ライフサイエンスコーパス: mutagen

1 erichia coli to grow in the presence of this mutagen.

2 im that cigarette smoke is a human germ cell mutagen.

3 sequence polymorphisms induced by a chemical mutagen.

4 mous transposon Activator (Ac) is a powerful mutagen.

5 reated Apc(Min/+) mice with a strong somatic mutagen.

6 r and sequences derived from the insertional mutagen.

7 5NO2 was found to be a potent direct acting mutagen.

8 sk factor for carcinogenesis because it is a mutagen.

9 These data reveal that 8-oxodGTP is a potent mutagen.

10 organic compounds, is a known carcinogen and mutagen.

11 hanisms, which may reflect the nature of the mutagen.

12 tion of ribavirin to be that of a potent RNA mutagen.

13 tinuously caused by endogenous and exogenous mutagens.

14 gen species to UV radiation to environmental mutagens.

15 of the DOC in contrast to the particle-bound mutagens.

16 or efficient DNA repair from a wide range of mutagens.

17 cell cycle and deleterious damage caused by mutagens.

18 ke, high-temperature cooking, and associated mutagens.

19 alysis of mutation spectra of DNA exposed to mutagens.

20 repair machinery, endogenous, and exogenous mutagens.

21 igen (PCNA) that is triggered by exposure to mutagens.

22 to within an order of magnitude of chemical mutagens.

23 n complement efforts using other insertional mutagens.

24 cyclic arylamines and their bioactivation to mutagens.

25 transferable to other high-copy insertional mutagens.

26 ionizing radiation and a number of chemical mutagens.

27 be caused by smoking and other environmental mutagens.

28 by which Msd proofreads the base milieu for mutagens.

29 epertoire to both purine and pyrimidine-like mutagens.

30 burden analysis and testing for exposure to mutagens.

31 ising from endogenous reactions or exogenous mutagens.

32 modification due to endogenous and exogenous mutagens.

33 -deoxycytidine are predicted to be efficient mutagens.

34 easily extended by adducts formed from other mutagens.

35 via the handling and metabolism of chemical mutagens.

36 ated and more sensitive to inhibition by RNA mutagens.

37 ehensive characterizations of other germline mutagens.

38 mutation frequency in the absence of tobacco mutagens.

39 fficacy against IQ and MeIQ tested as direct mutagens (10(-7) mol/plate), with a revertants percentag

40 s-anti-B[a]P-N(2)-dG), and one from the food mutagen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine

41 mutational events, this study defines such a mutagen, 3'-azidothymidine [zidovudine (AZT)], used wide

42 V553I, we also demonstrate resistance to the mutagen 5-azacytidine (5-AZC) and decreased accumulation

43 mes more sensitive to treatment with the RNA mutagen 5-fluorouracil (5-FU) than wild-type (WT)-ExoN(+

44 d two mutations conferring resistance to the mutagen 5-fluorouracil (5-FU): nsp12-M611F and nsp12-V55

45 oth in the presence of ribavirin and another mutagen, 5-azacytidine.

46 in MRC-5 cells in the presence of a chemical mutagen, 5-fluorouracil.

47 e examined the mutational specificity of two mutagens, 5-azacytidine and N-methyl-N'-nitro-N-nitroso-

48 ession combined with exposure to TPA and the mutagen 7,12-dimethylbenz(a)anthracene accelerated SCC d

49 g base excision DNA repair of the endogenous mutagen 8-oxoguanine.

50 ed to study the mechanism giving rise to the mutagens 8-oxoA and FAPyA.

51 As part of our studies of lethal viral mutagens, a series of 5-substituted cytidine analogues w

52 ntexts show variability in DNA distortion at mutagen adduct sites that could compromise DNA repair at

53 In this case, the total dose of mutagen administered to the host needs to be so high tha

54 yl methanesulfonate compared to the acridine mutagen agent.

55 against ethyl methanesulfonate and acridine mutagen agents.

56 e effects should be considered not only from mutagens alone, but also including possible comutagens a

57 eloped leukemia, even after treatment with a mutagen, although some of the older mice developed a non

58 on, a chemotherapeutic agent, a clastogen, a mutagen, an inducer of fragile sites and a carcinogen.

59 Benzo[a]pyrene is an important environmental mutagen and carcinogen.

60 (AalphaC), a food-derived heterocyclic amine mutagen and carcinogen.

61 Aflatoxin B1 (AFB1) is a mutagen and IARC (International Agency for Research on C

62 hypothesis that RBV could act both as an RNA mutagen and inhibit viral RNA synthesis in vivo, we stud

63 It is a potent mutagen and is of concern to public health.

64 of and protection from cadmium, a teratogen, mutagen and potentially lethal heavy metal.

65 -benz[de]anthracen-7-one, 3-NBA) is a potent mutagen and suspected human carcinogen identified in die

66 ic is, indeed, a potent gene and chromosomal mutagen and that its effects are mediated through the in

67 t was used to show that propionaldehyde is a mutagen and that mutation frequencies are increased in M

68 nt compartments receive different amounts of mutagen and that virions can migrate among compartments.

69 ermoid epithelia are continuously exposed to mutagens and are the most common target of cancer.

70 oxygen species (ROS), which represent human mutagens and are thought to be a major contributor to th

71 ad ways to the evolution of host genomes, as mutagens and as sources of genetic novelty (both coding

72 N-Nitrosamines are potent mutagens and carcinogens that can be formed during oxida

73 r (NER) excises bulky DNA lesions induced by mutagens and carcinogens.

74 DNA damage caused by sunlight, environmental mutagens and certain antitumor agents.

75 DNA that are generated by various alkylating mutagens and drugs.

76 igating the effects of physical and chemical mutagens and for exploring the potential of mutation bre

77 doneness level, and intake of specific meat mutagens and heme iron are associated with lung carcinom

78 NMF distinguished all three mutagens and in the pooled analysis IR was associated wi

79 testing of viral mutational tolerance to RNA mutagens and other selective pressures.

80 ants are constantly exposed to environmental mutagens and plant cells are totipotent, an understandin

81 mplate exposes the nontemplate DNA strand to mutagens and primes unscheduled error-prone DNA synthesi

82 ction are critical for the plant response to mutagens and proper plant development.

83 sporters protect embryos and stem cells from mutagens and pump morphogens that control cell fate and

84 antly to the carcinogenicity of a variety of mutagens and raises the possibility that genome-wide LOH

85 ential for the minimization of DNA damage by mutagens and reactive oxidizing species.

86 r (PTE) lesions that are induced by chemical mutagens and refractory to DNA repair have not been prev

87 in the tentative identification of possible mutagens and the positive identification of the nonmutag

88 ncluding 7,12-dimethylbenz[alpha]anthracene (mutagen) and camptothecin (topoisomerase inhibitor), as

89 ity of 2-aminoanthracene (2-AA), an indirect mutagen, and 4-nitroquinoline-N-oxide (4-NQO), a direct

90 ity of 2-aminoanthracene (2-AA), an indirect mutagen, and 4-nitroquinoline-N-oxide (4-NQO), a direct

91 nicity of 4-nitroquinoline-N-oxide, a direct mutagen, and benzo[a]pyrene, an indirect mutagen, toward

92 alleviation in response to treatment with a mutagen, and demonstrate that restriction alleviation se

93 d PAH attract much attention as carcinogens, mutagens, and as diagnostics for environmental forensics

94 Diet is a mixture of carcinogens, mutagens, and protective agents, many of which are metab

95 atalogues have the potential to identify the mutagens, and to reveal the mutagenic processes responsi

96 ity of 2-aminoanthracene (2-AA), an indirect mutagen; and 4-nitroquinoline-N-oxide (4-NQO), a direct

97 bination of this reporter-tagged insertional mutagen approach and zebrafish provides a powerful platf

98 Ribavirin is a viral mutagen approved for treatment of several virus infectio

99 show that in addition to genetic mutations, mutagens are also a powerful source of transcription err

100 emonstrated in cell culture models, but most mutagens are carcinogenic and are poorly tolerated.

101 ision repair, and repair of damage caused by mutagens are discussed.

102 The environmental arylamine mutagens are implicated in the etiology of various spora

103 ndividual's cumulative or recent exposure to mutagens; as a marker of individual hematopoietic progen

104 tations leading to cancer, or on the assumed mutagen-associated mutation rate, within the generally-a

105 but does not strongly depend on the assumed mutagen-associated mutation rate.

106 The mutagen-attenuated RVF MP-12 vaccine was determined to b

107 system provides the first random insertional mutagen available for germline genetic screens in mice.

108 of RAD51 to either spontaneously arising or mutagen-based DNA damage sites.

109 s were not due to differences in exposure to mutagens, because the patterns were still evident when c

110 old in cells by gamma radiation and chemical mutagens but not by UV treatment.

111 flammatory response or the production of DNA mutagens but rather by providing carbohydrate-derived me

112 identified that favipiravir likely acts as a mutagen, but the precise mutation bias that favipiravir

113 experimental animals, although it is a weak mutagen by itself.

114 These endogenous mutagens can alter genes, promote genomic rearrangements

115 Mutagens can be formed during meat process or digestion.

116 DNA damage induced by environmental mutagens can be resolved by disparate repair and/or repl

117 Mutations that are induced by chemical mutagens can occur anywhere in the genome.

118 that paternal exposure to a wide variety of mutagens can result in transgenerational instability man

119 No anti-mutagen capacity was noted for MeIQx and Glu-P-1 (10(-5)

120 -dG, which is the major adduct of the potent mutagen/carcinogen benzo[a]pyrene.

121 tantly exposed to chemical and environmental mutagens, causing lesions that can stall replication.

122 s further showed that cell cycle response to mutagen challenge was significantly enhanced in cells tr

123 combined) for sensitivity to four different mutagen challenges.

124 s anti-tumor agent, is known as an effective mutagen, clastogen and toxicant as well as an effective

125 controls and used in conjunction with a meat mutagen database to estimate intake of heterocyclic amin

126 r mutations, induced by the random germ line mutagen ENU (N-ethyl-N-nitrosourea), have disclosed key

127 This set allows rapid screening of potential mutagens, environmental conditions, or genetic loci for

128 genetic screening by an enhanced retroviral mutagen (ERM)-mediated random mutagenesis in the estroge

129 etics of transcription errors in response to mutagen exposure and find that DNA repair is required to

130 The relative risks associated with mutagen exposure compared to background rates are also s

131 ge responses repress induced mutations after mutagen exposure.

132 ology applications as well as an insertional mutagen for gene discovery during development.

133 In conclusion, RBV could work as a weak mutagen for HCV RNA in HCV-infected patients.

134 However, RBV can act as a potent mutagen for some RNA viruses.

135 An insertional mutagen for use in other mouse somatic cells would facil

136 hese elements as simple yet highly effective mutagens for both functional genomic and proteomic studi

137 ufficiently characterized source of chemical mutagens for consumers.

138 lications for the treatment of bacteria with mutagens, for the evolution of mutator strains in bacter

139 few studies have evaluated the role of meat mutagens formed during high cooking temperatures.

140 linked to databases for estimating intake of mutagens formed in meats cooked at high temperatures (he

141 blasts demonstrated that quercetin, a potent mutagen found in high levels in bracken fern (Pteridium

142 Environmental pollution including mutagens from wastewater effluents and discontinuity by

143 Thus, clinical translation of viral mutagens has been difficult, casting doubt on the clinic

144 y explains why DNA methylation, a well-known mutagen, has been maintained within coding sequences of

145 More than 24 different types of food mutagens have been identified till date from cooked meat

146 Forward genetic screens using chemical mutagens have been successful in defining the function o

147 oviruses, acting as somatic cell insertional mutagens, have been widely used to identify cancer genes

148 nsumption (type, cooking method, and related mutagens), heme iron, nitrite/nitrate, and prostate canc

149 le of well-done meat intake and meat-derived mutagen heterocyclic amine (HCA) exposure in the risk of

150 utagenesis were observed with both the viral mutagen (i.e., G-to-C mutations) and the host restrictio

151 ency virus type 1 (HIV-1) by use of chemical mutagens [i.e., 5-azacytidine (5-AZC)] as well as by hos

152 cellular proliferation and promoted acridine mutagen ICR191-induced transformation of MCF10A cells.

153 In vitro, ribavirin acts as a lethal mutagen in Hantaan virus (HTNV)-infected Vero E6 cells,

154 found that the 4-HNE-DNA adduct is a potent mutagen in human cells and is preferentially formed at c

155 strate that Tnt1 is an efficient insertional mutagen in M. truncatula, and could be a primary choice

156 ific L1HS-Ta subfamily acts as an endogenous mutagen in modern humans, reshaping both somatic and ger

157 acum) Tnt1 retrotransposon as an insertional mutagen in potato.

158 ng sexual reproduction, making Tnt1 an ideal mutagen in potato.

159 s induced by ultraviolet (UV) light, a major mutagen in several human cancers, in terms of extended (

160 mage suggests a role for L1 as an endogenous mutagen in somatic tissues.

161 ns of modification of p53 DNA exposed to the mutagen in vitro versus in vivo.

162 ansposons have been effectively exploited as mutagens in a variety of organisms.

163 ifficile has relied on the use of ermB-based mutagens in erythromycin-sensitive strains.

164 s far greater impact than any other external mutagens in mitochondria and is fundamentally linked to

165 superfamily, are widely used as insertional mutagens in numerous plant species.

166 een attributed to increased exposure time to mutagens in older individuals.

167 ement of chromatid breaks induced by various mutagens in short-term cultures of peripheral blood lymp

168 quantifying the chromatid breaks induced by mutagens in short-term cultures of peripheral blood lymp

169 These mutations may be caused by exposure to mutagens in the environment or by endogenous DNA-replica

170 als, which suggests differential exposure to mutagens in the urine.

171 ariety of carbocyclic and heterocyclic amine mutagens including PhIP.

172 of great importance in the bioactivation of mutagens, including the N-hydroxylation of arylamines.

173 regation is a unifying property of exogenous mutagens, including UV light and chemotherapy agents in

174 torting DNA lesions induced by a plethora of mutagens, including UV light.

175 licate ultraviolet radiation as the dominant mutagen, indicating a superficially located cell of orig

176 ygous mice (CBS(+/-) ) reduced the number of mutagen-induced aberrant colonic crypt foci.

177 dification (R-TDM) induced by spontaneous or mutagen-induced breaks.

178 ithin the same genetic background using only mutagen-induced changes as segregating markers.

179 ncreases of S and G(2) phase frequencies and mutagen-induced comets.

180 The probability of a cancer being mutagen-induced correlates across cancer sites with the

181 Levels of baseline and mutagen-induced DNA damage are intrinsically higher in P

182 We characterize this process in mutagen-induced mouse liver tumours and show that DNA re

183 We have established a mutagen-induced nonsense allele of the rat Apc gene on a

184 he conditional probabilities of cancer being mutagen-induced range between 7-96%.

185 isk and the probability of that cancer being mutagen-induced.

186 smokers) and the probability of cancer being mutagen-induced.

187 Thus, mutagen induction of LOH in embryonic stem cells suggest

188 us infection and improved resistance against mutagen/inflammation-induced colorectal tumorigenesis.

189 tations on viral replication, sensitivity to mutagen, inhibition by type I interferon (IFN), and tran

190 iation of red meat, processed meat, and meat mutagen intake with lung cancer risk in Environment And

191 Meat, well-done meat, and inferred meat mutagen intakes were evaluated.

192 red to the host needs to be so high that the mutagen is effective even in the refugia.

193 necessary to neutralize refugia and the less mutagen is necessary to achieve extinction at high migra

194 ling of a microbial pathogen with a chemical mutagen, is a potential broad-spectrum antiviral treatme

195 Genetic instability, provoked by exogenous mutagens, is well linked to initiation of cancer.

196 ed drinking water, is one of the most potent mutagens known.

197 The results of this study suggest that mutagens like DBPs may play an important role in enhanci

198 tions induced in the initial exposure to the mutagen, many of the lines are segregating or are now fi

199 production of mouse mutations with the point mutagen N-ethyl-N-nitrosourea (ENU) is a key strategy fo

200 ecessive mutations generated by the chemical mutagen n-ethyl-n-nitrosourea (ENU) mapped a new mutant

201 zygous for germline mutations induced by the mutagen N-ethyl-N-nitrosourea (ENU), numerous animals di

202 ved from males mutagenized with the germline mutagen N-ethyl-N-nitrosourea (ENU), we identified a rec

203 mutagenesis screen in C57BL/6 mice using the mutagen N-ethyl-N-nitrosourea (ENU).

204 opulations after treatment with the powerful mutagen N-ethyl-N-nitrosourea.

205 ue-Dawley rat that had been treated with the mutagen N-ethyl-N-nitrosourea.

206 ns against direct-acting and indirect-acting mutagens, namely 4-nitro-o-phenylenediamine, sodium azid

207 ing to the conclusion that generation of the mutagen nitrogen dioxide is peculiar to cell culture sys

208 repeat tract in a non-B conformation is the mutagen, not the sequence per se in the right-handed B h

209 iguous base-pairing capacity is an efficient mutagen of the PV genome.

210 In addition, mutagen or cancer-specific mutational background models

211 late the mutation rate, either by the use of mutagens or by selection (or genetic manipulation) of fi

212 ve been studied because of their activity as mutagens or drugs, but little is known regarding their i

213 natures that are causally linked to specific mutagens or susceptibility loci.

214 not affect viral replication, sensitivity to mutagen, or inhibition by IFN-beta compared to WT MHV.

215 ted with ultraviolet (UV) light and chemical mutagens, or by insertional mutagenesis.

216 NA, and these thymine analogs are well known mutagens, our observations raise the possibility that ha

217 sts, which are more exposed to environmental mutagens over time.

218 ugia, i.e., compartments that receive little mutagen, prevent extinction?

219 functional food ingredient with interesting mutagen preventing properties.

220 of the DNA bacteriophage T7 was grown with a mutagen, producing a genomic rate of 4 nonlethal mutatio

221 The essential oil showed mutagen-protective efficacy against IQ and MeIQ tested a

222 e), C. lechleri essential oil was tested for mutagen-protective properties (concentration range: 0.01

223 Mutagens related to meat cooking and processing, and var

224 at are known to be strong, moderate and weak mutagens, respectively.

225 A molecular dynamics simulation of RNA- and mutagen (RTP)-bound 3D(pol) revealed that the T19 residu

226 overed novel mutations in genes that include mutagen sensitive 206, single-strand annealing reducer,

227 d-joining (MMEJ) component, polymerase theta/mutagen-sensitive 308 (mus308), exhibits a sporadic thin

228 ere solely sensitive to MMS and define 8 new mutagen-sensitive genes (mus212-mus219).

229 The remaining 16 mutants define 14 new mutagen-sensitive genes (mus314-mus327).

230 an interaction between the gene (mus309, for mutagen-sensitive) encoding the Drosophila Bloom's syndr

231 of epidemiologic and genetic studies linking mutagen sensitivity and cancer risk.

232 We developed the first model incorporating mutagen sensitivity and epidemiologic factors to predict

233 re was a dose response between the degree of mutagen sensitivity and risk of SCCHN in non-Hispanic Wh

234 hly heritable, thereby validating the use of mutagen sensitivity as a cancer susceptibility factor.

235 city, we validated our previous finding that mutagen sensitivity as measured by the frequency of chro

236 When mutagen sensitivity data were incorporated, the AUC incr

237 r predisposition factor, the heritability of mutagen sensitivity has not been clearly established.

238 provides further support to the notion that mutagen sensitivity increases the risk of cancer.

239 Despite numerous studies showing that mutagen sensitivity is a cancer predisposition factor, t

240 us epidemiologic studies have suggested that mutagen sensitivity is a cancer susceptibility factor fo

241 nce is becoming increasingly convincing that mutagen sensitivity is a risk factor for cancer developm

242 the strongest and most direct evidence that mutagen sensitivity is highly heritable, thereby validat

243 notype and provided compelling evidence that mutagen sensitivity is highly heritable.

244 of genetic and environmental factors on the mutagen sensitivity phenotype and provided compelling ev

245 of genetic and environmental factors on the mutagen sensitivity phenotype.

246 Mutagen sensitivity was measured in peripheral blood lym

247 Mutagen sensitivity, a measurement of chromatid breaks i

248 We measured DNA damage, mutagen sensitivity, and reactive oxygen species (ROS) i

249 Mutagen sensitivity, measured by quantifying the chromat

250 r studies are required to fully characterize mutagen sensitivity, which could have important implicat

251 s study is to identify genetic predictors of mutagen sensitivity.

252 -epoxide (BPDE)-induced chromatid breaks (by mutagen-sensitivity assay) and DNA damage (by comet assa

253 C3B (A3B), the primary candidate as a cancer mutagen, shows little association with immune cell types

254 ith those linked to a specific environmental mutagen, specifically ionizing radiation or cigarette sm

255 igated the association between meat and meat mutagens, specifically PhIP, and prostate cancer risk in

256 The results show that mutagens such as fast neutrons (used for the induction o

257 Mutagens, such as UV light, were implicated in unexpecte

258 entify mutated genes, and argue that the two mutagens target the same set of genes.

259 ethyltransferase (M.EcoRII) and that it is a mutagen that can form productive base pairs with either

260 nexpectedly, we found trichostatin A to be a mutagen that caused DNA damage and mutagenesis at least

261 m transfer DNA (T-DNA) is an effective plant mutagen that has been used to create sequence-indexed T-

262 5-aza-2'-deoxycytidine (KP1212), a selective mutagen that induces A-to-G and G-to-A mutations in the

263 These agents define a specific class of mutagen that promotes template-switching and acts by sta

264 and could be extended to the arylamine food mutagens that are biologically relevant in humans.

265 Reactive oxygen species are ubiquitous mutagens that have been linked to both disease and aging

266 etroviruses are powerful insertional somatic mutagens that have been used for many landmark discoveri

267 ng in enhanced sensitivity of CVB3 to lethal mutagens that is dependent on the size of the viral popu

268 Mutagens that strongly and specifically affect this clas

269 transposons are "copy-and-paste" insertional mutagens that substantially contribute to mammalian geno

270 emonstrate that TEs are potent episodic (epi)mutagens that, thanks to marked chromatin tropisms, limi

271 erited DNA repair deficiencies or exposed to mutagens, the pleotropic effects of these contexts could

272 ss of viral drug resistance: resistance to a mutagen through increased fidelity.

273 Fast neutron radiation has been used as a mutagen to develop extensive mutant collections.

274 transposon system has been used as a somatic mutagen to identify candidate cancer genes.

275 y transposon to act as a somatic insertional mutagen to identify genes involved in solid tumour forma

276 wide BiFC screen with an enhanced retroviral mutagen to identify new LMP1-binding proteins.

277 se screens to compare the efficiency of each mutagen to isolate mutants and to identify mutated genes

278 The use of transposons as insertional mutagens to identify cancer genes in mice has generated

279 d 4-nitroquinoline-N-oxide (4-NQO), a direct mutagen toward Salmonella typhimurium TA 98 and TA 100.

280 d 4-nitroquinoline-N-oxide (4-NQO), a direct mutagen toward Salmonella typhimurium TA 98 and TA 100.

281 d 4-nitroquinoline-N-oxide (4-NQO), a direct mutagen toward Salmonella typhimurium TA 98 and TA 100.

282 ect mutagen, and benzo[a]pyrene, an indirect mutagen, toward Salmonella typhimurium TA 98 and TA 100.

283 A mutagen-treated CHO cell line, in which LRP-1 is express

284 e of perinatal lethality was observed in the mutagen-treated cohort compared with an untreated backcr

285 d this issue in the esophageal epithelium of mutagen-treated mice.

286 Surprisingly, our results demonstrate mutagen treatment did not increase mitochondrial point o

287 embryonic stem cells to nontoxic amounts of mutagens triggers a marked increase in the frequency of

288 ype E. coli in <24 h, outperforming chemical mutagens, ultraviolet light and the mutator strain XL1-R

289 the type and concentration of flavonoids and mutagen used.

290 s potential as a random germline insertional mutagen useful for in vivo gene trapping in mice.

291 -frame exon traps in the enhanced retroviral mutagen vector.

292 The positive identification of mutagens was hampered by a lack of commercially availabl

293 omatic hydrocarbons (PAHs) and other organic mutagens were assessed by quantification of urinary PAH

294 summary, red meat, processed meat, and meat mutagens were independently associated with increased ri

295 Each mutagen, whether used alone or in combination, resulted

296 mito-APOBEC1 acts as a potent mutagen which exclusively induces C:G>T:A transitions wi

297 eat, meat cooking methods, and inferred meat mutagens with SSL risk and in comparison to risk of othe

298 luated meat cooking methods and meat-derived mutagens with SSL risk.

299 ting HIV-1 infection in which use of a viral mutagen would over multiple rounds of replication lead t

300 densely ionizing radiation than by chemical mutagens, x-rays, or endogenous aging processes.