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1 division, are considered reliable markers of biological aging.
2 psychoactive medication do further impact on biological aging.
3 may be a key factor in HIV-related premature biological aging.
4 Telomere length may be a marker of biological aging.
5 ium surfaces, indicating a titanium-specific biological aging.
6 nditions of oxidative stress observed during biological aging.
7 Reduced telomere length may be a marker of biological aging.
8 ementia and mortality and may be a marker of biological aging.
9 ybrid rats, a well accepted animal model for biological aging.
10 on during development, oxidative stress, and biological aging.
11 ks support the applicability of the model to biological aging.
12 els under conditions of oxidative stress and biological aging.
13 chemical or photochemical modifications, not biological aging.
14 help us to better comprehend the process of biological aging.
15 onsequences contributing to disease risk and biological aging.
21 ights into molecular processes that underlie biological aging and, perhaps more importantly, potentia
22 thelium that are known to be associated with biological aging, and cellular senescence markers in HIV
24 e whether MDD is associated with accelerated biological aging, and whether depression characteristics
25 osclerosis is also associated with premature biological aging, as atherosclerotic plaques show eviden
26 ent diseases in the United States, caused by biological aging, autoimmune conditions, trauma, or iatr
27 no evidence for salient differences in neuro-biological aging between the two sensory regions, the ob
28 Modern programmed (adaptive) theories of biological aging contend that organisms including mammal
29 the same chronological age varied in their "biological aging" (declining integrity of multiple organ
32 nking internalizing disorders to accelerated biological aging in the first half of the life course, p
35 ross-sectional data suggest that accelerated biological aging may be a mechanism through which sleep
36 Thus, the overproduction of noggin during biological aging may result in impaired osteoblast forma
38 S-mediated DNA damage results in accelerated biological aging of hVSMCs via 2 mechanisms: (1) Acute S
39 eloping MDD are characterized by accelerated biological aging, operationalized as shortened telomere
40 r the AHP amplitude is strictly dependent on biological aging or is modified by the training procedur
42 oxidative modification of CaM during normal biological aging results in a reduced calcium sensitivit
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