ライフサイエンスコーパス: aging

1 ealth often deteriorates during reproductive aging.

2 tion contributes to inflammation, cancer and aging.

3 pproach for studying its role in disease and aging.

4 ansformation of stem cells that characterize aging.

5 might further clarify the prognostic role of aging.

6 ants for 12-36 h to allow oocytes to undergo aging.

7 stable pigments during fermentation and wine aging.

8 ls, renal function gradually declines during aging.

9 bryonic development, disease progression and aging.

10 identify mechanisms underlying physiological aging.

11 portant roles in neurodegeneration and brain aging.

12 eage commitment was radiation sensitive with aging.

13 rogenitor cells, and in preventing premature aging.

14 heir genetic clearance can delay features of aging.

15 of skeletal muscle, is important for healthy aging.

16 he canopy of central African forests are now aging.

17 e trend of variation with the endplate after aging.

18 tabolism might also have a role in mammalian aging.

19 ing an increase in methylome disorder during aging.

20 esized by NSCs and increases in the SGZ with aging.

21 midbrain dopaminergic neurons (mDANs) during aging.

22 loped countries, is strongly associated with aging.

23 ce of the microbiome, and how they relate to aging.

24 o genotoxic stress and confer fitness during aging.

25 s of dopaminergic neurons over the course of aging.

26 rogen sulfide and other mercaptans during AR-aging.

27 foundation for rejuvenating immunity during aging.

28 ation and tissue atrophy, and in accelerated aging.

29 ve oxygen species metabolism and accelerated aging.

30 a and impaired epidermal stratification upon aging.

31 d pathways may potentially alter the rate of aging.

32 ociated epigenetic changes are implicated in aging.

33 ibutes to developmental defects, cancer, and aging.

34 d genetic mechanisms that control organismal aging.

35 tic brain injury, prolonged wakefulness, and aging.

36 are independent signals for cellularity and aging.

37 a variety of human diseases as well as human aging.

38 reatment of infections and malignancy during aging.

39 gmentation is a critical determinant of skin aging.

40 in the population-based Mayo Clinic Study of Aging.

41 stress resemble trajectories observed during aging.

42 germ line predisposition, inflammation, and aging.

43 alization reverses the behavioral effects of aging.

44 rk in the endplate and the interaction after aging.

45 in metabolic disease, neurodegeneration, and aging.

46 traviolet A (TMP/UVA) during development and aging.

47 ion on retinal structure and function during aging.

48 o be associated with overall cancer risk and aging.

49 h may protect against cancer, radiation, and aging.

50 is regarded as a disease of accelerated lung aging.

51 molecular mechanisms that contribute to HSC aging.

52 or [3], and alterations in processes such as aging [4] and brain disorders [5], highlighting the impo

53 [3, 4], tissue repair [5-8], and organismal aging [9].

54 articipants were in the Mayo Clinic Study of Aging, a population-based study that uses a medical reco

55 tanding mechanisms of SC maintenance and how aging affects SC function are of special importance, bot

56 , and humans that demonstrates how cognitive aging affects the navigational computations supported by

57 earning and memory, the review discusses how aging affects the perception and integration of spatial

58 The Successful Aging after Elective Surgery study enrolled dementia-fre

59 hology according to US National Institute on Aging-Alzheimer's Association neuropathological criteria

60 and loss of proteostasis is associated with aging and age-related chronic disease.

61 ed our technology to quantify the effects of aging and age-related genetic and chemical factors in th

62 Oregon Health and Science University Layton Aging and Alzheimer Disease Center and Oregon Brain Bank

63 were studied from 1997 to 2007 in the Health Aging and Body Composition study.

64 ice had reduced macrophage infiltration with aging and CalpTG mice produced less IL-1alpha and IL-1be

65 evidence supports a general hypothesis that aging and cancer are diseases related to energy metaboli

66 of how defective FA signaling contributes to aging and cancer at the energy metabolism level.

67 Both aging and chronic inflammation produce complex structura

68 se activity, which accelerated the molecular aging and clearance of intestinal alkaline phosphatase (

69 has uncovered genetic contributions to skin aging and confirmed previous findings, showing that pigm

70 lterations that invariably lead to premature aging and death.

71 tential for organoids to serve as models for aging and describe how current organoid techniques could

72 cs, i.e., energy metabolism, occur in normal aging and disturbed bioenergetics may be an important co

73 ion, increases most aspects of health during aging and extends lifespan in diverse species, including

74 between reproductive senescence and somatic aging and give an overview of the involvement of nutrien

75 formance is affected by neurodegeneration in aging and has the potential to be used as a clinical mar

76 onal design of small molecules that modulate aging and hence alter the propensity for a host of age-r

77 e changes in tissue structure seen in normal aging and in chronic inflammation to altered lung mechan

78 progressive process affecting kidneys during aging and in chronic kidney disease (CKD), regardless of

79 imaging during microvascular development and aging and in models of brain ischemia and Alzheimer's di

80 Calorie restriction (CR) retards aging and increases longevity in many animal models.

81 rocess of cellular growth arrest linked with aging and inflammation.

82 rotein aggregates, which are associated with aging and many human diseases such as Alzheimer's diseas

83 abnormalities, genomic instability, and HSC aging and might promote hematological malignancies with

84 diac hypertrophy induced by stresses such as aging and neurohumoral activation is an independent risk

85 g 28 y in the Swedish Adoption/Twin Study of Aging and parental social class based on the Swedish soc

86 than the waking brain, and is slowed in the aging and posttraumatic brain.

87 l which incorporates genetic effect, natural aging and prolonged oral environmental toxicity administ

88 Our results suggest that both biological aging and reduced regenerative capacity contribute to ca

89 MPP phenotypes are reminiscent of premature aging and stressed hematopoiesis, and indeed progressed

90 depleted glutathione levels, which occur in aging and stroke, will give rise to dysfunctional CBF re

91 lial cells (ECs) in regulating hematopoietic aging and support further research to identify the rejuv

92 -driver mutations (CHDMs) occurs with normal aging and these mutations have been detected in more tha

93 onary syndrome (ACS) to promote premature EC aging and thrombogenicity.

94 mitophagy is thought to contribute to normal aging and to various neurodegenerative and cardiovascula

95 is also implicated as an underlying cause of aging and tumorigenesis.

96 Alzheimer's disease (AD), it also occurs in aging and various neurological, medical, and psychiatric

97 are also able to demonstrate that epigenetic aging and white matter tract integrity also share common

98 METHODS AND The Health, Aging, and Body Composition study is a prospective cohor

99 At entry into the Health, Aging, and Body Composition study, men and women who lat

100 s in mt DNA background variation on obesity, aging, and cancer risk.

101 betes, obesity, neurodegenerative disorders, aging, and cancer, making the TOR pathway an attractive

102 HSCs, with implications for blood disorders, aging, and immunity.

103 three of the main regulators of metabolism, aging, and longevity, are components of the same pathway

104 y.A cross-sectional subset of the Nutrition, Aging, and Memory in Elders cohort who had undergone MRI

105 es, regeneration of tissues, cell divisions, aging, and pathological conditions observed in many canc

106 probably served as combination fermentation, aging, and serving vessels.

107 ular process can directly influence cellular aging, and thus could provide guidance for the design of

108 e further subjected to Accelerated Reductive aging (AR) and analyzed for free and Brine Releasable (B

109 sms underlying altered beta-cell function in aging are poorly understood in mouse and human islets, a

110 sal event, and yet the key events that drive aging are still poorly understood.

111 gical stress, and interventions that reverse aging-associated deficits.

112 We further observed an aging-associated increase in the incidence of goblet cel

113 sts an involvement of PV+ ependymal cells in aging-associated ventricle stenosis.

114 uptake and intracellular accumulation of the aging biomarker lipofuscin.

115 hat nucleolar size and activity can serve as aging biomarkers.

116 tes from the Baltimore Longitudinal Study of Aging (BLSA) to determine whether impaired mitochondrial

117 Two ubiquitous features of the aging brain are the intracellular accumulation of aggreg

118 ption may be one key factor that renders the aging brain vulnerable to Abeta deposition and the devel

119 could imply loss of cellular identity in the aging brain, and provide a link between aging-related mo

120 on of the autophagy-lysosomal pathway in the aging brain.

121 nctional mitochondria has been implicated in aging, but a deeper understanding of mitochondrial dynam

122 on has been associated with many diseases of aging, but the mechanisms responsible for producing this

123 tivates protein kinase A (PKA) to accelerate aging by inhibiting transcription factors Msn2/4.

124 has long been hypothesized to play a role in aging, cancer, and viral and bacterial evolution.

125 California, San Francisco (UCSF) Memory and Aging Center (collected between 1999-2015) and 11,381 in

126 ampal FKBP1b overexpression also counteracts aging changes in gene transcriptional networks.

127 f Foxp1 in bone marrow MSCs led to premature aging characteristics, including increased bone marrow a

128 d up participants with HIV from the Veterans Aging Cohort Study for a minimum of 3 years between Jan

129 e on or after April 1, 2003, in the Veterans Aging Cohort Study were included.

130 However, the mechanisms by which aging contributes to neurodegeneration remain elusive.

131 Of these aging-dependent genes, 876 (37%) also showed altered exp

132 Corneal nerve damage produced by aging, diabetes, refractive surgeries, and viral or bact

133 Change in population size, population aging, disease prevalence or incidence, service utilizat

134 72/876, 99.5%) in the direction opposite the aging effect and closer to levels in YCs.

135 Knowledge of the aging effect on airway inflammation and asthma control i

136 No significant aging effect was observed in [(18) F]Nifene binding over

137 n aged controls (ACs) compared with YCs (the aging effect).

138 mycin has previously been shown to have anti-aging effects in cells and organisms.

139 Although the anti-aging effects of lactic acid bacteria (LAB) have been ob

140 over a novel mutational signature in healthy aging endocrine cells.

141 pted increased or de novo rhythmicity during aging, enriched for stress-response functions.

142 With an aging ESRD population and continued organ shortage, pres

143 Our data indicate that redistribution of aging factors from aged cells to their progeny can be a

144 x the retention of DNA circles, which act as aging factors in the mother cell.

145 ocyte aneuploidy and spontaneous abortion in aging females.

146 ss of ISCs coupled with tissue demand and in aging flies, underscoring the generality of this mechani

147 Aging, genetics and environmental toxicity are important

148 ic Epidemiology Research on Adult Health and Aging (GERA) cohort individuals provided 1,342,814 systo

149 ic Epidemiology Research in Adult Health and Aging (GERA) cohort, in four race/ethnicity groups: non-

150 During aging, germ cells with reduced E(z) activity cannot meet

151 ities to improve health and longevity for an aging global population.

152 ve dysfunction in normative and pathological aging has been linked to hyperexcitability in the aged C

153 Genome-wide studies of aging have identified subsets of genes that show age-rel

154 isms underlying the effects of probiotics on aging have rarely been assessed.

155 Upon aging, hematopoietic stem cells (HSCs) undergo changes i

156 et to ameliorate neurogenesis-defects in the aging hippocampus.

157 ractions between intestinal microbes and the aging host.

158 emia-associated genes, commonly occurs among aging human hematopoietic stem cells.

159 eets generated with long-term passaged (P10) aging human mesenchymal stromal cells (MSCs) could be us

160 Repeated cell divisions and aging impair stem cell function.

161 that extensive long-term culture-induced MSC aging impaired their osteogenic ability and subsequent b

162 Aging impairs the ability of alveolar macrophages to lim

163 H2A.J also accumulates in mice with aging in a tissue-specific manner and in human skin.

164 d to modulate the biological consequences of aging in breast.

165 upling is impaired as a consequence of brain aging in later life, contributing to cognitive and memor

166 of participants in the Mayo Clinic Study of Aging in Olmsted County, Minnesota.

167 typic systems that recapitulate hallmarks of aging in order to better understand and to modulate the

168 tive assessments of age-related trends after aging, including mean diameter, volume fraction and conn

169 his affliction shows all of the hallmarks of aging, including telomere shortening, cellular senescenc

170 reates an inescapable double bind that makes aging inevitable in multicellular organisms.

171 f numerous molecular changes associated with aging, insights into the driver mechanisms of this funda

172 oxical findings that aging itself and slowed aging interventions can both be characterized by slower

173 Aging is a biologically universal event, and yet the key

174 Aging is a major international concern that brings formi

175 fore, that chronological resistance arterial aging is a prominent factor leading to weakened vasodila

176 Aging is accompanied by major changes in adipose tissue

177 Aging is associated with increased risk for type 2 diabe

178 fining the structure of the notochord during aging is critical for investigations relating to IVD fun

179 Unraveling the complexity of aging is crucial for understanding its mechanisms and it

180 The generally accepted paradigm is that such aging is gradual and its origin is in slower than expone

181 Aging is linked to deficiencies in immune responses and

182 mitochondrial dynamics and mitophagy during aging is missing.

183 t an early stage of differentiation and that aging is not an obligate requirement for a CD19(neg) sta

184 MLR and MLR-associated proteins on neuronal aging is unknown.

185 ry signaling and microglial sensitization in aging, its implications in psychological stress, and int

186 nt may explain the paradoxical findings that aging itself and slowed aging interventions can both be

187 Decreased Sesn2 levels in aging lead to a blunted ischemic AMPK activation, altera

188 ersely, psychological stress may also induce aging-like sensitization of microglia and increase react

189 (-)-P7C3-S243 safely protected aging male and female wild-type and TgF344-AD rats from

190 levels were positively associated with skin aging manifestation, including score of pigment spots on

191 ollution is known to be associated with skin aging manifestations.

192 sociations between CES-D scores and cellular aging markers.

193 nal data suggest that accelerated biological aging may be a mechanism through which sleep influences

194 pulation is widely promoted as 0.8 g . d(-1) Aging may increase protein requirements, particularly to

195 ns in some elderly subjects, indicating that aging may negatively affect the ability of B cells to di

196 e often-reported posterior-anterior shift in aging may not reflect a global sensory-processing defici

197 ing function, which is found in normal brain aging, may play an important role in the pathogenesis of

198 he associations of adult height with healthy aging measured by a full spectrum of health outcomes, in

199 mportance of skeletal muscle inflammation in aging-mediated insulin resistance, and our findings furt

200 ti-inflammatory cytokine in the treatment of aging-mediated insulin resistance.

201 cross-links in genomic DNA may contribute to aging, neurodegeneration, and cancer.

202 s Consortium (ADGC), a National Institute on Aging (NIA)-funded national data repository (reflecting

203 ause both proteins are expressed in normally aging non-HGPS individuals, and most hallmarks of normal

204 Upon oxidative stress and aging, Nrf2 (NFE2-related factor2) triggers antioxidant

205 an alternative, but many functional signs of aging occur at the level of tissues rather than cells an

206 PS individuals, and most hallmarks of normal aging occur in progeria, research on HGPS can identify m

207 We observe noise reduction during normal aging of a cell, followed by a short catastrophe phase i

208 Here, we determined that aging of endothelial cells (ECs), a critical component o

209 Pre-maturation aging of immature oocytes may adversely affect the fate

210 aged HSCs to thrombin-cleaved OPN attenuates aging of old HSCs, resulting in increased engraftment, d

211 e of the enzyme acid sphingomyelinase in the aging of stored units of packed red blood cells (pRBCs)

212 Aging of the hematopoietic system is associated with an

213 n, maintenance, neuromuscular disorders, and aging of the NMJ, focusing on communications among moton

214 bute to reduced burden of dementia given the aging of the population is not known.

215 ients and health care systems, and given the aging of the population worldwide, the incidence of fall

216 ere, we provide an overview of the impact of aging on both the allograft and the recipient and its ef

217 ponents of immunity, including the effect of aging on cells of the (mostly adaptive) immune system, o

218 in mouse and human islets, and the impact of aging on intraislet communication has not been character

219 es and how these relationships change during aging or disease states.

220 xt for understanding how feedback altered by aging or injuries may influence the ability to regulate

221 To enquire how the circadian system protects aging organisms, here we compare circadian transcriptome

222 of the supportive housing program for youths aging out of foster care and the need for such programs

223 With an aging patient population and increasing complexity in pa

224 CI: 6%, 11%) decrease in the odds of healthy aging per SD (0.062 m) increase in height.

225 nment, was sufficient to drive hematopoietic aging phenotypes in young HSCs.

226 The issue of the aging physician and when to cease practice has been cont

227 lantation and will likely increase given the aging population and nonalcoholic fatty liver disease as

228 This fact conspires with an aging population in many countries to make rigorous asse

229 rates of adult obesity and DM along with an aging population, NAFLD-related liver disease and mortal

230 cular event affecting most individuals in an aging population, there is little consensus regarding it

231 pose an extraordinary threat to the world's aging population, yet no disease-modifying therapies are

232 gly important problem of hearing loss in our aging population.

233 incurable neurodegenerative disorders in the aging population.

234 s and decreased responses to vaccines in the aging population.

235 autosomal mosaic events >2 Mb in size in the aging population.

236 velopment of disease and the acceleration of aging, possibly in a gender-specific manner.

237 We now demonstrate that obesity and aging precipitate alterations of TRIM28-dependent transc

238 es cancer development and contributes to the aging process has progressed rapidly.

239 aging, research suggests that targeting the aging process itself could ameliorate many age-related p

240 ssion of cancer and diabetes, as well as the aging process.

241 ins and Klotho, which further accelerate the aging process.

242 unction may be particularly sensitive to the aging process.

243 ple develop presbyopia as part of the normal aging process.

244 in sleep pattern are typical for the normal aging process.

245 have identified major roadblocks that normal aging processes impose on tissue regeneration.

246 Therapeutic approaches that target aging processes may be beneficial for halting the progre

247 sis, and report that nucleoli also expand as aging progresses in cells derived from healthy individua

248 ficial effects exerted by strawberry against aging progression.

249 ders Study (n = 492) and the Rush Memory and Aging Project (n = 487).

250 States (the National Social Life, Health and Aging project).

251 ldwide highlights the need to understand how aging promotes CVD in order to develop new strategies to

252 Aging promotes inflammation, a process contributing to f

253 ers suggesting increased BBB permeability in aging rats.

254 Skin aging-reducing strategies should incorporate the sex dif

255 mice were subjected to the investigation of aging-related cardiac hypertrophy.

256 a new therapeutic approach for obesity- and aging-related diseases associated with mitochondrial dys

257 prevent telomere-associated diseases, namely aging-related diseases, including cancer.

258 the aging brain, and provide a link between aging-related molecular changes and functional decline.

259 mechanism for therapeutic intervention into aging-related neuronal disorders.

260 n of Pofut1 in skeletal myofibers can induce aging-related phenotypes in cis within skeletal myofiber

261 r, the long-term effects of irradiation with aging remain unclear.

262 tain proteostasis undergoes a decline during aging, rendering the organism susceptible to these patho

263 the two and that synaptic homeostasis during aging requires autophagy to regulate protein homeostasis

264 Proteostasis is one of the seven "pillars of aging research" identified by the Trans-NIH Geroscience

265 rent organoid techniques could be applied to aging research.

266 r from understanding the biological basis of aging, research suggests that targeting the aging proces

267 e4), and the Sacramento Area Latino Study on Aging (SALSA) (n = 1,294, 11 APOE-e4/e4).

268 rging themes, including the contributions of aging, selective vulnerability and non-cell-autonomous f

269 recent evidence, however, implicates FMOs in aging, several diseases, and metabolic pathways.

270 ach with a number of murine models of slowed aging shows that, compared to controls, energetic resour

271 espread effects on the transcriptome with an aging signature.

272 To examine whether epigenetic aging signatures are slowed by longevity-promoting inter

273 Aging significantly degrades contrast sensitivity.

274 health also helps move more industrialized, aging societies from a focus on material consumption to

275 r men in the Veterans Affairs (VA) Normative Aging Study.

276 an increase in immunological tolerance with aging suppresses disease onset after late young adulthoo

277 in protection is more likely associated with aging than the virus infection and could be compensated

278 discuss CRTC deregulation as a new driver of aging that integrates the link between age and disease r

279 Telomere length is a marker of biological aging that may provide a cellular memory of exposures to

280 Upon aging, the development of Wnt activated mammary carcinom

281 Upon aging, the expression of osteopontin (OPN) in the murine

282 When fully controlled for chronologic aging, the fibrosis progression rate was accelerated dur

283 nditions that are characteristic of the mice aging, the function of Roquin was examined in immune cel

284 coupling of cellular, tissue, and organismal aging through inhibition of ISC proliferation and provid

285 Functional status declines with aging, thus impeding autonomy.

286 ndicate that dissolution, concentration, and aging time are important factors that influence Cu extra

287 The nanoparticle aging time course is characteristic of nucleation and pa

288 Senescent cell accumulation in aging tissues is linked to age-associated diseases and d

289 dependence and interactions between cells in aging tissues.

290 rain networks during progression from normal aging to Alzheimer disease dementia (AD) has also been o

291 se findings broaden the concept of cognitive aging to include evidence of Alzheimer's disease-related

292 85146 near SLC45A2 is associated with a skin aging trait at genome-wide significance (P = 4.1 x 10(-9

293 ased studies, the NHATS (National Health and Aging Trends Study) linked to the NSOC (National Study o

294 mimics a form of accelerated cardiovascular aging, we also studied age-related cardiac remodeling.

295 show that human islet function declines with aging, which can reduce insulin action and may contribut

296 stulated to play a role on sarcopenia during aging, which is believed to be due alterations in glucos

297 ssociation of epigenetic age and immune cell aging with sleep in the Women's Health Initiative study

298 from these ADP factors may be important for aging without significant ADP.

299 e (21% vs. 31% and 49%, respectively) and an aging workforce that is less likely to be in private pra

300 fur density, and renal function in both fast aging Xpd(TTD/TTD) and naturally aged mice.