ライフサイエンスコーパス: aged mice

1 ell deletion rejuvenates pulmonary health in aged mice.

2 re HSC function and the immune repertoire in aged mice.

3 associated with declining levels of IL-2 in aged mice.

4 a-cell mass, leading to islet hyperplasia in aged mice.

5 impaired dopamine homeostasis and release in aged mice.

6 nd decreased bone marrow fat accumulation in aged mice.

7 investigated the origin of CD25(lo) Tregs in aged mice.

8 MI checkpoint is compromised in oocytes from aged mice.

9 ion studies show altered dopamine release in aged mice.

10 Tregs, naive T cells, and memory T cells in aged mice.

11 gnitive decline and enhances neurogenesis in aged mice.

12 ted to increase the generation of neurons in aged mice.

13 icity and overall behavioral capabilities of aged mice.

14 nt-binding protein (CREB)-regulated genes in aged mice.

15 tional defect in fine odor discrimination in aged mice.

16 se results in transgenic, non-transgenic and aged mice.

17 well as strengthening of damaged muscles of aged mice.

18 first 24 weeks of adult life but depleted in aged mice.

19 n both fast aging Xpd(TTD/TTD) and naturally aged mice.

20 ranscriptional changes in the hippocampus of aged mice.

21 rulonephritis and a range of malignancies in aged mice.

22 acetylation at the c-fos promoter region in aged mice.

23 d neuron formation and olfactory function in aged mice.

24 endent "context discrimination (CS) test" in aged mice.

25 , after fear conditioning were diminished in aged mice.

26 ted fibrosis, was observed in both adult and aged mice.

27 evels were diminished in CD8(+) T cells from aged mice.

28 ed effector CD8+ T cell polyfunctionality in aged mice.

29 ein kinase signaling in satellite cells from aged mice.

30 rkers of the effects of haloperidol (HAL) in aged mice.

31 icity and hippocampal-dependent cognition in aged mice.

32 ntly improved HAL effects on the CAR test in aged mice.

33 tore T cell responses and TriVax efficacy in aged mice.

34 evented ischemia-mediated tissue necrosis in aged mice.

35 gene expression changes in quiescent HSCs of aged mice.

36 ppocampus and improves cognitive function in aged mice.

37 g autophagy and improving vessel function in aged mice.

38 -derived products after being transferred to aged mice.

39 neutralization of sFasL reduced CNV only in aged mice.

40 reversal learning from both young and middle-aged mice.

41 lated from adipose or bone marrow tissues of aged mice.

42 icantly lower in amplitude in cartilage from aged mice.

43 ere evident when the mutation was induced in aged mice.

44 enance of normal motor behavior in adult and aged mice.

45 nce of performing preclinical assessments in aged mice.

46 insulin resistance in the skeletal muscle of aged mice.

47 ads to reduced insulin sensitivity in middle-aged mice.

48 revented by long-term caloric restriction in aged mice.

49 n and increased replication of beta cells in aged mice.

50 scriptomes of microglia of healthy adult and aged mice.

51 ro and in vivo, resembling EPCs derived from aged mice.

52 ease of central serotonin in young-adult and aged mice.

53 k the size and location of axonal boutons in aged mice.

54 ssociated metabolic disorders in fat-fed and aged mice.

55 ty and enhanced thrombotic susceptibility in aged mice.

56 ow chimeras were performed between young and aged mice.

57 oodborne sFasL, and reduced CNV in young and aged mice.

58 well as primary preadipocytes isolated from aged mice.

59 nti-Gr-1 boosted DT effects in young but not aged mice.

60 usceptibility to various types of cancers in aged mice.

61 ode dysfunction under stressed conditions in aged mice.

62 antly attenuated at the NMJs of 27-month-old aged mice.

63 D31(hi)Emcn(hi) vessel and bone formation in aged mice.

64 (PR8), both of which cause severe disease in aged mice.

65 challenge, although effects were greater in aged mice.

66 clones are introduced into the repertoire of aged mice.

67 diminished microgliosis and astrogliosis in aged mice.

68 8 wk of age but was significantly reduced in aged mice.

69 pecific immunity and reduced tumor growth in aged mice.

70 dent effect of apoE on Abeta accumulation in aged mice.

71 tion following stringent lethal challenge in aged mice.

72 es of BACE1, causes reduced spine density in aged mice.

73 dent effect of apoE on Abeta accumulation in aged mice.

74 c adaptational changes to chronic hypoxia in aged mice.

75 hroughput RNA-Sequencing of kidney tissue in aged mice.

76 ecretions and plasma in both young adult and aged mice.

77 ag in polycythemic response were observed in aged mice.

78 rotein upregulation were not affected in the aged mice.

79 sion was decreased in the cerebral cortex of aged mice.

80 rarily restored normal sequence structure in aged mice.

81 een neuroinflammation and hypermetabolism in aged mice.

82 -renewal and restored immune cell content in aged mice.

83 ot only in the skin but also in the serum of aged mice.

84 cline of the affected SVZ-stem cell niche in aged mice.

85 jury and restored endogenous HSC function in aged mice.

86 tions to voluntary wheel running in young or aged mice.

87 re naive T cell homeostatic proliferation in aged mice.

88 +) dynamics in eggs from young and naturally-aged mice.

89 uvenated the aged HSCs and MuSCs in normally aged mice.

90 tiated after stroke, would delay recovery in aged mice.

91 ted with the extent of cognitive deficits in aged mice.

92 slow gamma activity but not SWR abundance in aged mice.

93 as determined by Morris water maze (MWM), in aged mice.

94 binol rescued the barrier deficiency even in aged mice.

95 chanism of active zone proteins in NMJs from aged mice.

96 and improve measures of healthspan in middle-aged mice.

97 Here, we show that aged mice (18-19 months) had reduced functional recovery

98 In the current study, aged mice (22-25 months old) exhibited significantly inc

99 n, astrocytic Apoe dramatically decreased in aged mice, a decrease that was prevented by exercise.

100 In aged mice, a single injection of HT-0712 significantly b

101 Conversely, loss of FGF21 function in middle-aged mice accelerated thymic aging, increased lethality,

102 In aged mice, accumulation of RanGAP1 together with polyglu

103 lts, young C57BL/6 mice (age 3-4 mo), middle-aged mice (age 10-12 mo), and aged mice (age 24-26 mo) w

104 -4 mo), middle-aged mice (age 10-12 mo), and aged mice (age 24-26 mo) were subjected to left anterior

105 neurons, effects that were also observed in aged mice, albeit to a lesser extent, indicating preserv

106 Increased GDF11 levels in aged mice also improved muscle structural and functional

107 ment of liver fibrosis was also increased in aged mice and correlated with high numbers of liver fibr

108 ctor CD8+ T cell apoptosis in both young and aged mice and enhanced effector CD8+ T cell polyfunction

109 ce the functions of stem/progenitor cells in aged mice and extend lifespan.

110 rses long-term memory (LTM) deficits in both aged mice and flies.

111 ry T cells (Treg) significantly increases in aged mice and humans.

112 m, whereas myeloid-biased HSCs accumulate in aged mice and humans.

113 ed 7KCh and microglia to the outer retina of aged mice and investigated 7KCh effects on retinal micro

114 determined that NETosis is more prevalent in aged mice and investigated the role of PAD4/NETs in age-

115 Furthermore, macrophages from aged mice and normal human elderly volunteers displayed

116 on in the thymus ameliorates thymopoiesis in aged mice and offer a strategy to combat the age-associa

117 minished in uterine (and tail) arteries from aged mice and post-menopausal women.

118 sine in skeletal muscle, brain, and heart of aged mice and promoted the accumulation of carnosinylate

119 ignificantly improves learning and memory in aged mice and reduces 5hmC abundance in mouse hippocampu

120 e behavioral and molecular effects of HAL in aged mice and that these effects occur via modulation of

121 nd it is increased within the hippocampus of aged mice and young heterochronic parabionts.

122 ystemic challenge relative to Prevnar-immune aged mice and young mice that had received either vaccin

123 ased levels of H3K9me3 in the hippocampus of aged mice, and improved performance in the objection loc

124 ainst C. difficile toxin A were depressed in aged mice, and vancomycin treatment reduced antibody res

125 Blood flow and angiogenesis in aged mice are also enhanced on administration of bisphos

126 Two-thirds of MuSCs from aged mice are intrinsically defective relative to MuSCs

127 udies suggested that macrophages from middle-aged mice are more susceptible to cell death, as well as

128 nt a large majority of memory CD8 T cells in aged mice, are not memory cells that develop in response

129 prefrontal cortex was significantly lower in aged mice as compared with young mice.

130 changes in motor behavior in young-adult or aged mice as evaluated by an extensive array of motor be

131 Aged mice as well as mice with reduced DC function had d

132 burdens were found in the spleens of middle-aged mice at 24 and 60 h and in the livers at 60 h posti

133 ost MHC genes remained more downregulated in aged mice at day 3.

134 d with lower levels of ICAM-1 in wounds from aged mice at early time points.

135 thway is strongly de-regulated in MuSCs from aged mice because of insufficient attachment to the nich

136 ICOS contributed to Treg maintenance in aged mice, because in vivo Ab blockade of ICOSL led to a

137 on, we found that after being transferred to aged mice, bone marrow from young mice gave rise to NK c

138 tected in the absence of injury or stress in aged mice but not in young mice.

139 Surprisingly, aged mice but not mice with genetically altered DC funct

140 regulatory T cell accumulation in naturally aged mice, but not inflammatory infiltration.

141 Partial restoration of cognitive ability in aged mice, by lymphopenia-induced homeostasis-driven pro

142 The changes in synaptic transmission in aged mice can be partially rescued by improving calcium

143 s to IL-10 production from CD4(+) T cells in aged mice, causing attenuated responses of CD8(+) T cell

144 ate cellular and humoral immune responses of aged mice comparable to levels seen in young mice.

145 monstrate an eosinophilic immunopathology in aged mice comparable to that seen in mice immunized with

146 d, and recovery from infection was slower in aged mice compared to young mice.

147 gamma but not IL-1beta or TNF also protected aged mice, consistent with the notion that poly(I.C) pre

148 Calorie-restricted aged mice contain less visceral fat and displayed reduce

149 revious studies have shown B-1a cell Ig from aged mice contains abundant nontemplated (N)-additions.

150 Neonatal B1 B cells and their CLL progeny in aged mice continued to express moderately up-regulated c

151 enhanced contextual fear memory in adult and aged mice demonstrating improved hippocampal function.

152 In addition to neurodegeneration, aged mice developed a degenerative myopathy, with scatte

153 Nonetheless, Pneumovax-immunized aged mice developed limited bacteremia following respira

154 However, in aged mice, disease pathogenesis was significantly reduce

155 p defective long-term potentiation (LTP) and aged mice display spatial learning and memory deficits t

156 Although aged mice displayed a larger number of effector memory T

157 Although septic aged mice displayed equivalent or increased numbers of c

158 Aged mice displayed increased intraplatelet expression o

159 ally improved the survival outcome of middle-aged mice during both polymicrobial sepsis and sterile e

160 lations that produce interleukin-6 in middle-aged mice during systemic inflammation.

161 to either sublethally irradiated or normally aged mice effectively depleted SCs, including senescent

162 PERK expression in the hippocampus of middle-aged mice enhances hippocampal-dependent learning and me

163 Aged mice exhibit increased bacterial colonization and d

164 Here we demonstrated that aged mice exhibit poor effector CD8+ T cell polyfunction

165 animals during infection, but TFH cells from aged mice exhibit significant differences, including red

166 Aged mice exhibited reduced pulmonary immune profiles an

167 ent peritoneal cells from endotoxemic middle-aged mice exhibited reduced viability and produced eleva

168 ution and morphology of retinal terminals in aged mice exhibiting varying levels of axonal transport

169 e data suggest that loss of BMP signaling in aged mice exposed to neonatal oxygen is associated with

170 wed that a majority of accumulating Tregs in aged mice expressed low levels of CD25, and their accrua

171 Although most aged mice failed to develop clinical disease during thei

172 Although eggs from aged mice feature a reduced ability to replenish intrace

173 Aged mice fed a control diet were exquisitely more susce

174 In contrast, DT increased MDSCs in young and aged mice following MC-38 tumor challenge, although effe

175 ting cell frequencies were 10-fold higher in aged mice following Pneumovax immunization relative to y

176 The administration of JAK inhibitor to aged mice for 10 wk alleviated both adipose tissue and s

177 Furthermore, the 1918 VLPs fully protected aged mice from 2009 pandemic H1N1 virus challenge 16 mon

178 tion of apoE4 in astrocytes does not protect aged mice from apoE4-induced GABAergic interneuron loss

179 t, deletion of apoE4 in neurons does protect aged mice from both deficits.

180 separates satellite cell gene expression in aged mice from that in young mice.

181 We found that bone marrow from young and aged mice gave rise to CD27(-) mature NK cells similarly

182 ever, in either case, melatonin treatment of aged mice generally altered these parameters so that the

183 Importantly, aged mice given PspA plus a combination of pFL and CpG O

184 mics of NG2(+) glial cells in the mature and aged mice gray matter.

185 ondrial function in the pancreatic islets of aged mice (>/=24 months), the result of 52% and 57% defe

186 skin and serum increase in otherwise normal, aged mice (>12 months).

187 Aged mice had a relative inability to upregulate gene ex

188 and Enterobacteriaceae were mostly similar, aged mice had a significant change in the Firmicutes to

189 iN cells from aged mice had apparently normal active and passive neuro

190 d mediator metabololipidomics, we found that aged mice had both delayed resolution and reduced SPMs.

191 Aged mice had higher levels of sFasL in the blood compar

192 use model of RSV pathogenesis, we found that aged mice had impaired Ag-specific CD8(+) T cell respons

193 polymicrobial sepsis, and subsequently, the aged mice had increased mortality and defective peritone

194 Importantly, in aged mice harboring a genetic burden relevant for human

195 Also, more influenza specific T cells in aged mice have a regulatory phenotype, which could contr

196 A study reveals that aged mice have decreased hippocampal expression of the D

197 Here, we find that MII oocytes from aged mice have less securin than oocytes from young mice

198 Reprogramming of fibroblasts from adult and aged mice, however, has not yet been explored in detail.

199 and improves cognitive function in adult and aged mice; however, whether neuronal Cav-1 overexpressio

200 This study in juvenile-adolescent aged mice identifies a novel form of synaptic plasticity

201 ic administration of young blood plasma into aged mice improved age-related cognitive impairments in

202 In addition, thymopoiesis of aged mice improved with a single intrathymic administrat

203 gnaling, and that antagonism of miR-19a/b in aged mice improves blood flow recovery after ischemia an

204 d in microvascular density between young and aged mice in normoxia and at 2 and 3weeks of hypoxia.

205 ial delay in cerebral angiogenic response in aged mice in the first week of hypoxia, no significant d

206 restored protein solubility in the lenses of aged mice in vivo and in human lenses ex vivo.

207 cell densities were increased in lesions of aged mice in which remyelination was enhanced by parabio

208 In aged mice, increased voiding frequency and enhanced low

209 Finally, in aged mice, increasing cellular excitability and activati

210 IgE was significantly increased in only the aged mice infected with influenza virus.

211 cate that the insulin resistance observed in aged mice is mainly mediated through the S-nitrosation o

212 ments indicate that impaired regeneration in aged mice is reversible by exposure to a young circulati

213 Notably, increased white matter repair in aged mice is translated into significant poststroke moto

214 stics under stressed conditions in young and aged mice is unknown.

215 Aged mice lacking MR in SMCs (SMC-MR) have reduced vascu

216 ral analysis of young adult and intermediate-aged mice lacking NGF-TrkA signaling demonstrates that t

217 Moreover, aged mice lacking Tec kinase developed a mild autoimmune

218 Thus, reduced bacterial diversity in aged mice may contribute to increased P. gingivalis colo

219 st that reduced DC numbers in lymph nodes of aged mice may involve the effect of advanced glycation e

220 In aged mice, novel nano-proresolving medicines carrying as

221 that Sirt1 activators increase bone mass in aged mice, our results also suggest that Sirt1 could be

222 rity of murine trauma and shock in young and aged mice over time, and by examining the response in is

223 during aging, we tested the hypothesis that aged mice overexpressing the antioxidant enzyme glutathi

224 , the number of virus-specific precursors in aged mice prior to infection was decreased up to 10-fold

225 We found that, after extended training, aged mice produced shorter actions and displayed squeeze

226 Importantly, TNF blockade in tumor-bearing, aged mice receiving IT displayed significant anti-tumor

227 In response to a s.c. injection of KC, aged mice recruited fewer neutrophils at increasing dose

228 Treatment of diabetic and aged mice recruits fibroblasts to the wound bed and redu

229 or extracellular matrix content in young or aged mice, regardless of running activity.

230 the residual functional MuSC population from aged mice, rejuvenating its potential for regeneration a

231 obulin G (IgG) levels in Pneumovax-immunized aged mice relative to other groups.

232 l and macrophage recruitment was observed in aged mice relative to young mice despite equivalent leve

233 Unexpectedly, we find that aged mice remain behaviorally circadian and that their e

234 indicated that post-training TSA infusion in aged mice rescued aging-associated deregulation of H4 ac

235 Overexpression of beta(2)AR in aged mice rescued glucose intolerance and insulin releas

236 , we found that NK cells from both young and aged mice responded vigorously to priming by pathogen-de

237 Strikingly, alpha-Toc supplementation of aged mice resulted in a 1000-fold lower bacterial lung b

238 fully promote an IL-4/IL-4Ralpha response in aged mice resulted in attenuated arginase (M2a associate

239 endent, spontaneous inflammasome activity in aged mice resulted in impaired glucose tolerance that co

240 r, prior in vivo depletion of macrophages in aged mice resulted in lesser cytokine levels, increased

241 systemic cancer IT regimens or LPS given to aged mice resulted in rapid and lethal toxicities affect

242 NF knockout mice and in vivo TNF blockade in aged mice resulted in significant increases in survival

243 steady-state conditions is also impaired in aged mice, resulting in a decreased proportion of CD27(-

244 atin marks in activated satellite cells from aged mice, resulting in the specific induction of Hoxa9

245 on of FOXN1 in the fully involuted thymus of aged mice results in robust thymus regeneration characte

246 Depletion experiments in aged mice revealed TIMP2 to be necessary for the cogniti

247 methyltransferase Dnmt3a2; re-expression in aged mice reverses memory deficits, and knockdown in you

248 trikingly, most haematopoietic stem cells in aged mice share these altered metabolic and functional f

249 Notably, SCs in aged mice show altered beta1-integrin activity and insen

250 However, aged mice show an increase in the amount of sleep, where

251 Aged mice showed a significant decline in spatial refere

252 creased with advancing age, such that middle-aged mice showed much more pronounced differences compar

253 ecific c-Kit overexpression (c-KitbetaTg) in aged mice showed significantly increased islet vasculatu

254 Aged mice showed significantly poorer contextual and tra

255 gly, introducing just the activated APC into aged mice significantly enhances otherwise compromised A

256 In aged mice, skeletal blood flow and endothelial Notch act

257 At 2 d postinfection, aged mice suffered 1000-fold higher pulmonary bacterial

258 or transformation were observed in young and aged mice, suggesting old animals were responsive to the

259 pS214-Tau was not observed in normal aged mice, suggesting that it arises with the evolutiona

260 d self-renewal of NPCs were also impaired in aged mice, suggesting that the down-regulation of protea

261 after satellite cell depletion in young and aged mice suggests that Pax3+ cells may compensate for a

262 Here, we demonstrate in aged mice that spontaneously elevated TNF represents a c

263 and lifespan extension were achieved in mid-aged mice that were locally implanted with healthy hypot

264 In aged mice, this response was induced by brain-derived si

265 tigen-specific immune responses in young and aged mice through the upregulation of immunomodulatory g

266 uggest that alpha-Toc enhances resistance of aged mice to bacterial pneumonia by modulating the innat

267 eus accumbens shell and prefrontal cortex of aged mice to levels comparable with those observed in yo

268 e to sepsis, the increased susceptibility of aged mice to sepsis appears not to be due to an exaggera

269 noted a dramatic decrease in the ability of aged mice to support survival and homeostatic proliferat

270 ontrast, subjecting the MuSC population from aged mice to transient inhibition of p38alpha and p38bet

271 Our data indicate that exposure of aged mice to young blood late in life is capable of reju

272 Exposure of aged mice to youthful systemic factors or GDF11 decrease

273 In aged mice, topical HOCl attenuated age-dependent product

274 In aged mice, total Abeta levels and amyloid plaque load we

275 These findings were recapitulated in aged mice treated with an MCD inhibitor (CBM-3001106), a

276 se studies examined beta cell replication in aged mice under basal conditions and in response to spec

277 bsence of Pax7+ satellite cells in young and aged mice using an inducible Pax7(CreER) -R26R(DTA) mode

278 Both young and aged mice vaccinated with H(2)O(2)-inactivated WNV-KUNV

279 Conversely, a reduction of inflammation in aged mice via transgenic expression of alpha-1-antitryps

280 Overt tau pathology in the aged mice was accompanied by spatial memory deficits.

281 The majority of CD8 T cells from uninfected aged mice was CD44(Hi) and had increased expression of i

282 phocytes from inflamed versus healthy middle-aged mice, we found elevated numbers of T follicular hel

283 By using multiorgan genome-wide analysis of aged mice, we found that the choroid plexus, an interfac

284 cine-elicited RSV-specific CD8(+) T cells in aged mice, we used a peptide vaccine approach.

285 Enhanced platelet activation responses in aged mice were also prevented by polyethylene glycol-cat

286 In contrast, the Piccolo levels in NMJs from aged mice were comparable to levels in adult mice.

287 Young and aged mice were laser treated to induce CNV.

288 of human exposure, whereas concentrations in aged mice were low to undetectable.

289 l analysis revealed that nearly all Tregs in aged mice were of an effector phenotype (CD44(hi)CD62L(l

290 Macrophages from young and aged mice were tested for sFasL-mediated cytokine produc

291 Young and aged mice were treated with a matrix metalloprotease (MM

292 ite cell function and muscle regeneration in aged mice, whereas overexpression of Hoxa9 mimics ageing

293 s response in activated satellite cells from aged mice, which limits satellite cell function and musc

294 Synaptic transmission is degraded in aged mice, which may contribute to the decline in neural

295 D8(+) T-cell-dependent tumour elimination in aged mice, which requires IFN-gamma.

296 tissue, cervical lymph nodes, and spleen of aged mice, which were equivalent to those in young adult

297 We hypothesized that treatment of aged mice with agonistic anti-CD137 (41BB) mAb will part

298 r captopril on wound healing in diabetic and aged mice with further validation in older diabetic pigs

299 Intranasal pretreatment of aged mice with poly(I.C) (a TLR3 agonist) and, to a less

300 ownregulated upon wounding in both young and aged mice, with an exception of acute upregulation of mi