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1 ry metabolites of fungi that cause toxic and carcinogenic effects.
2 ted with supply chain production, except for carcinogenic effects.
3 and mutations are well established for their carcinogenic effects.
4 olic dysfunctions that lead to ER stress and carcinogenic effects.
5 ls of Lsm1 protein have been shown to induce carcinogenic effects.
6 on (IR) is a public concern due to its known carcinogenic effects.
7 to understand the mechanisms involved in PAH carcinogenic effects.
8 y discontinued for fear of possible toxic or carcinogenic effects.
9 uses a wide range of toxic, teratogenic, and carcinogenic effects.
10 which early-life iAs exposure elicits latent carcinogenic effects.
11 require metabolic activation to exert their carcinogenic effects.
12 f anti-inflammatory, anti-platelet, and anti-carcinogenic effects.
13 3,000, 6,000, and 12,000 ppm caused multiple carcinogenic effects.
14 omatic hydrocarbon with strong mutagenic and carcinogenic effects.
16 rstanding of how nickel exerts its toxic and carcinogenic effects at a molecular level may be importa
18 th studies demonstrates the lack of cultural carcinogenic effects, but suggests cultural influences o
20 the first time, that arsenite may exert its carcinogenic effect by targeting cysteine residues in th
21 f dose-dependent cancer risks, incorporating carcinogenic effects, cell killing, and, additionally, p
22 radiation oncology, has potentially greater carcinogenic effect compared with sparsely ionizing radi
23 ility of multigenerational transmission of a carcinogenic effect from exposure to a maternal diet hig
24 hat may be responsible for the genotoxic and carcinogenic effects observed in this transgenic model,
26 onclusion, ADM significantly contributes the carcinogenic effect of AHR and tobacco combustion produc
27 n cell cycle machinery are implicated in the carcinogenic effect of arsenite, the molecular mechanism
31 the ability of MGMT expression to block the carcinogenic effect of MNU even in cancer prone mice.
33 h an increased risk of skin cancers, and the carcinogenic effect of PAHs is thought to involve both t
36 (AGT) protects cells from the mutagenic and carcinogenic effects of alkylating agents by removing O(
37 anisms against the cytotoxic, mutagenic, and carcinogenic effects of alkylating agents by transferrin
38 tein that protects tissues against toxic and carcinogenic effects of alkylating agents, is degraded t
39 a DNA repair enzyme that protects cells from carcinogenic effects of alkylating agents; however, MGMT
40 2B) cells that was adapted to study the anti-carcinogenic effects of all-trans-retinoic acid (RA).
41 literature has long hypothesized potentially carcinogenic effects of antihypertensive agents, but to
42 he exact molecular mechanisms underlying the carcinogenic effects of arsenic remain incompletely unde
45 doses greater than 5 Gy seems to lessen the carcinogenic effects of breast irradiation, most likely
47 hanisms involved including withdrawal of the carcinogenic effects of calcineurin inhibitors and/or th
48 men are not more susceptible than men to the carcinogenic effects of cigarette smoking in the lung.
51 ammals and their cells against the toxic and carcinogenic effects of electrophiles and reactive forms
52 esponse protects cells against the toxic and carcinogenic effects of environmental insults by upregul
58 n carcinogenesis and suggests that the known carcinogenic effects of inflammation may be at least par
59 ntributing to second cancer risk include the carcinogenic effects of ionizing radiation and chemother
60 d is one of the most sensitive organs to the carcinogenic effects of IR, and we have recently highlig
64 ptor (AHR) is known to mediate the toxic and carcinogenic effects of polycyclic aromatic hydrocarbons
65 n factors that mediate many of the toxic and carcinogenic effects of polyhalogenated aromatic hydroca
66 otects animal cells from the deleterious and carcinogenic effects of quinones and other electrophiles
69 plays a critical role in protection from the carcinogenic effects of simple alkylating agents by repa
71 , which is believed to play some role in the carcinogenic effects of sun exposure, the present study
72 Since UVB is responsible for most of the carcinogenic effects of sun exposure, we investigated th
76 s known about the possible proliferative and carcinogenic effects of these particles on cells of the
78 NER) is a major cellular defense against the carcinogenic effects of ultraviolet light from the sun.
79 V-induced DNA damage profoundly modulate the carcinogenic effects of UV exposures, and these response
86 urrently exposed to molecules with potential carcinogenic effects such as 17beta-estradiol, the most
87 erintuitive conclusion that UVR has anti-BCC carcinogenic effects that can explain, at least in part,
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