (Gal-3BP) with carotid plaque formation (focal intima-media thickness >1.5 mm)

177 SV-induced calcium release, viral entry, and plaque formation following infection with acyclovir-sens

178 ction, pseudorevertant alleles that restored plaque formation for lysis-defective mutants of Rz and R

179 n rescues early and late gene expression and plaque formation for SV40 HR viruses, has been shown to

180 perimentation and analysis considering phage plaque formation from the perspective of selection actin

181 there were stark differences in gap junction plaque formation, gap junctional intercellular communica

182 has been related to several factors such as plaque formation, hormonal modifications, and viral infe

183 e is characterized by severe atherosclerotic plaque formation, hypertension, type 2 diabetes, obesity

184 nt during viral entry but completely blocked plaque formation if present postentry, reduced plaque si

185 We found a significant reduction in brain plaque formation, improved cognitive function and increa

186 kness (CCA-IMT) and new focal carotid artery plaque formation (IMT >1.5 mm) over median 7 years.

187 oduction of viral particles, as indicated by plaque formation in a bacterial lawn.

188 pose-tissue inflammation and atherosclerotic plaque formation in a mouse model of obesity.

189 calcium significantly accelerates Randall's plaque formation in a murine model.

190 g strains for adherence to, invasion of, and plaque formation in A549 cells.

191 eta pathology and provides new insights into plaque formation in AD.

192 ing basement membrane, blood physiology, and plaque formation in Alzheimer disease.

193 s peptide translocation across membranes and plaque formation in Alzheimer's disease, are discussed.

194 orexin receptor antagonist decreased, Abeta plaque formation in amyloid precursor protein transgenic

195 s are necessary and sufficient for psoriatic plaque formation in an experimental disease model that c

196 ulation of cerebral Abeta levels and amyloid plaque formation in animal models, and accumulating evid

197 t here that overexpression of hDDAH1 reduces plaque formation in ApoE(-/-) mice by lowering ADMA.

198 ngiotensin II (Ang-II)-mediated atheromatous plaque formation in ApoE(-/-) mice.

199 eta plaques in vivo, but rather it inhibited plaque formation in APPPS1 mice coexpressing SNCA(A30P)

200 by which they infect cells and contribute to plaque formation in arterial walls are not well understo

201 izes ox-LDL which leads to the initiation of plaque formation in arteries.

202 different pathophysiological mechanisms for plaque formation in athletic versus sedentary men.

203 ces of the CT domain of the F protein slowed plaque formation in both avian and COS-7 cells.

204 DNA binding mutant of C/EBP-alpha, enhances plaque formation in bovine cells.

205 We observed increased plaque formation in CD47 null mice compared to wild-type

206 pathways may therapeutically reduce amyloid plaque formation in cerebral vessels and the brain paren

207 s DksA is required for stress resistance and plaque formation in cultured cell monolayers, a measure

208 and RstBA systems are required for wild-type plaque formation in cultured epithelial cells.

209 cellular survival in macrophages and reduced plaque formation in HeLa cells.

210 We found that mengovirus plaque formation in HeLa or L cells was inhibited nearly

211 lexneri degP mutant, which was defective for plaque formation in Henle cell monolayers, had a reduced

212 We induced atherosclerotic plaque formation in hypercholesterolemic ApoE mice by pl

213 DL associated with decreased atherosclerotic plaque formation in hyperlipidemia.

214 C also significantly reduced atherosclerotic plaque formation in hyperlipidemic LDLR(-/-) mice.

215 onounced defect in viral gene expression and plaque formation in limited-passage human fibroblasts.

216 ven metabolic changes reduce atherosclerotic plaque formation in mice, thereby underscoring the impor

217 es IL-17A, IL-17F, and IL-22 in psoriasiform plaque formation in mice.

218 for growth in primary murine macrophages and plaque formation in monolayers of L2 fibroblasts, thus v

219 Plaque formation in native coronary bifurcations and neo

220 ta in blood plasma and is thought to inhibit plaque formation in peripheral tissue.

221 ns reduce spongiform degeneration and hinder plaque formation in prion disease.

222 hotosensitive dye Rose bengal, and monitored plaque formation in real time using multiphoton microsco

223 The Y328 and F328 viruses allowed plaque formation in the absence of trypsin, whereas the

224 n, however the exact role of aggregation and plaque formation in the aetiology of Alzheimer's disease

225 eptide generation and thereby reduce amyloid plaque formation in the brain, a neuropathological hallm

226 ased soluble Abeta species and extracellular plaque formation in the brain.

227 hibits Abeta generation and diminishes Abeta plaque formation in the brain.

228 The specific role of nZVI-derived root iron plaque formation in the safe production of rice has been

229 sCD163 was associated with plaque formation in virally suppressed HIV+ men (RR 1.52

230 POPG blocked viral plaque formation in vitro by 4 log units, and markedly s

231 efficiency of trypsin independent growth and plaque formation in vitro: R-R-R-R > R-K-A-R > R-Q-P-R >

232 one or more of these compounds may modulate plaque formation in vivo, which is a prerequisite for th

233 increase in Abeta40 would accelerate amyloid plaque formation in vivo.

234 phage cholesterol efflux and atherosclerotic plaque formation in vivo.

235 h a B-independent phenotype, as evaluated by plaque formation in wild-type cells.

236 gher than the wild-type SER virus and caused plaque formation, in contrast to the wild-type virus whi

237 like mice from premature mortality, cerebral plaque formation, increased beta-amyloid levels, protein

238 e pentose phosphate pathway had no effect on plaque formation, indicating that it is not critical for

239 pathways in abdominal aortic aneurysm versus plaque formation, inhibiting the former pathology but pr

240 how that eosinophils support atherosclerotic plaque formation involving enhanced von Willebrand facto

241 Atherosclerotic plaque formation is fueled by the persistence of lipid-l

242 Developing a better understanding of phage plaque formation is relevant because of the ubiquity of

243 ) the mechanism of capillary amyloidosis and plaque formation is similar, (b) the cells of monocyte/m

244 cells (both of which mediate atherosclerotic plaque formation) lacking sortilin had reduced secretion

245 amyloid precursor protein results in amyloid plaque formation, McGowan et al. have produced mice that

246 roups according to extent of VCAM-1-positive plaque formation (median CEU videointensity, 1.8 [95% CI

247 myloid beta (Abeta) production, aggregation, plaque formation, microglia/immunological responses, inf

248 ere remarkably resistant to ligation-induced plaque formation (n=6).

249 We analyzed brain exosome content, amyloid plaque formation, neuronal degeneration, sphingolipid, A

250 autoimmune diseases, cancer, atherosclerotic plaque formation, numerous neurological disorders, etc.

251 phage foam cells, central to atherosclerotic plaque formation, occurs as a result of imbalance betwee

252 riven gamma oscillations before the onset of plaque formation or cognitive decline in a mouse model o

253 response improves resistance to Abeta, slows plaque formation or increases plaque degradation, and ma

254 apoE(-/-) recipients significantly decreased plaque formation (P<0.001).

255 This leads to an increase of plaque formation, particularly in early stages of the di

256 ero monolayers, in MDBK cells, after initial plaque formation, plaque size actually decreased and, wi

257 rowth was more prominent early after initial plaque formation: plaques grew faster in 6-month-old com

258 8 mice with 1,25(OH)2D3 during the period of plaque formation reduced soluble and insoluble plaque-as

259 yet the precise role of alpha-syn in amyloid plaque formation remains elusive.

260 rmation, and time-course studies showed that plaque formation represents MNGC death.

261 ells knocked down for Bim showed delayed VZV plaque formation, resulting in longer survival of VZV-in

262 Atherosclerotic plaque formation results from chronic inflammation and f

263 rease in sCD14 was associated with increased plaque formation (risk ratio [RR] 1.24, 95% confidence i

264 ere with helper phage reproduction, blocking plaque formation, sharply reducing burst size and enhanc

265 Abca1(BSM) mice had reduced atherosclerotic plaque formation, similar to mice transplanted with bone

266 y, overexpression of Bim resulted in earlier plaque formation, smaller plaques, reduced virus replica

267 encephalopathy characterized by abundant PrP plaque formation, spongiform change, and gliosis.

268 text that would recapitulate major events in plaque formation such as infiltration of inflammatory ce

269 that CXADR is induced in macrophages during plaque formation, suggesting a mechanism by which entero

270 se alterations correlated with the extent of plaque formation, suggesting a plaque-independent mechan

271 d wall thickness progression and risk of new plaque formation, suggesting arterial injury in this coh

272 unctions resulted in a dramatic reduction in plaque formation, suppressed systemic and organ inflamma

273 rmits the control of the determinant step of plaque formation, that is calcification of the plaque.

274 biological membranes are involved in fibril plaque formation, the role of lipid membrane composition

275 us salivarius, contribute to tooth decay and plaque formation; therefore, it is essential to develop

276 ICP0-null HSV-1 and wt HCMV replication and plaque formation; therefore, this study reveals that MOR

277 nome foci, stimulated ICP0-null mutant HSV-1 plaque formation to near wild-type levels, and efficient

278 al in macrophages and significantly enhanced plaque formation upon prolonged infection in L2 fibrobla

279 tivated Langerin(neg) cDCs trigger psoriatic plaque formation via IL-23-mediated activation of innate

280 ooth muscle cells alleviates atherosclerosis plaque formation via up-regulating autophagy in ApoE(-/-

281 ) controls, although atherosclerotic luminal plaque formation was attenuated.

282 ce of the glycolytic pathway in invasion and plaque formation was confirmed by testing the effect of

283 The in vivo results revealed that plaque formation was inhibited/reduced by chlorhexidine

284 rus plaque number, an increase in pseudotype plaque formation was observed.

285 rrelation in young APP/PS1 mice before Abeta plaque formation was proportional to the amount of regio

286 In addition, atherosclerotic plaque formation was significantly reduced in the aorta

287 virus, which was not viable on the level of plaque formation, was characterized.

288 To examine the role of CXCL16 in plaque formation, we created CXCL16-deficient mice (CXCL

289 isingly, whereas beta-amyloid production and plaque formation were unaltered, synaptic loss, astrogli

290 xpression of immediate-early genes and viral plaque formation) were substantially reduced in cells tr

291 M-A(-/-)apoe-/- mice showed increased aortic plaque formation when compared with trJAM-A(+/+) apoe(-/

292 ar calcium deposition in the early stages of plaque formation, when active uptake mechanisms are the

293 he origin efficiently and were inhibitory to plaque formation, whereas constructs whose N terminus is

294 ctivities in the absence of detectable viral plaque formation, whereas mixed deleted and complete for

295 n alone results in the drastic inhibition of plaque formation which can be partially relieved by an i

296 or near residue 359 were shown to potentiate plaque formation, while other C-terminal truncations wer

297 ith BAC20 resulted in complete inhibition of plaque formation with as little as 50 nM of the drug, wh

298 on and cell death, enabling studies of viral plaque formation with single-cell resolution.

299 p53-/- mice demonstrated increased aortic plaque formation, with increased rates of cell prolifera

300 mutant, XG4J, was not viable on the level of plaque formation without X174 J gene complementation.