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1 untreated mice, diminished retinal oxidative stress to 70% of the untreated level, and markedly ameli
3 ved in cross-linked networks by distributing stress to a small fraction of highly strained connected
4 ished in the past year have linked oxidative stress to a variety of upper gastrointestinal insults.
6 o significantly blunted the ability of acute stress to activate c-Fos expression within the anterior
7 rats, reduces or blocks the ability of acute stress to activate hindbrain neurons that are immunoreac
9 t couple detection of pathogens and cellular stress to activation of Caspase-1, and consequent IL-1be
12 nked quantitative and qualitative aspects of stress to adolescent and adult outcomes, a number of que
13 treatments with exogenous ABA or dehydration stress to advance our understanding of the features requ
15 l that cells detect and respond to oxidative stress to allow adaptation and repair damage, the underl
17 en appears to act in synergy with epithelial stress to allow intraepithelial cytotoxic T cells to kil
18 n factor that undergoes self-cleavage during stress to allow the expression of DNA repair functions a
19 trolled in response to a variety of cellular stresses to allow the rapid reprogramming of cellular ge
20 of B-Raf reduces T cell resistance to shear stress to alpha4beta1 integrin ligands vascular cell adh
21 sothermal titration calorimetry with osmotic stress to also measure hydration changes accompanying li
24 respectively, are regulated during oxidative stress to alter O-GlcNAcylation are not fully characteri
30 These in vitro findings linking oxidative stress to amyloid fibril formation may be significant to
34 a stress that can act additively with other stresses to arrest cells in G1 in a p38-dependent fashio
37 core with ceftriaxone the capacity of acute stress to augment the acquisition of cocaine self-admini
40 ication of lipid peroxide-mediated oxidative stress to be different in survivors and non-survivors.
42 mechanisms of drug action and resistance was stressed to be essential for the design of new agents an
43 n a silica cladding allows large anisotropic stresses to be set into the crystalline material so that
47 of a kappa antagonist administered following stress to block forced swim stress-induced reinstatement
49 en both milk samples were subjected to shear stress to break the curd system at constant shear rate,
53 as miR-451 depletion synergizes with oxidant stress to cause profound anemia in zebrafish embryos.
54 Using a novel apparatus to apply mechanical stress to cell-cell junctions, we showed that knockdown
56 ve suggested one potential mechanism linking stress to cellular aging, disease and mortality in human
57 Brain circuits are plastic and remodeled by stress to change the balance between anxiety, mood contr
60 f PTSD and suggests the potential of ongoing stress to compound initial stress reactions and lead to
61 cells actively exert physical forces (solid stress) to compress tumour blood vessels, thus reducing
62 his report we have examined the use of shear stress to condition synthesized material prior to applic
64 e renin angiotensin system and macrophage ER stress to contribute to the development of hypertension
65 that functions under conditions of metabolic stress to control systemic energy homeostasis and the ov
67 ncentrations of aldosterone increase oxidant stress to convert GC to an NO(.)-insensitive state, resu
68 RAD52 colocalizes with OGG1 after oxidative stress to cultured cells, but not after the direct induc
69 KD1-dependent mechanism that links oxidative stress to decreased CREB protein abundance is predicted
71 ced swim stress that adds to the interaction stress to determine the global contractility or extensib
72 strains with differential responsiveness to stress to determine whether CRH might also differentiall
73 ged the amygdala, a brain region involved in stress, to determine whether its resting metabolic activ
75 was activated by extracellular hyperosmotic stress to directly phosphorylate c-Jun in the serine 63
80 ver, the potential for oxidative/nitrosative stress to elicit an autoimmune response or to contribute
81 ibly manipulated between 0-8 GPa compressive stresses to enable systematic and reversible changes in
82 xert harmful effects, ranging from oxidative stress to endothelial dysfunction, nitric oxide disarray
83 is a strategy employed by plants exposed to stress to enhance resistance against future stress episo
84 utrients and growth factors and inhibited by stress to ensure that cells grow only during favorable c
85 ost-transcriptional regulation under uranium stress to enter a cellular dormant state, thereby provid
88 al epithelia require a higher level of shear stress to evoke a cytosolic calcium increase than do mou
89 the DA system may underlie the propensity of stress to exacerbate psychotic disorders or predispose a
90 revisiae cells treated with and without salt stress to explore population variation and identify cell
91 We used zebrafish with FLD and hepatic ER stress to explore the relationship between Atf6 and stea
92 the symmetry between tensile and compressive stresses to facilitate mesoscale network contraction of
94 fic regions of the VTA both during and after stress to fuel later escalated cocaine taking and seekin
96 t the gamble to induce systemic self-harming stress to harm pathogens may not pay off in the end.
99 le reviews recent studies connecting chronic stress to health outcomes in parents of children with in
100 had similar aortic dimensions and wall shear stress to healthy volunteers and younger patients with B
101 that silencing Nup88 in IMCD3 cells acutely stressed to hypertonic conditions reduces nuclear retent
102 n Ganges and Prayon plants in response to Cd stress to identify transporter genes that were more high
103 er the NLRP3 inflammasome connects metabolic stress to IL-1beta-mediated inflammation and provides a
105 ts define a pathway linking vascular oxidant stress to immune activation and aortic stiffening and pr
106 PFC is critically involved in females during stress to impair subsequent learning and does so via com
107 uture decades, we can expect deficit-related stress to increase and consequently Douglas fir growth t
108 s to acute stress, and blunts the ability of stress to increase anterior pituitary release of adrenoc
109 r 1 (HSF1) mediates the cellular response to stress to increase the production of heat shock protein
110 rated rats were subjected to water avoidance stress (to induce visceral hypersensitivity), then given
111 st-menopausal women underwent a passive heat stress to induce hot flushes at baseline and follow-up.
112 es suggest that FAAH is required for chronic stress to induce hyperactivity and structural remodeling
113 FC derived from tumour cells is required for stress to induce lymphatic remodelling and that this dep
114 ground, Rps27l disruption triggers ribosomal stress to induce p53 and apoptosis, whereas under Trp53(
115 iption factor that binds HSP promoters after stress to induce their transcription, interacts with the
116 which is activated upon heat shock and other stresses to induce the expression of molecular chaperone
117 ertilization interacted with competition and stress to influence biomass and changes in height, respe
118 nonsynonymous OXTR SNP interacted with early stress to influence relevant behavioral stress reactivit
120 rnight fast by blocking the ability of acute stress to inhibit food intake, and by attenuating stress
122 ctivation, to clarify the relationship of ER stress to intra-acinar trypsinogen activation in pancrea
124 degrees C following 60 min 42 degrees C heat stress to investigate specifically the early events in t
125 ngle neutron scattering coupled with osmotic stress to investigate the hydration of two proteins, lys
126 tant exhibiting constitutive plastid osmotic stress to investigate the molecular and genetic pathways
127 (Populus x canescens) were exposed to water stress to investigate xylem sap sulfate and ABA, stomata
128 etabolic derangement and excessive oxidative stress to ion channel/transporter dysfunction that predi
130 ex vivo perfusion of arterial laminar shear stress to isolated veins further confirmed the correlati
131 involvement in adaptive threat-biases under stress, to its chronic engagement in anxiety disorders i
132 ory activation of autophagy during prolonged stress to keep the levels of this process under a safe a
133 ytes increased their resistance to oxidative stress to levels that were comparable with stimulated yo
134 suggest a novel mechanism linking oxidative stress to ligand-independent cleavage of p75(NTR), resul
136 e heart under conditions of in vivo cellular stress to likely modulate vascular responses to neurohor
138 escence microscopy, we applied defined shear stress to low- or high-affinity LFA-1 and imaged the spa
139 ts performed better than the wild type under stress to maintain a favorable instantaneous water use e
143 ases degrading collagen are activated during stress to make proline available, and proline oxidase, t
144 eptibility of mutants sensitive to oxidative stress to MalE-LacZ lethality indicates that ROS contrib
148 endotoxin (LPS) model of evoked inflammatory stress to measure plasma IL-1 receptor antagonist (IL1RA
151 xR is a redox regulator that senses peroxide stress to mediate antibiotic resistance in P. aeruginosa
153 acid (ABA) is induced in response to abiotic stress to mediate plant acclimation to environmental cha
156 al stability of nanobeams under high tensile stress to minimize thermal buckling effects, therefore k
160 ession networks before and after exposure to stress to model the effect of stress on mutational robus
163 N is the critical link that allows oxidative stress to modulate nSMase2 phosphorylation and function.
165 inuously reorganize, adapting in response to stress to modulate the calcium signaling apparatus.
167 l the channel banks create just enough shear stress to move the median-sized gravel particles on the
168 importance of cell contractility and tissue stress to multicellular vertex formation and resolution,
169 the ratio of horizontal compressive tectonic stresses to near-surface gravitational stresses is relat
170 ess (>300 kPa) in the cap can intensify this stress to nearly 600 kPa when the cap thickness is <65 m
172 f control on behavior, led even controllable stress to now produce functional desensitization of DRN
174 s suggested defense reactions towards biotic stress to occur which did not lead to adequate responses
175 is definition to include the transmission of stress to offspring via early postnatal care, as animal
176 strategy based on tolerating the effects of stress to one of escaping the stress via reproduction.
177 in its toxicity profile from mainly membrane stress to one that exhibited not only sustained membrane
178 ing to multiple insults, including oxidative stress to orchestrate apoptotic and autophagic cell deat
181 riments use thermal, chemical, or mechanical stress to perturb the folding equilibrium for examining
182 Intriguingly, while application of oxidative stress to phase I and II iron-limited cells similarly ox
183 oles in the signaling steps that link biotic stresses to plant defense responses and growth changes.
185 uopathies, but the consequences of genotoxic stress to postmitotic neurons are poorly understood.
187 ly exacerbating and buffering the effects of stress, to predict anthropometry during childhood, and b
189 ulates vascular function by limiting oxidant stress to preserve bioavailable nitric oxide (NO(*)).
190 chondria must buffer the risk of proteotoxic stress to preserve bioenergetics, but the role of these
191 endothelial cells during elevated oxidative stress to preserve functional viability of the intima.
193 buffer external (environmental) or internal stresses to preserve the biological integrity of the org
194 al for targeting IL-33, ILC2s, and oxidative stress to prevent and/or treat asthma development relate
195 evolved to cope with endogenous or exogenous stress to prevent chromosomal instability and maintain c
196 kinase Rad53 is activated during replication stress to prevent fork collapse, an essential but poorly
198 egrity by clearance of individual HSCs after stress to prevent propagation of damaged stem cells.
199 uitinases associate more with Rsp5 upon heat-stress to prevent the assembly of K63-linked ubiquitin o
200 llular checkpoints that respond to damage or stress to prevent tumorigenesis, the transcriptional con
203 a/delta can repress this oncogene-induced ER stress to promote senescence in accordance with its role
207 , we propose that autophagy limits metabolic stress to protect the genome, and that defective autopha
209 nd respond dynamically to pH and temperature stresses to protect client proteins from aggregation.
210 2/RelB and IKK2-p65, is activated by various stresses to protect or damage the liver, in context-spec
211 re was no indication of diminished oxidative stress to proteins or lipids, and no evidence for anti-i
213 s then underwent a period of whole-body heat stress to raise oral temperature 0.8-1.0 degrees C above
214 present study, we determined if hyperosmotic stress to rat hippocampal slices activates p38 and JNK a
215 on the GR, monitoring the level of cellular stress to redirect glucocorticoid-regulated signaling th
217 at Dps acts as a checkpoint during oxidative stress to reduce initiations, providing an opportunity f
218 Here, we show that cells can sense nitrogen stress to reduce target of rapamycin complex-1 (TORC1) a
220 switch, which is activated during oxidative stress to regulate the balance between cell survival by
221 ient status, growth factor availability, and stress, to regulate cellular and organismal growth.
223 -cleaved SERPINB11 was unable to undergo the stressed-to-relaxed transition typical of inhibitory typ
224 regulated proteolysis of cTnI during cardiac stress to remove the unique cardiac N-terminal extension
225 undant molecular responses to neutralize the stress, to repair the damage and to eventually grow insi
227 obtained from our previous rest study by the stress-to-rest TIAC ratio obtained from the rest-stress
228 latory pathway in Manduca sexta enables heat stress to reveal a hidden reaction norm of larval colora
229 a means of reducing the effect of oxidative stress to RPE cells in age-related macular degeneration.
231 ted within blood vessels by high-fluid shear stresses to selectively target drugs to sites of vascula
232 ansiently increases in response to oxidative stress to sequester and oxidize Fe2+, which would otherw
234 ne inactivation of Rps27l triggers ribosomal stress to stabilize Mdm2, which degrades Mdm4 to reduce
236 advances have allowed the study of oxidative stress to tackle fundamental questions and have provided
237 s the first study (to our knowledge) to link stress to telomere length in a non-WEIRD population, our
238 for a mechanism linking cumulative childhood stress to telomere maintenance, observed already at a yo
239 ecological momentary assessment of patients' stress to test hypotheses about clonidine's behavioral m
240 We examined the effects of a modest heat stress to test the hypothesis that SSNA responses could
242 echanism to eliminate cells during metabolic stress to the advantage of a multicellular organism.
244 However, they can also mislocalize and cause stress to the bacterial cell, which is dealt with by the
248 meability can be modulated by applying shear stress to the droplet interfaces, inducing flow parallel
253 host inflammatory response confer oxidative stress to the gastric epithelium during H. pylori infect
254 triggers represents a qualitatively distinct stress to the host immune system, yet our understanding
255 des insight into a new paradigm linking cell stress to the immune response, and serves as a template
256 ities in IECs, thus linking cell-specific ER stress to the induction of organ-specific inflammation.
257 caspase-2-dependent mechanism that relays ER stress to the mitochondria to promote inflammation, inte
258 redox regulatory switch that links oxidative stress to the modulation of TDP-43 and its downstream ta
260 ted States recover from acid deposition, the stress to the most susceptible populations of native col
261 eration of contractility following oxidative stress to the myocardium, particularly through a decreas
263 e not only for contribution of mitochondrial stress to the pathology of ITP, but also clinical potent
264 Functional radiography provides the maximum stress to the pelvic floor, resulting in levator ani rel
266 that link pathogen recognition and cellular stress to the processing of the proinflammatory cytokine
267 sensing of microbial products and metabolic stress to the proteolytic activation of the proinflammat
268 owth, and a molecular mechanism linking this stress to the regulation of growth in developing organs,
272 madelta T cells are activated in response to stress to the surrounding tissue and perform a number of
273 cell-free virus did not reflect the level of stress to the VZV-infected cell that was seen after inoc
275 resulting in a delay in the transmission of stresses to the intracranial cavity and lower intracrani
277 long with caspase-8 activation and oxidative stress, to their synergistic cytotoxic effects in leukem
278 fficient, defined as the ratio of protrusive stress to tissue-substrate friction, that allows classif
279 ction was observed in the transmission of ER stress to TLR4 KO macrophages, consistent with the fact
280 1P1 responds to S1P as well as laminar shear stress to transduce flow-mediated signaling in endotheli
281 logies to use nanoparticle-induced oxidative stress to treat disease in a site-specific fashion.
282 atin-remodelling factor that is activated by stress to trigger aberrant gene expression and cardiac m
284 se motors generate sufficient thick-filament stress to trigger the transition to its long-periodicity
285 ability of cortisol, released in response to stress, to trigger a cascade of adaptive genomic and non
286 r the past 2 decades, the contribution of ER stress to various forms of liver diseases has been exami
288 ins in the endoplasmic reticulum (ER) causes stress to which an unfolded protein response is activate
289 adiation (IR) is a physiologically important stress to which cells respond by the activation of multi
293 riving force derives from the high degree of stress to which the DNA is subjected in the viral capsid
294 important source of environmental oxidative stress to which the skin is exposed, especially during s
297 acental angiogenesis depends on the type of 'stress' to which the pregnancy is subjected, and also di
298 l pathway, but rather one guided by uniaxial stress, to which the nanothreads consistently align.
299 of the airways modulate both the mechanical stresses to which the airways are exposed as well as the
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