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1 gonist (yohimbine; used as a pharmacological stressor).
2 rfusion injury (IRI), a common type of renal stressor.
3 ting time as an additional work-related time stressor.
4 ediately following the first exposure to the stressor.
5 e also induced in wild-type mice by an acute stressor.
6 tic conditions altered vulnerability to this stressor.
7 ed as a result of direct experience with the stressor.
8 nce, dominance, and warmth) responses to the stressor.
9 Radiation is a prevalent environmental stressor.
10 ulates a conserved survival response to this stressor.
11 nd 5.5% for peak cortisol levels following a stressor.
12 ly depended upon the presence of the natural stressor.
13 ponse to an inflammatory challenge or social stressor.
14 amine can be prophylactic against subsequent stressors.
15 properties against endogenous and exogenous stressors.
16 for mental disorders arising through social stressors.
17 y occurs when mitochondria adapt to tolerate stressors.
18 organismal capacity to respond to additional stressors.
19 n exposures and integrate risk from multiple stressors.
20 istinct context, likely triggered by similar stressors.
21 T to VE to see if they differ with different stressors.
22 after a recurrent exposure to environmental stressors.
23 organism's capacity to respond to additional stressors.
24 lethal exposure to natural and anthropogenic stressors.
25 or bodily responses to internal and external stressors.
26 is association across a large range of acute stressors.
27 ays a critical role in resistance to various stressors.
28 general case in adaptation to environmental stressors.
29 ccount for increased complexity and multiple stressors.
30 ns are linked to adaptation to environmental stressors.
31 and the relative importance of anthropogenic stressors.
32 he many other coastal systems facing similar stressors.
33 at varying levels of one or more additional stressors.
34 igenetic memory in response to environmental stressors.
35 response to combined climate change-related stressors.
36 rders, as well as sensitivity to compounding stressors.
37 not lead to adequate responses to the biotic stressors.
38 er risk of adverse outcomes after even minor stressors.
39 more resources to tolerate and recover from stressors.
40 proteins to survive the sudden appearance of stressors.
41 ific biological systems impacted by external stressors.
42 te samples that are exposed to environmental stressors.
43 e to acidification as well as the additional stressors.
44 ems maintenance, is altered by anthropogenic stressors.
45 change, food availability, and human-related stressors.
46 that have the potential to act as additional stressors.
47 s been linked to reduced ability to adapt to stressors.
48 to drugs of abuse, drug-associated cues, and stressors.
49 environmental contaminants and psychosocial stressors.
50 entrally controls responses to environmental stressors.
51 oral reefs isolated from other anthropogenic stressors.
52 s overseas, and loneliness as post-migration stressors.
53 ate change when such change results in novel stressors.
55 estments to counteract land- and ocean-based stressors: (1) marine restoration should be prioritised
56 arrhythmias after exposure to QT-prolonging stressors, 10 had other LQTS pathogenic mutations, and 1
59 mechanisms by which different environmental stressors affect plasmodesmal permeability are not well
61 e relatively inhibited in the absence of the stressor and mounted robust responses upon stressor pres
62 rossover study addressed the impact of daily stressors and a history of major depressive disorder (MD
63 eing implemented to relieve areas from local stressors and allow populations to restore to natural le
65 ging support is needed to identify potential stressors and available social support in order to promo
68 t-migration potentially traumatic events and stressors and mental health, and assessed the moderating
69 d periphyton communities exposed to chemical stressors and show that effects on primary production un
70 he interplay of regional scale environmental stressors and the lack of long-term instrumental data of
71 ntory of Stressful Events assessed prior day stressors and the Structured Clinical Interview for DSM-
73 explained by the genetic vulnerability, the stressors and their interactions, we fitted linear mixed
75 yloidogenic LC production as an intrinsic PC stressor, and identifies stress-responsive pathways as n
77 the influence of biological sex, early-life stressors, and genetic and epigenetic factors in individ
78 y vulnerable to adverse effects of perinatal stressors, and impaired cBF integrity results in lasting
79 e valence systems), reactivity to subsequent stressors, and, ultimately, risk for psychopathology.
80 ain baseline, predisposing and precipitating stressors, angiographic features, revascularization, use
81 to affect the transcriptome's response to a stressor.Animals' response to acute stress is known to b
83 logical reserve and diminished resistance to stressors; approximately 10% of those in the elderly pop
86 cellular stress and found that the oxidative stressor arsenite and heat shock-activated stress respon
87 biological communities respond to concurrent stressors at local-to-regional scales remains largely un
89 they did not allow responding to the biotic stressors attack adequately, leading to the observed gro
91 and atolls are less exposed to direct human stressors but are becoming increasingly vulnerable becau
92 umulative risk assessments consider multiple stressors but it is impractical to test every chemical c
93 .SIGNIFICANCE STATEMENT Everyone experiences stressors, but how we respond to them can range from pro
94 capable of adapting to internal and external stressors by undergoing structural plasticity, and failu
95 As expected, for a woman with no prior day stressors, C-reactive protein (CRP), serum amyloid A (SA
96 iated microbiota in mice exposed to a social stressor (called social disruption), as well as non-stre
99 ndividuals, exposure to severe or cumulative stressors can lead to an array of pathological condition
100 s into the mechanism through which emotional stressors can lead to cardiovascular disease in human be
101 y vulnerable period when chronic exposure to stressors can precipitate the onset of a broad spectrum
103 ecipitation (ChIP) analysis showed that this stressor caused substantial gene-dependent increases in
107 any single etiological agent, environmental stressors compromising coral condition might play a larg
108 mg Cl(-)/L), ethanol-vehicle control, or no-stressor control) and subsequently tested their toleranc
110 mixture gene expression profiles from single stressor data were able to better predict effects on rep
111 tems on Earth, yet the extent to which human stressors determine species occurrences, compared with b
113 increases in phenotypes relevant to anxiety/stressor disorders and alcohol addiction, including anxi
114 ence the pathologic outcome or response to a stressor due to the release of a plethora of substances,
115 difications associated with early transplant stressors (e.g., cold ischemia time) and donor aging.
116 Models developed specifically for groups of stressors (e.g., either cyanobacteria or insecticides) p
120 de variety of both natural and anthropogenic stressors encountered by corals in the Anthropocene.
124 we found that neutrophils and monocytes from stressor-exposed mice expressed higher levels of IL-1bet
129 tes multiple neurobehavioral consequences of stressor exposure, including long-lasting biases towards
133 nflammation, suggesting that like many other stressors, extended sleep disruption may lead to a state
134 ted by activation of the receptor during the stressor followed by a persistent, ligand-independent co
135 ate adaptive autonomic responses to physical stressors (for example, hypotension, hemorrhage and pres
137 bitat patches within a landscape to modulate stressors from extreme climate events, and animal distri
138 The aggregate exposure pathway (AEP) tracks stressors from sources to the exposures and serves as a
139 ations between cortisol response following a stressor, functional brain activity to reward, and depre
143 -related differences disappeared-because the stressors heightened CRP, SAA, sICAM-1 and sVCAM-1 respo
144 for extrapolation of laboratory findings of stressor impacts on specific components of the axis.
145 ng genetic factors, environmental toxins and stressors, impaired immune responses, mitochondrial dysf
146 ely studied, showing that there are multiple stressors implicated in colony declines, one stressor be
147 led the pleotrophic acts of an environmental stressor in a complex stress system relevant to public h
149 etamine should be administered relative to a stressor in order to maximize its antidepressant and/or
150 , first shown with an intermittent footshock stressor in rats trained to self-administer heroin, gene
154 d be predicted based on the effects of these stressors in isolation, suggesting that OA increases the
160 red in a prophylactic manner 1 week before a stressor, in order to protect against heightened fear re
161 uced by arsenite, a thiol-directed oxidative stressor, in the absence of eIF2alpha phosphorylation su
163 ), a conserved eukaryotic response to myriad stressors including hypoxia, may play a role in hypoxia-
164 ytic phenotype when evaluated using multiple stressors including open-field, elevated plus maze, hole
165 nditions in addition to multiple, additional stressors including thermal stress, food-limitation, and
167 onfounding factors were resettlement related stressors, including loneliness (odds ratio 1.17, 95% CI
168 enhanced stability against extreme external stressors, including organic solvents, proteases, and et
170 Freshwater ecosystems are exposed to many stressors, including toxic chemicals and global warming,
173 esearch showing: (1) that exposure to social stressors increases proinflammatory activity, (2) that i
174 l confinement (SC), a moderate environmental stressor, increases tic-like responses and elicits TS-li
176 ting host social and communicative behavior, stressor-induced behavior, and performance in learning a
177 The potent HN analogue HNG protects from stressor-induced cell death in fibroblasts, cardiomyobla
180 How the duration and timing of exposure to stressors interact to shape critical windows and influen
181 ms have evolved in response to environmental stressors, interactions dictated by physical forces that
186 rupt reorganizations in response to changing stressors, known as regime shifts or critical transition
188 lnerability of mitochondria to mitochondrial stressors, leading to elevated superoxide release and re
190 es have shown that exposure to psychological stressors leads to inflammation throughout the body.
193 se results suggest that repeated exposure to stressors may differentially alter the neural circuits u
194 known about the influence that environmental stressors may have on genome-wide methylation patterns,
195 designed experiments to test how exposure to stressors may induce resource trade-offs that shape crit
196 s support that deficiencies in recovery from stressors may result in attenuated tolerance to stress t
197 s where rivers are already degraded by other stressors may undermine efforts to conserve biodiversity
199 are increasingly threatened by a variety of stressors, no comprehensive global analysis of change in
200 esponse to projected multiple climate change stressors (ocean acidification and warming) on Antarctic
201 lation should be considered as an additional stressor of marine ecosystems in a similar way to ocean
206 tigated the effect of a single-episode acute stressor on generalization of aversive learning when str
207 ique to assess for the effects of additional stressors on an LCx estimate in a consistent framework,
208 and chemical (elevated metal concentrations) stressors on benthic macroinvertebrate communities.
209 ognitive, emotional, sensorimotor, and mixed stressors on driver arousal and performance with respect
210 model to quantify the roles of anthropogenic stressors on hydrologic alteration and biodiversity in U
211 ences (such as famine and exposures to other stressors) on the long-term persistence of specific patt
212 dent following the six-cycle exposure to the stressor, on Day 6 post-C. rodentium challenge, and pers
218 we propose as an additional, fourth putative stressor (pathogens), which may adversely impact the end
219 ible growth arrest triggered by a variety of stressors, plays important roles in normal physiology an
221 us) to one of seven natural or anthropogenic stressors (predator cue (Anax spp.), 0.5 or 1.0 mg carba
224 entially traumatic events and post-migration stressors related to asylum process and resettlement wer
225 athogenetic role by transmitting trauma- and stressor-related disorders (TSRD) across generations.
227 cellular stress responses elicited by these stressors represents a key step in understanding potenti
228 , have historically been considered negative stressors, requiring responses that are strictly defensi
229 tosynthetic efficiency, tolerance to abiotic stressors, resistance to fungal pathogens and grain qual
230 sticide tolerance results from a generalized stressor response in organisms, and would be induced fol
232 do not themselves harm cells through complex stressors resulting from their design or operational con
236 ptom Scale-Interview Version (PSS-I) and the stressor-specific Posttraumatic Stress Disorder Checklis
238 ophy as well as decreased basal, diurnal and stressor-stimulated plasma corticosterone secretion and
239 t, our findings for the main effects of life stressors (strong risk factor) and 5-HTTLPR genotype (no
240 elated traits and when challenged by certain stressors, succumb to enhanced tumour development and an
243 l circuits, and from environmental energetic stressors such as food deprivation and physical exertion
246 could worsen glycemic control by activating stressors such as higher neighborhood crime, lower housi
248 n fail to account for ongoing changes due to stressors such as land use change and climate change and
250 ers that stabilize proteins to environmental stressors such as refrigeration and elevated temperature
251 were or were not (controls) exposed to cell stressors such as tumor necrosis factor and adherent-inv
252 al vulnerability who experience an exogenous stressor, such as prone/side sleeping or soft bedding, d
255 e can play a role in mitigating the negative stressors, such as the symptoms of HS, on patients' ment
256 mbination of environmental and psychological stressors superimposed on genetic vulnerability, the neu
260 died using social disruption (SDR), a social stressor that involves repeated social defeat in subordi
262 Repeated social defeat (RSD) is a murine stressor that recapitulates key physiological, immunolog
263 hough this endosomal pathway is activated by stressors that also activate mitochondrial autophagy, en
264 and exponential functional relationships to stressors that could cause a nonlinear decrease in seagr
268 pret this as evidence that the environmental stressors that limit tree height also act as ecological
269 important response of animal microbiomes to stressors that reduce the ability of the host or its mic
271 amined cortisol responses to an experimental stressor, the Trier Social Stress Test (TSST), in 208 of
272 tragenerational purging, whereas for abiotic stressors, there appeared to be an interaction between p
274 ightening their responsiveness to subsequent stressors, this enhanced sensitivity probably increases
275 n particular the ability to quickly quantify stressor thresholds in conjunction with dynamic compensa
277 While the epigenome remains sensitive to stressors throughout life, we propose two key principles
278 regarding the power of chronic environmental stressors to accelerate biological aging across multiple
279 makes it possible for childhood psychosocial stressors to affect immune system development, which in
280 tivity are widely considered to be the major stressors to ocean ecosystems induced by emissions of CO
281 g the partial contributions of each of these stressors to programming of cardiovascular dysfunction.
282 host cells links a chemotherapeutic agent-a stressor-to immune modulation and cancer metastasis.
285 Catalase was induced by the canonical ER stressor, tunicamycin, and by I/R in cardiac myocytes fr
286 in ways not directly predictable from single stressors, underscoring the complex and trait-specific m
287 Higher total cortisol output following a stressor was associated with increased depression severi
289 fects development by acting as an early life stressor, we examined birthweight, litter size, maternal
290 s of cortisol responses to a prolonged acute stressor, we identified three distinct trajectories of c
292 lls treated with four types of mitochondrial stressors, we identify activating transcription factor 4
294 entially traumatic events and post-migration stressors were positively associated with PTSD and sever
297 est that post-migration resettlement-related stressors were the most important correlates of mental h
299 lished protocols, one that combines a social stressor with physical alcohol cue exposure, and one tha
300 tem is continuously exposed to environmental stressors with non-linear interrelationships between abi
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