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1 s to oxidative stress, a common mechanism of environmental insult.
2 ial responsiveness to this bacterial-derived environmental insult.
3 cellular protection against this ubiquitous environmental insult.
4 n must be maintained during growth and under environmental insult.
5 range for the negative impact of diet as an environmental insult.
6 nk between defense of genome and host during environmental insult.
7 to damage and collapse at the trigger of an environmental insult.
8 tivity, function and response to disease and environmental insult.
9 ield that guards mechanosensory neurons from environmental insult.
10 immunological barrier against pathogens and environmental insults.
11 n establishment of biofilms and tolerance of environmental insults.
12 ed by phosphorylation in response to adverse environmental insults.
13 se states, including infectious diseases and environmental insults.
14 ogy and provides cell wall integrity against environmental insults.
15 types can moderate children's sensitivity to environmental insults.
16 and are produced by numerous endogenous and environmental insults.
17 The oral cavity is exposed to a variety of environmental insults.
18 tatic mechanism in response to metabolic and environmental insults.
19 asticity, and the response to endogenous and environmental insults.
20 esponse of myocardium to diverse genetic and environmental insults.
21 nscription for defense against pathogens and environmental insults.
22 stable cell forms, highly resistant to harsh environmental insults.
23 y is a period of particular vulnerability to environmental insults.
24 ells and protects them from host-related and environmental insults.
25 an alter epithelial function and response to environmental insults.
26 f inadequate nutrient intake plus additional environmental insults.
27 e reactive oxygen species produced by severe environmental insults.
28 he face of a broad spectrum of intrinsic and environmental insults.
29 for protection of skin and other organs from environmental insults.
30 ponse to invading pathogens and a variety of environmental insults.
31 the ability to respond to potentially toxic environmental insults.
32 perior access to nutrients and resistance to environmental insults.
33 sive spore wall that protects the spore from environmental insults.
34 em to damage by opportunistic infections and environmental insults.
35 on, olfactory sensory neurons are exposed to environmental insults.
36 ) modulates host responses to infectious and environmental insults.
37 esulting from normal metabolic activities or environmental insults.
38 sociated with pathogenicity and responses to environmental insults.
39 play key roles in protecting the lungs from environmental insults.
40 of gene mutations, chromosomal anomalies or environmental insults.
41 o regulate lung inflammatory responses to an environmental insult, a function directly relevant to di
43 response, are one of the earliest sensors of environmental insult and have been shown to play a role
44 the submandibular and lacrimal glands via an environmental insult and LTalpha; 2) amplification of lo
45 isms that evolved to protect the genome from environmental insult and that serve to obscure observati
46 ch as maintaining a physical barrier against environmental insults and allergens and providing a tiss
47 rial spores are extraordinarily resistant to environmental insults and are vectors of various illness
48 iated signaling in inflammatory responses to environmental insults and DC-T cell communication in ant
49 ructures designed to protect the genome from environmental insults and deliver it to the host cell.
53 e in the response of brain cells to prenatal environmental insults and may be a key component in the
54 en demonstrated to confer protection against environmental insults and prevent disease or inhibit the
55 ddition to telomere shortening, a variety of environmental insults and signaling imbalances can elici
57 n significantly if they promote tolerance to environmental insults and thus prevent the general deter
58 ing the normal cell cycle and in response to environmental insult, and have demonstrated that the che
60 survival of one or more subpopulations upon environmental insult, and therefore plays an important r
63 ms that detect microbial substances, sterile environmental insults, and molecules derived from host c
64 It is the combination of bacterial factors, environmental insults, and the host immune response that
66 cantholysis in the fragile epidermis because environmental insults are more stringent and wound heali
68 t line of defense against microbes and other environmental insults at mucosal tissues and are thus th
69 s an important approach to understanding how environmental insults at particular developmental junctu
71 rs of relapse are immunologic challenges and environmental insults, both of which associate with chan
72 sHsps are not only activated in response to environmental insults, but also exert developmental and
73 body from infection, dehydration, and other environmental insults by creating an impermeable barrier
74 me at which the interval between devastating environmental insults by impact exceeded the timescale f
75 gainst the toxic and carcinogenic effects of environmental insults by upregulating an array of genes
78 turbances caused by susceptibility genes and environmental insults during early neurodevelopment init
80 ding that pathological genetic variation and environmental insults during sensitive periods in brain
81 ould be potentially vulnerable to early-life environmental insults, during the maturation of parvalbu
82 n ATP-independent mechanism that responds to environmental insult (e.g., heat shock and ethanol treat
83 ) is hypothesized as one of the responses to environmental insults, e.g. attack by fungivorous insect
84 netic insufficiencies predispose for PLE and environmental insults, e.g. viral infections and inflamm
85 or direct exposure of the child to the index environmental insult has sparked interest in transgenera
89 enetic defect, accident, injury, disease, or environmental insult; however, most persons develop this
91 increasing the resilience of the airways to environmental insults in addition to improving strategie
92 ultiple susceptibility genes and one or more environmental insults in early life, resulting in altere
94 per-reactivity and remodeling in response to environmental insults in the absence of overt Th2-type i
96 The niche may also protect stem cells from environmental insults including cytotoxic chemotherapy a
98 on yeast Spc1/StyI MAPK is activated by many environmental insults including high osmolarity, oxidati
99 MAP kinases, Sty1 is activated by a range of environmental insults including osmotic stress, hydrogen
100 of lymphocytes that are poised to respond to environmental insults including viral infections with th
102 ive stress that defends against a variety of environmental insults, including electrophile attacks an
103 vide a crucial first line of defense against environmental insults, including infection, trauma, and
104 on of mucus to help protect the lung against environmental insults, including pathogens and pollution
105 gers, may assist plants in coping with harsh environmental insults, including soil and water pollutan
106 rovide a protective barrier against numerous environmental insults, including ultraviolet radiation (
109 irect evidence of genetic susceptibility and environmental insult interactions leading to a unique an
110 action, in which an individual's response to environmental insults is moderated by his or her genetic
111 irways, caused by many different genetic and environmental insults, is known as tracheomalacia in hum
112 RNA), whose deregulation may be sensitive to environmental insult leading to altered phenotypes.
114 omes of cortical malformation as a result of environmental insults may still be amenable to explanati
115 lly due to different genetic deficits and/or environmental insults, neural computations and the behav
117 sceptibility to pulmonary fibrosis following environmental insults or cytotoxic cancer therapies has
118 ted by dopamine and its metabolites and that environmental insults or genetic defects may disrupt thi
119 n of the endodermal layer of the yolk sac by environmental insults or genetic manipulations during th
121 pond to stress, protecting itself from harm (environmental insults or infections), to ultimately, dea
123 can occur as a result of immunosuppression, environmental insult, or aging; however, the cause of re
124 that can be instigated by microbial toxins, environmental insults, or the genetic predisposition of
125 ssociated with increased cell survival after environmental insult, our data suggest that ultraviolet
126 t removed rsbR, -S, and -T; however, only an environmental insult required RsbU to reactivate RsbV.
127 gene products or with the by-products of the environmental insult, resulting in a greater than additi
128 Mechanosensory hair cells are vulnerable to environmental insult, resulting in hearing and balance d
130 s of Entamoeba and Giardia protect them from environmental insults, stomach acids, and intestinal pro
131 etic trait and probably requires an inciting environmental insult such as a viral infection to trigge
132 male germ cells are exquisitely sensitive to environmental insults such as heat and oxidative stress.
136 of antigen-specific suppression elicited by environmental insults, such as ultraviolet (UV)-B radiat
137 y commensal sulfate-reducing bacteria, is an environmental insult that potentially contributes to chr
138 ged with endogenous metabolic byproducts and environmental insults that can lead to nearly a million
139 elopmental perturbations, disease states, or environmental insults that cause ectopic cell death woul
140 e PFC may render it especially vulnerable to environmental insults that impact PFC function in adulth
141 n rates and spectra, as well as the roles of environmental insults that influence these processes.
142 ients with SFTPC mutations may be related to environmental insults that ultimately overwhelm the home
143 at ATF3 is induced by a very large number of environmental insults, this study supports involvement o
144 ased upon mechanisms that protect cells from environmental insult thus contributing to the survival a
145 ith a means of responding to a wide range of environmental insult, thus maintaining DNA integrity and
146 nutrition is a modulator of vulnerability to environmental insults; thus, it is timely to consider nu
147 ion between both genetic barrier defects and environmental insults to the barrier with AD suggests th
148 ich protects the dormant spore's genome from environmental insults, uses the protein SpoIVA as a scaf
149 ed in response to many types of cellular and environmental insults via mechanisms involving post-tran
150 osure to smoking, alcohol and other putative environmental insults was collected using a structured q
151 systemic protection against tissue damage by environmental insults, we identified artemisitene as a n
152 cteria are tolerant of antibiotics and other environmental insults, whereas their isogenic, rapidly g
153 iated with HCC could influence the effect of environmental insults, yielding a predilection for tumor
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