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1 ield that guards mechanosensory neurons from environmental insult.
2 s to oxidative stress, a common mechanism of environmental insult.
3 ial responsiveness to this bacterial-derived environmental insult.
4 cellular protection against this ubiquitous environmental insult.
5 ase inflammation associated with a secondary environmental insult.
6 ia-like behavior, even when combined with an environmental insult.
7 n must be maintained during growth and under environmental insult.
8 range for the negative impact of diet as an environmental insult.
9 nk between defense of genome and host during environmental insult.
10 to damage and collapse at the trigger of an environmental insult.
11 tivity, function and response to disease and environmental insult.
12 to ensure safeguarding of germline DNA from environmental insults.
13 osition and increased vulnerability to early environmental insults.
14 sive spore wall that protects the spore from environmental insults.
15 em to damage by opportunistic infections and environmental insults.
16 on, olfactory sensory neurons are exposed to environmental insults.
17 f physical and immunological defense against environmental insults.
18 esulting from normal metabolic activities or environmental insults.
19 sociated with pathogenicity and responses to environmental insults.
20 play key roles in protecting the lungs from environmental insults.
21 of gene mutations, chromosomal anomalies or environmental insults.
22 immunological barrier against pathogens and environmental insults.
23 n establishment of biofilms and tolerance of environmental insults.
24 ed by phosphorylation in response to adverse environmental insults.
25 s to be less subtle for disease-predisposing environmental insults.
26 se states, including infectious diseases and environmental insults.
27 ipates in protecting the organism's DNA from environmental insults.
28 types can moderate children's sensitivity to environmental insults.
29 and are produced by numerous endogenous and environmental insults.
30 that together increase resistance to common environmental insults.
31 The oral cavity is exposed to a variety of environmental insults.
32 tatic mechanism in response to metabolic and environmental insults.
33 eostasis (EH) in response to mild or intense environmental insults.
34 ue to ensure barrier function in response to environmental insults.
35 n development and a time of vulnerability to environmental insults.
36 l for muscle homeostasis and the response to environmental insults.
37 used by direct damage to the skin barrier by environmental insults.
38 ulnerable to damage by genetic mutations and environmental insults.
39 aks (DSBs) arising from physiological and/or environmental insults.
40 protect the host from microbes, injury, and environmental insults.
41 rtant source of innate cytokine responses to environmental insults.
42 cuits particularly vulnerable to genetic and environmental insults.
43 de the epidermis with an optimal response to environmental insults.
44 ) modulates host responses to infectious and environmental insults.
45 lectively vulnerable to numerous genetic and environmental insults.
46 ogy and provides cell wall integrity against environmental insults.
47 asticity, and the response to endogenous and environmental insults.
48 esponse of myocardium to diverse genetic and environmental insults.
49 nscription for defense against pathogens and environmental insults.
50 stable cell forms, highly resistant to harsh environmental insults.
51 y is a period of particular vulnerability to environmental insults.
52 ells and protects them from host-related and environmental insults.
53 an alter epithelial function and response to environmental insults.
54 hen regulation is lost due to genetic and/or environmental insults.
55 f inadequate nutrient intake plus additional environmental insults.
56 e reactive oxygen species produced by severe environmental insults.
57 e interaction of genetic vulnerabilities and environmental insults.
58 he face of a broad spectrum of intrinsic and environmental insults.
59 for protection of skin and other organs from environmental insults.
60 ponse to invading pathogens and a variety of environmental insults.
61 the ability to respond to potentially toxic environmental insults.
62 perior access to nutrients and resistance to environmental insults.
63 o regulate lung inflammatory responses to an environmental insult, a function directly relevant to di
66 response, are one of the earliest sensors of environmental insult and have been shown to play a role
67 the submandibular and lacrimal glands via an environmental insult and LTalpha; 2) amplification of lo
68 isms that evolved to protect the genome from environmental insult and that serve to obscure observati
69 ch as maintaining a physical barrier against environmental insults and allergens and providing a tiss
70 rial spores are extraordinarily resistant to environmental insults and are vectors of various illness
71 sma membrane (PM) homeostasis in response to environmental insults and changes in lipid metabolism.
73 iated signaling in inflammatory responses to environmental insults and DC-T cell communication in ant
74 ructures designed to protect the genome from environmental insults and deliver it to the host cell.
78 genetic alterations across generations after environmental insults and how this may impact the develo
79 e in the response of brain cells to prenatal environmental insults and may be a key component in the
80 haride-based capsules that protect them from environmental insults and play a role in virulence, host
81 en demonstrated to confer protection against environmental insults and prevent disease or inhibit the
82 immune response functions to a wide array of environmental insults and remain poised for future patho
83 ity of the mitochondrial network to overcome environmental insults and respond to physiological cues.
84 ddition to telomere shortening, a variety of environmental insults and signaling imbalances can elici
86 n significantly if they promote tolerance to environmental insults and thus prevent the general deter
87 ing the normal cell cycle and in response to environmental insult, and have demonstrated that the che
89 survival of one or more subpopulations upon environmental insult, and therefore plays an important r
92 ms that detect microbial substances, sterile environmental insults, and molecules derived from host c
93 It is the combination of bacterial factors, environmental insults, and the host immune response that
94 milder variants increasing susceptibility to environmental insults are associated with age-related ca
96 cantholysis in the fragile epidermis because environmental insults are more stringent and wound heali
99 ncer cells must resist numerous internal and environmental insults associated with neoplasia that jeo
100 t line of defense against microbes and other environmental insults at mucosal tissues and are thus th
101 s an important approach to understanding how environmental insults at particular developmental junctu
103 rs of relapse are immunologic challenges and environmental insults, both of which associate with chan
104 sHsps are not only activated in response to environmental insults, but also exert developmental and
105 body from infection, dehydration, and other environmental insults by creating an impermeable barrier
106 me at which the interval between devastating environmental insults by impact exceeded the timescale f
107 gainst the toxic and carcinogenic effects of environmental insults by upregulating an array of genes
108 critical time in offspring development where environmental insults can have damaging impacts on the f
109 ew, the cholangiocyte response to genetic or environmental insults can lead to a heterogeneous respon
112 Impaired NMDAR signalling through genetic or environmental insults causes a constellation of neurodev
114 rogeneity of clinical symptoms, pathologies, environmental insults contributing to the disease, and d
116 turbances caused by susceptibility genes and environmental insults during early neurodevelopment init
118 ding that pathological genetic variation and environmental insults during sensitive periods in brain
120 ould be potentially vulnerable to early-life environmental insults, during the maturation of parvalbu
121 n ATP-independent mechanism that responds to environmental insult (e.g., heat shock and ethanol treat
122 ) is hypothesized as one of the responses to environmental insults, e.g. attack by fungivorous insect
123 netic insufficiencies predispose for PLE and environmental insults, e.g. viral infections and inflamm
124 strate how fetal growth can be influenced by environmental insults (for example, maternal infections)
125 or direct exposure of the child to the index environmental insult has sparked interest in transgenera
126 ll-derived cytokine that responds rapidly to environmental insult, has a critical role in initiating
130 enetic defect, accident, injury, disease, or environmental insult; however, most persons develop this
133 pan-stress" markers for responses to diverse environmental insults implicated in miscarriage Cell Sig
134 increasing the resilience of the airways to environmental insults in addition to improving strategie
135 tic component combined with random potential environmental insults in an immunologically susceptible
136 ultiple susceptibility genes and one or more environmental insults in early life, resulting in altere
138 sceptibilities and inflammatory reactions to environmental insults in humans with impaired skin barri
139 2s) respond rapidly to allergen exposure and environmental insults in mucosal organs, producing type
141 per-reactivity and remodeling in response to environmental insults in the absence of overt Th2-type i
143 GMM escape, bacteria to be protected against environmental insults including antibiotics and low pH,
144 The niche may also protect stem cells from environmental insults including cytotoxic chemotherapy a
146 on yeast Spc1/StyI MAPK is activated by many environmental insults including high osmolarity, oxidati
147 MAP kinases, Sty1 is activated by a range of environmental insults including osmotic stress, hydrogen
148 of lymphocytes that are poised to respond to environmental insults including viral infections with th
149 ical barrier to protect host tissues against environmental insults, including dietary antigens, aller
152 ive stress that defends against a variety of environmental insults, including electrophile attacks an
153 vide a crucial first line of defense against environmental insults, including infection, trauma, and
154 ripheral organs, the cochlea is subjected to environmental insults, including loud, damage-inducing s
156 a layer of protection for the bacterium from environmental insults, including other bacteria and the
157 on of mucus to help protect the lung against environmental insults, including pathogens and pollution
158 gers, may assist plants in coping with harsh environmental insults, including soil and water pollutan
159 rovide a protective barrier against numerous environmental insults, including ultraviolet radiation (
160 porting a combination of genetic factors and environmental insults, including viral infection during
166 irect evidence of genetic susceptibility and environmental insult interactions leading to a unique an
168 action, in which an individual's response to environmental insults is moderated by his or her genetic
169 survival to a potential plethora of diverse environmental insults is underpinned by coordinated comm
170 irways, caused by many different genetic and environmental insults, is known as tracheomalacia in hum
171 RNA), whose deregulation may be sensitive to environmental insult leading to altered phenotypes.
173 s arising from a contribution of genetic and environmental insults, many of which molecularly converg
174 omes of cortical malformation as a result of environmental insults may still be amenable to explanati
175 lly due to different genetic deficits and/or environmental insults, neural computations and the behav
177 sceptibility to pulmonary fibrosis following environmental insults or cytotoxic cancer therapies has
178 ted by dopamine and its metabolites and that environmental insults or genetic defects may disrupt thi
179 n of the endodermal layer of the yolk sac by environmental insults or genetic manipulations during th
181 pond to stress, protecting itself from harm (environmental insults or infections), to ultimately, dea
183 can occur as a result of immunosuppression, environmental insult, or aging; however, the cause of re
184 e from errors during biosynthesis, damage by environmental insults, or imbalances in enzymatic and me
185 that can be instigated by microbial toxins, environmental insults, or the genetic predisposition of
186 ssociated with increased cell survival after environmental insult, our data suggest that ultraviolet
188 hether cell types exposed to a high level of environmental insults possess cell type-specific prosurv
189 tivation (MIA) as a rodent model of prenatal environmental insult, previous results have reported den
190 t removed rsbR, -S, and -T; however, only an environmental insult required RsbU to reactivate RsbV.
191 gene products or with the by-products of the environmental insult, resulting in a greater than additi
192 Mechanosensory hair cells are vulnerable to environmental insult, resulting in hearing and balance d
194 The skin is the primary barrier against environmental insults, safeguarding the body from mechan
195 s of Entamoeba and Giardia protect them from environmental insults, stomach acids, and intestinal pro
196 etic trait and probably requires an inciting environmental insult such as a viral infection to trigge
197 male germ cells are exquisitely sensitive to environmental insults such as heat and oxidative stress.
200 serve as crucial, yet vulnerable barriers to environmental insults such as pathogens, allergens, and
203 of antigen-specific suppression elicited by environmental insults, such as ultraviolet (UV)-B radiat
204 y commensal sulfate-reducing bacteria, is an environmental insult that potentially contributes to chr
205 erstanding of how lung stem cells respond to environmental insults that affect the lung epithelial ba
206 ged with endogenous metabolic byproducts and environmental insults that can lead to nearly a million
207 elopmental perturbations, disease states, or environmental insults that cause ectopic cell death woul
208 e PFC may render it especially vulnerable to environmental insults that impact PFC function in adulth
209 n rates and spectra, as well as the roles of environmental insults that influence these processes.
212 ients with SFTPC mutations may be related to environmental insults that ultimately overwhelm the home
213 at ATF3 is induced by a very large number of environmental insults, this study supports involvement o
214 ased upon mechanisms that protect cells from environmental insult thus contributing to the survival a
215 ith a means of responding to a wide range of environmental insult, thus maintaining DNA integrity and
216 nutrition is a modulator of vulnerability to environmental insults; thus, it is timely to consider nu
217 est a model in which 1) genetic and/or early environmental insults to excitatory signaling in layer 3
218 (TLR)3/4-TBK1-IRF3 pathway activation links environmental insults to IL-33 induction in the skin and
219 g cellular integrity in normal cells against environmental insults to prevent disease onset, whereas
220 ion between both genetic barrier defects and environmental insults to the barrier with AD suggests th
221 leiotropic mechanisms, including genetic and environmental insults to the brain, contribute to neurod
222 ich protects the dormant spore's genome from environmental insults, uses the protein SpoIVA as a scaf
223 ed in response to many types of cellular and environmental insults via mechanisms involving post-tran
224 osure to smoking, alcohol and other putative environmental insults was collected using a structured q
225 systemic protection against tissue damage by environmental insults, we identified artemisitene as a n
226 o IL-33 overexpression unless they encounter environmental insults, whereas developing lungs are high
227 cteria are tolerant of antibiotics and other environmental insults, whereas their isogenic, rapidly g
229 iated with HCC could influence the effect of environmental insults, yielding a predilection for tumor