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2 ssure approximately parallels the overburden stress to a depth of 17,640 ft (5,377 m) subsea and ther
3 ites not only promotes the interfacial shear stress to a high level and thus results in significantly
4 demonstrate that a 'soft' robot causes less stress to a jellyfish while handling compared to a tradi
5 ved in cross-linked networks by distributing stress to a small fraction of highly strained connected
7 o significantly blunted the ability of acute stress to activate c-Fos expression within the anterior
8 f mRNA translation occurs pervasively during stress to activate gene expression programs; however, th
9 rats, reduces or blocks the ability of acute stress to activate hindbrain neurons that are immunoreac
10 t couple detection of pathogens and cellular stress to activation of Caspase-1, and consequent IL-1be
13 nked quantitative and qualitative aspects of stress to adolescent and adult outcomes, a number of que
14 treatments with exogenous ABA or dehydration stress to advance our understanding of the features requ
17 l that cells detect and respond to oxidative stress to allow adaptation and repair damage, the underl
20 en appears to act in synergy with epithelial stress to allow intraepithelial cytotoxic T cells to kil
21 n factor that undergoes self-cleavage during stress to allow the expression of DNA repair functions a
22 of B-Raf reduces T cell resistance to shear stress to alpha4beta1 integrin ligands vascular cell adh
24 senses metabolic changes during nutritional stress to alter gene expression programs is less known.
26 respectively, are regulated during oxidative stress to alter O-GlcNAcylation are not fully characteri
29 highlights the contribution of environmental stress to anhedonia (loss of pleasure and/or motivation)
32 ent (KO) mice endowed with chronic oxidative stress to assess the influence of aging-associated redox
35 core with ceftriaxone the capacity of acute stress to augment the acquisition of cocaine self-admini
36 agy is turned off during prolonged oxidative stress, to avoid overeating and destruction of essential
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
44 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
48 en both milk samples were subjected to shear stress to break the curd system at constant shear rate,
52 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
61 f PTSD and suggests the potential of ongoing stress to compound initial stress reactions and lead to
62 cells actively exert physical forces (solid stress) to compress tumour blood vessels, thus reducing
63 his report we have examined the use of shear stress to condition synthesized material prior to applic
65 e renin angiotensin system and macrophage ER stress to contribute to the development of hypertension
66 that functions under conditions of metabolic stress to control systemic energy homeostasis and the ov
68 een insufficient study of mechanisms linking stress to CVD or of methods to attenuate stress' patholo
69 cultured endothelial cells exposed to shear stress to decrease CSE expression and treated with solve
70 static conditions or exposed to fluid shear stress to decrease CSE expression; and (3) cultured endo
71 biofilms can generate sufficient mechanical stress to deform and even disrupt soft epithelial cell m
73 ced swim stress that adds to the interaction stress to determine the global contractility or extensib
74 ged the amygdala, a brain region involved in stress, to determine whether its resting metabolic activ
77 was activated by extracellular hyperosmotic stress to directly phosphorylate c-Jun in the serine 63
78 dy utilized the sensitivity of semen to heat stress to discriminate the heat-tolerance ability of pig
80 thway from adverse childhood experiences and stress to disruption of the development of neural system
83 ver, the potential for oxidative/nitrosative stress to elicit an autoimmune response or to contribute
84 ibly manipulated between 0-8 GPa compressive stresses to enable systematic and reversible changes in
85 xert harmful effects, ranging from oxidative stress to endothelial dysfunction, nitric oxide disarray
86 f the plant defense system against oxidative stress to engineer tolerant plants in the climate change
89 is a strategy employed by plants exposed to stress to enhance resistance against future stress episo
90 utrients and growth factors and inhibited by stress to ensure that cells grow only during favorable c
91 ost-transcriptional regulation under uranium stress to enter a cellular dormant state, thereby provid
94 the DA system may underlie the propensity of stress to exacerbate psychotic disorders or predispose a
95 revisiae cells treated with and without salt stress to explore population variation and identify cell
96 We used zebrafish with FLD and hepatic ER stress to explore the relationship between Atf6 and stea
97 the symmetry between tensile and compressive stresses to facilitate mesoscale network contraction of
99 fic regions of the VTA both during and after stress to fuel later escalated cocaine taking and seekin
101 t the gamble to induce systemic self-harming stress to harm pathogens may not pay off in the end.
104 le reviews recent studies connecting chronic stress to health outcomes in parents of children with in
105 had similar aortic dimensions and wall shear stress to healthy volunteers and younger patients with B
106 d, culture, and apply calibrated fluid shear stress to hEMVs (takes 1-7 d); and how to assess vascula
107 response to paraquat (PQ)-induced oxidative stress to identify pre-symptomatic signatures of impendi
109 n Ganges and Prayon plants in response to Cd stress to identify transporter genes that were more high
110 er the NLRP3 inflammasome connects metabolic stress to IL-1beta-mediated inflammation and provides a
112 ts define a pathway linking vascular oxidant stress to immune activation and aortic stiffening and pr
113 uture decades, we can expect deficit-related stress to increase and consequently Douglas fir growth t
114 s to acute stress, and blunts the ability of stress to increase anterior pituitary release of adrenoc
115 Importantly, nitrogen interacted with heat stress to increase bleaching severity up to twofold when
116 r 1 (HSF1) mediates the cellular response to stress to increase the production of heat shock protein
117 rated rats were subjected to water avoidance stress (to induce visceral hypersensitivity), then given
118 st-menopausal women underwent a passive heat stress to induce hot flushes at baseline and follow-up.
119 es suggest that FAAH is required for chronic stress to induce hyperactivity and structural remodeling
120 FC derived from tumour cells is required for stress to induce lymphatic remodelling and that this dep
121 lin C leaves the nucleus following cytotoxic stress to induce mitochondrial fragmentation and apoptos
122 ground, Rps27l disruption triggers ribosomal stress to induce p53 and apoptosis, whereas under Trp53(
124 which is activated upon heat shock and other stresses to induce the expression of molecular chaperone
125 ertilization interacted with competition and stress to influence biomass and changes in height, respe
126 nonsynonymous OXTR SNP interacted with early stress to influence relevant behavioral stress reactivit
128 rnight fast by blocking the ability of acute stress to inhibit food intake, and by attenuating stress
129 ctivation, to clarify the relationship of ER stress to intra-acinar trypsinogen activation in pancrea
130 degrees C following 60 min 42 degrees C heat stress to investigate specifically the early events in t
131 tant exhibiting constitutive plastid osmotic stress to investigate the molecular and genetic pathways
132 (Populus x canescens) were exposed to water stress to investigate xylem sap sulfate and ABA, stomata
133 etabolic derangement and excessive oxidative stress to ion channel/transporter dysfunction that predi
135 ex vivo perfusion of arterial laminar shear stress to isolated veins further confirmed the correlati
136 involvement in adaptive threat-biases under stress, to its chronic engagement in anxiety disorders i
137 ory activation of autophagy during prolonged stress to keep the levels of this process under a safe a
139 suggest a novel mechanism linking oxidative stress to ligand-independent cleavage of p75(NTR), resul
141 e heart under conditions of in vivo cellular stress to likely modulate vascular responses to neurohor
144 escence microscopy, we applied defined shear stress to low- or high-affinity LFA-1 and imaged the spa
145 ts performed better than the wild type under stress to maintain a favorable instantaneous water use e
146 be protected from genotoxic and proteotoxic stress to maintain a healthy pool throughout life(1-3).
150 ases degrading collagen are activated during stress to make proline available, and proline oxidase, t
151 eptibility of mutants sensitive to oxidative stress to MalE-LacZ lethality indicates that ROS contrib
154 clinical evidence linking specific types of stress to maternal inflammatory load during pregnancy.
157 endotoxin (LPS) model of evoked inflammatory stress to measure plasma IL-1 receptor antagonist (IL1RA
160 acid (ABA) is induced in response to abiotic stress to mediate plant acclimation to environmental cha
163 al stability of nanobeams under high tensile stress to minimize thermal buckling effects, therefore k
165 re exists a window of opportunity even after stress to mitigate its impact with a second surge of exo
168 ession networks before and after exposure to stress to model the effect of stress on mutational robus
171 N is the critical link that allows oxidative stress to modulate nSMase2 phosphorylation and function.
172 esponse transducer IRE1alpha under genotoxic stress to modulate repair programs and sustain cell surv
174 inuously reorganize, adapting in response to stress to modulate the calcium signaling apparatus.
176 l the channel banks create just enough shear stress to move the median-sized gravel particles on the
177 importance of cell contractility and tissue stress to multicellular vertex formation and resolution,
178 the ratio of horizontal compressive tectonic stresses to near-surface gravitational stresses is relat
183 ther oncogenes, BRAF(V600E) causes oncogenic stress to normal cells, leading to growth arrest (senesc
184 f control on behavior, led even controllable stress to now produce functional desensitization of DRN
186 s suggested defense reactions towards biotic stress to occur which did not lead to adequate responses
187 is definition to include the transmission of stress to offspring via early postnatal care, as animal
188 strategy based on tolerating the effects of stress to one of escaping the stress via reproduction.
189 in its toxicity profile from mainly membrane stress to one that exhibited not only sustained membrane
190 ing to multiple insults, including oxidative stress to orchestrate apoptotic and autophagic cell deat
192 riments use thermal, chemical, or mechanical stress to perturb the folding equilibrium for examining
193 Intriguingly, while application of oxidative stress to phase I and II iron-limited cells similarly ox
194 oles in the signaling steps that link biotic stresses to plant defense responses and growth changes.
196 uopathies, but the consequences of genotoxic stress to postmitotic neurons are poorly understood.
198 ly exacerbating and buffering the effects of stress, to predict anthropometry during childhood, and b
200 chondria must buffer the risk of proteotoxic stress to preserve bioenergetics, but the role of these
201 endothelial cells during elevated oxidative stress to preserve functional viability of the intima.
203 al for targeting IL-33, ILC2s, and oxidative stress to prevent and/or treat asthma development relate
204 kinase Rad53 is activated during replication stress to prevent fork collapse, an essential but poorly
206 Multiple pathways counteract DNA replication stress to prevent genomic instability and tumorigenesis.
207 egrity by clearance of individual HSCs after stress to prevent propagation of damaged stem cells.
208 uitinases associate more with Rsp5 upon heat-stress to prevent the assembly of K63-linked ubiquitin o
210 deacetylase (HDAC) inhibition, caused adult stress to produce changes similar to those induced by ad
213 Our study demonstrated that HFD induces ER stress to promote chondrocyte death and subchondral bone
214 ast-Thbs4, emerged after induction of tissue stress to promote fibrosis in the absence of smooth musc
216 a/delta can repress this oncogene-induced ER stress to promote senescence in accordance with its role
217 tifs are sufficient to bear normal and shear stress to promote significant and tunable adhesive prope
220 pression is up-regulated in response to cell stress to protect against pathological cell death in mul
222 ance vessels develop resilience to oxidative stress to protect functional integrity and tested this h
223 nd respond dynamically to pH and temperature stresses to protect client proteins from aggregation.
224 2/RelB and IKK2-p65, is activated by various stresses to protect or damage the liver, in context-spec
225 re was no indication of diminished oxidative stress to proteins or lipids, and no evidence for anti-i
226 on the GR, monitoring the level of cellular stress to redirect glucocorticoid-regulated signaling th
227 Here, we show that cells can sense nitrogen stress to reduce target of rapamycin complex-1 (TORC1) a
229 ow NOD1 and NOD2 sense microbes and cellular stress to regulate host responses that can affect diseas
230 switch, which is activated during oxidative stress to regulate the balance between cell survival by
232 ient status, growth factor availability, and stress, to regulate cellular and organismal growth.
233 red on the intricacies of how cells use such stresses to regulate their internal mechanical integrity
234 regulated proteolysis of cTnI during cardiac stress to remove the unique cardiac N-terminal extension
235 undant molecular responses to neutralize the stress, to repair the damage and to eventually grow insi
237 x transrepressor directly transduces osmotic stress to repress stomatal development to improve plant
239 obtained from our previous rest study by the stress-to-rest TIAC ratio obtained from the rest-stress
240 a means of reducing the effect of oxidative stress to RPE cells in age-related macular degeneration.
241 olded protein response/endoplasmic reticulum stress to secretory optimization, coordinated with cell
242 ted within blood vessels by high-fluid shear stresses to selectively target drugs to sites of vascula
243 hile hydrogen peroxide distributes oxidative stress to sensitize the network to mitochondrial critica
244 suggesting the role of endocannabinoids and stress to sexual differentiation of the brain and cerebe
245 gated to a conjugated state under mechanical stress to significantly change their properties, we deve
246 ne inactivation of Rps27l triggers ribosomal stress to stabilize Mdm2, which degrades Mdm4 to reduce
248 CREB dysfunction, and promote survival under stress to support the hypothesis that lower molecular we
249 advances have allowed the study of oxidative stress to tackle fundamental questions and have provided
250 s the first study (to our knowledge) to link stress to telomere length in a non-WEIRD population, our
251 for a mechanism linking cumulative childhood stress to telomere maintenance, observed already at a yo
252 ecological momentary assessment of patients' stress to test hypotheses about clonidine's behavioral m
253 We examined the effects of a modest heat stress to test the hypothesis that SSNA responses could
255 echanism to eliminate cells during metabolic stress to the advantage of a multicellular organism.
258 meability can be modulated by applying shear stress to the droplet interfaces, inducing flow parallel
260 n inhibitor of tumor progression by altering stress to the endoplasmic reticulum, down-regulating per
261 des insight into a new paradigm linking cell stress to the immune response, and serves as a template
262 n appear to link energy balance and cellular stress to the intracellular signal transduction pathways
263 caspase-2-dependent mechanism that relays ER stress to the mitochondria to promote inflammation, inte
264 redox regulatory switch that links oxidative stress to the modulation of TDP-43 and its downstream ta
266 ted States recover from acid deposition, the stress to the most susceptible populations of native col
270 e not only for contribution of mitochondrial stress to the pathology of ITP, but also clinical potent
271 Functional radiography provides the maximum stress to the pelvic floor, resulting in levator ani rel
272 that link pathogen recognition and cellular stress to the processing of the proinflammatory cytokine
273 owth, and a molecular mechanism linking this stress to the regulation of growth in developing organs,
276 cell-free virus did not reflect the level of stress to the VZV-infected cell that was seen after inoc
278 ellular status information, such as cellular stress, to the integrity of microtubules in order to ins
279 evant conditions, ranging from environmental stresses to the biotechnological production of small mol
282 fficient, defined as the ratio of protrusive stress to tissue-substrate friction, that allows classif
283 ction was observed in the transmission of ER stress to TLR4 KO macrophages, consistent with the fact
284 1P1 responds to S1P as well as laminar shear stress to transduce flow-mediated signaling in endotheli
286 logies to use nanoparticle-induced oxidative stress to treat disease in a site-specific fashion.
287 atin-remodelling factor that is activated by stress to trigger aberrant gene expression and cardiac m
290 se motors generate sufficient thick-filament stress to trigger the transition to its long-periodicity
291 consecutive MDE it may take lower levels of stress to trigger these neurotoxic pathways, leading to
292 ability of cortisol, released in response to stress, to trigger a cascade of adaptive genomic and non
293 therapeutic potential of blocking Chop or ER stress to unleash T cell-mediated antitumor immunity.
294 r the past 2 decades, the contribution of ER stress to various forms of liver diseases has been exami
295 ins in the endoplasmic reticulum (ER) causes stress to which an unfolded protein response is activate
299 l pathway, but rather one guided by uniaxial stress, to which the nanothreads consistently align.