戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (1語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 1,316 (46%) were hypoxic, and 450 (16%) were hyperoxic.
2 c, 553 (46%) were hypoxic and 256 (21%) were hyperoxic.
3 ly when rabbits breathed air made hypoxic or hyperoxic.
4                                              Hyperoxic (100% O(2)) and hypercapnic (5% CO(2), 21% O(2
5 ured in diabetic rats housed for 48 hr under hyperoxic (100% O(2)), hypoxic (11% O(2)), or normoxic (
6 0% helium), limitedly and fully aerobic, and hyperoxic (100% oxygen) conditions.
7                                       In the hyperoxic 140-day fetal baboon BPD model, p66(Shc) expre
8 ted under either physiologic (5%) or chronic hyperoxic (40%) oxygen conditions.
9 immediately placed in normoxic (room air) or hyperoxic (70% oxygen) conditions for 3 days.
10 were then grown in a normoxic (20% O(2)), or hyperoxic (80% O(2)), atmosphere.
11 e considered that Ang2 might be important in hyperoxic acute lung injury (ALI).
12                                              Hyperoxic acute lung injury (HALI) is characterized by a
13 on, and apoptosis, which are the features of hyperoxic acute lung injury (HALI).
14   Prolonged exposure to hyperoxia results in hyperoxic acute lung injury (HALI).
15                                A hallmark of hyperoxic acute lung injury is the influx of inflammator
16 the role of genetic imprinting in regulating hyperoxic acute lung injury survival time using a mouse
17 B cell hyperplasia and confers protection in hyperoxic acute lung injury.
18 nstrate that IL-13 has protective effects in hyperoxic acute lung injury.
19 rgic P2X7 receptor to cause inflammation and hyperoxic acute lung injury.
20 inflammation and the inhibition of injury in hyperoxic acute lung injury.
21 measured when breathing normoxic followed by hyperoxic air (1.0 FIO2 ) to acutely attenuate periphera
22 pithelial necrosis with an important role in hyperoxic ALI and pulmonary edema.
23 n vitro and neonatal rat ECFCs isolated from hyperoxic alveolar growth-arrested rat lungs mimicking b
24 er transplantation was the same in livers of hyperoxic and control rats.
25 tilatory responses to hypercapnia under both hyperoxic and hypoxic conditions were assessed both with
26 uring superoxide bursts in macrophage cells, hyperoxic and hypoxic conditions, and in responses to H(
27       By subjecting the mouse to alternating hyperoxic and hypoxic conditions, strong and weak functi
28 natively spliced products are produced under hyperoxic and hypoxic conditions.
29 alcium and mitochondrial calcium in both the hyperoxic and hypoxic group.
30 f CCN1 becomes abnormally reduced during the hyperoxic and ischemic phases of ROP modeled in the mous
31 ic neonate group (156+/-14.2) compared to WT hyperoxic animals (255+/-35.1).
32                           Moreover, EVs from hyperoxic animals induced not only the pathological hall
33    Chemoafferent degeneration in chronically hyperoxic animals was accompanied by marked hypoplasia o
34 nd the total number of nuclei was greater in hyperoxic animals.
35 xic animals, there was minimal disruption in hyperoxic animals.
36 s with detachments, but was decreased in the hyperoxic animals.
37 s telomerase and are relatively resistant to hyperoxic apoptosis.
38 ts of these studies find that hyperbaric and hyperoxic approaches resulted in increased cardiac fibro
39 onary sensory inputs and perfusing them with hyperoxic artificial cerebral spinal fluid to minimize p
40  higher in untreated cells after growth in a hyperoxic atmosphere than in untreated cells grown in a
41                  After 6 days of growth in a hyperoxic atmosphere, the thyroxine-treated cells were 2
42 e hypothesis that BLP mediates BPD using the hyperoxic baboon model.
43 ical evidence of chronic lung disease in the hyperoxic baboon model.
44 gates pulmonary inflammation and fibrosis in hyperoxic baboons, we hypothesized that ionizing radiati
45       Cell culture is often considered to be hyperoxic, but pericellular oxygen levels, which are aff
46 cking the protein had the same response to a hyperoxic challenge as did their wild-type siblings.
47                                     Relative hyperoxic challenge during reoxygenation causes myocardi
48                                     In vivo, hyperoxic challenge induced p21-dependent differentiatio
49                           Exposure of CFs to hyperoxic challenge-induced transcription of smooth musc
50 expression was significantly reduced in both hyperoxic compared to normoxic groups (P<0.05).
51  mice, prolonged survival was observed under hyperoxic condition.
52 wn for 2 weeks in physiological (5% O(2)) or hyperoxic conditions (40% O(2)) in the presence or absen
53    C57BL/6J mice were transiently exposed to hyperoxic conditions (75% O2) between postnatal day 7 (P
54                 Gigantism has been linked to hyperoxic conditions because oxygen concentration is a k
55      In this study, we show that exposure to hyperoxic conditions during the evolution of pneumonia r
56                          The reduction under hyperoxic conditions from 0.75 +/- 0.34 to 0.49 +/- 0.09
57 as analyser measurements during normoxic and hyperoxic conditions in pregnant sheep.
58   The lack of change in the ASL signal under hyperoxic conditions is consistent with the hypothesis t
59                     Expression is optimal in hyperoxic conditions or in air and is reduced under hypo
60 sults demonstrate that culturing cells under hyperoxic conditions reduces their ability to efficientl
61                                              Hyperoxic conditions were established by ventilating the
62 RX1(-/-) mice showed reduced mortality under hyperoxic conditions, and apoptotic cell death and caspa
63                                        Under hyperoxic conditions, overexpressors had increased longe
64 e panel of 21 brain organoids to hypoxic and hyperoxic conditions, we identify hundreds of gene regul
65 abolic lesions, exacerbated by storage under hyperoxic conditions, were ameliorated by hypoxic storag
66 ression of YHB1 is optimal under normoxic or hyperoxic conditions, yet respiring yeast cells have low
67 dy labeling in the detachments maintained in hyperoxic conditions.
68 ty to isoprenaline seen under these slightly hyperoxic conditions.
69 ately 0.11), separated by 30 min of control, hyperoxic conditions.
70 on of pulmonary blood flow under hypoxic and hyperoxic conditions.
71 ed to evaluate HRMVECs following hypoxic and hyperoxic conditions.
72 ROS, SA-beta-gal, and AF normally induced by hyperoxic conditions.
73  cultured cells and intact animals die under hyperoxic conditions.
74 ubated, and exposed to normoxic, hypoxic, or hyperoxic conditions.
75 has a shorter lifespan under both normal and hyperoxic conditions; (iii) develops an atypical (tip-to
76 t CO protects cultured epithelial cells from hyperoxic damage.
77 rference (RNAi) knockdown of Bcl-XL enhanced hyperoxic death of cells expressing p21, whereas overexp
78  two components would be expected, and under hyperoxic (end-tidal PO2 = 200 Torr) conditions, when th
79  aurantiacus since this bacterium lives in a hyperoxic environment and is subject to high UV radiatio
80  Prolonged exposure of porcine TM cells to a hyperoxic environment led to an increase in ROS producti
81                                      Using a hyperoxic environment, the concentration was 50% using 3
82                                      Using a hyperoxic environment, the concentration was 50% using 3
83  be a behavioural strategy for responding to hyperoxic environments.
84 , using the modified Oxford technique during hyperoxic eucapnia, hyperoxic hyperpnoea and hyperoxic h
85 nt increase of MVD in the TG group following hyperoxic exposure (85+/-12) in comparison to the WT hyp
86                                        After hyperoxic exposure (O2 > 95%), neonatal (<12 hours old)
87 sion is increased from P7 to P17, altered by hyperoxic exposure and relative hypoxic recovery and mod
88 ivity or chelation of cellular iron prior to hyperoxic exposure decreased reactive iron levels in the
89                             In HPAECs, a 3-h hyperoxic exposure enhanced the tyrosine phosphorylation
90 idant enzymes in preventing lung injury from hyperoxic exposure has been implicated in a number of ea
91                                              Hyperoxic exposure increases the activation of CD103(+),
92 preventing oxidant-mediated lung injury from hyperoxic exposure is negligible, and other cellular ant
93 petrosal ganglion neurones were sensitive to hyperoxic exposure only during the early postnatal perio
94 h GM-CSF (9 micro g/kg/day) during 4 days of hyperoxic exposure resulted in decreased apoptosis in th
95 rth, indicating that even a relatively short hyperoxic exposure was sufficient to derange normal chem
96                         We hypothesized that hyperoxic exposure, a predisposing factor to bronchopulm
97                 Two to four months after the hyperoxic exposure, treated rats were compared with untr
98 ell viability in lung primary cultures after hyperoxic exposure.
99 increased markers of oxidative injury before hyperoxic exposure.
100 number of myelinated axons was unaffected by hyperoxic exposure.
101 is massively up-regulated in the lungs after hyperoxic exposure.
102 gocytic activity for yeast; however, similar hyperoxic exposures in iron-supplemented media significa
103 abilization and at O(2) levels that would be hyperoxic for most tissues.
104 eatment-limiting consequence of therapy with hyperoxic gas mixtures.
105 k rate, but with EIAH prevented by inspiring hyperoxic gas or work of breathing reduced via a proport
106         Extreme aviators continually inspire hyperoxic gas to mitigate risk of hypoxia and decompress
107 c exposure (85+/-12) in comparison to the WT hyperoxic group (62+/-8.4), (P<0.05).
108     EPC's showed significant reduction in WT hyperoxic group compared to others (P>0.05).
109                                    Among the hyperoxic groups, both RNA and protein of VEGF expressio
110 ly, we proposed tyrosine as a marker for the hyperoxic growth phase.
111  to the carboniferous era, in regulating the hyperoxic growth phase.
112 ents were performed under normoxic (21%) and hyperoxic (&gt;95%) conditions.
113 hrenic nerve discharge (PND) at rest, during hyperoxic hypercapnia (10% CO(2)), and during peripheral
114 n with cyanide, but only mildly activated by hyperoxic hypercapnia (central chemoreceptor stimulation
115                     We studied the effect of hyperoxic hypercapnia (CO2) on the variational activity
116 hyperoxic eucapnia, hyperoxic hyperpnoea and hyperoxic hypercapnia (end-tidal P(CO(2)) + 5 mmHg above
117 O(2) : ~48 mmHg, P(ET) CO(2) : ~34 mmHg) and hyperoxic hypercapnia (P(ET) O(2) : ~524 mmHg, P(ET) CO(
118 tivation of central chemoreceptors with mild hyperoxic hypercapnia also causes resetting of the arter
119  experiments in fourteen rats, we found that hyperoxic hypercapnia and poikilocapnic hypoxia also res
120 f experiments, the animals were subjected to hyperoxic hypercapnia and poikilocapnic hypoxia.
121                                  Progressive hyperoxic hypercapnia and progressive isocapnic hypoxia
122 tivation of central chemoreceptors with mild hyperoxic hypercapnia does not affect arterial pressure,
123                     In the FD group, whereas hyperoxic hypercapnia induced normal cardiovascular and
124  threshold and sensitivity of RTN neurons to hyperoxic hypercapnia nor their activation by peripheral
125 tilatory and occlusion pressure responses to hyperoxic hypercapnia with and without added resistive l
126 g progressive isocapnic hypoxia, progressive hyperoxic hypercapnia, and during recovery from moderate
127                Heart rate is elevated during hyperoxic hypercapnia, but this response is not differen
128 ties to acute isocapnic hypoxia (G(pO2)) and hyperoxic hypercapnia, the latter divided into periphera
129 mined the closed- and open-loop responses to hyperoxic hypercapnia.
130  ventilatory responses to isocapnic-hypoxia, hyperoxic-hypercapnia, and exercise; breath-hold toleran
131  did not have any worsening in symptoms, her hyperoxic hypercapnic rebreathing ventilatory response w
132 ation was sustained during exercise, despite hyperoxic-hypercapnic ventilatory responsiveness being n
133                                        Under hyperoxic/hyperoxic incubation (control), hepatocytes we
134  Oxford technique during hyperoxic eucapnia, hyperoxic hyperpnoea and hyperoxic hypercapnia (end-tida
135 evere end-apnoea hypoxaemic hypercapnia, and hyperoxic hyperventilation designed to ablate hypoxaemia
136 ilation) and hyperoxaemic hypercapnia (prior hyperoxic hyperventilation) impact free radical-mediated
137                          Under conditions of hyperoxic, hypocapnic apnoea, the mean threshold for ind
138 ormoxic, normocapnic perfusate), to inhibit (hyperoxic, hypocapnic perfusate) or to stimulate (hypoxi
139 antly decreased after 2 continuous cycles of hyperoxic-hypoxic-hyperoxic treatments compared with wil
140        Mean respiratory variables (baseline, hyperoxic/hypoxic responses) were not severely influence
141                              Replicating the hyperoxic in vivo pO(2) of 53 mm Hg in the ex vivo retin
142                                Under hypoxic/hyperoxic incubation (reoxygenation), however, loss of t
143 extracellular lung compartment contribute to hyperoxic-induced lung damage and that overexpression of
144      To study the biologic role of EC-SOD in hyperoxic-induced pulmonary disease, we created transgen
145  room air value, or deltaPO(2), in mm Hg) to hyperoxic inhalation challenge.
146 , DA restored lung ability to clear edema in hyperoxic-injured rat lungs.
147 ial cells (HLMVEC) are a principal target of hyperoxic injury (hyperoxia).
148 n, and proliferation during remodeling after hyperoxic injury also require FGF signaling.
149                        IRAK-M may potentiate hyperoxic injury by suppression of key antioxidant pathw
150  data suggest that: (1) iron uptake promotes hyperoxic injury to AM; and (2) hyperoxia impairs the ca
151 erve to protect the neonatal lung from acute hyperoxic injury via inhibition of apoptosis.
152  the importance of the endothelium in lethal hyperoxic injury, 2) HO-1 and CO require endothelial STA
153                              The elements of hyperoxic injury, which result in high rates of lethalit
154 lveolarization during recovery from neonatal hyperoxic injury.
155 ects the neonatal pulmonary vasculature from hyperoxic injury.
156 e lung structure and function after neonatal hyperoxic injury.Methods: Newborn mice were exposed to 7
157 ge and promotes proper vascular repair after hyperoxic insult in the OIR model.
158 in the neonatal dog, revascularization after hyperoxic insult involves a period of marked vasoprolife
159 ditions and to the pulmonary defense against hyperoxic insult is very limited.
160  However, glutathione supplementation during hyperoxic insult restored the ability of Nrf2(-/-) cells
161 als at different time points during or after hyperoxic insult were analyzed.
162 sed mortality following a normally sublethal hyperoxic insult, accompanied by alveolar epithelial cel
163 ls and intravitreal neovascularization after hyperoxic insult.
164 t mortality following an otherwise nonlethal hyperoxic insult.
165 ibited using dopamine (5 to 10 microg/kg) or hyperoxic lactated Ringer's solution.
166 date the specific roles of HO-1 and STAT3 in hyperoxic lung and endothelial cell injury.
167 e P326TAT ameliorates barrier dysfunction of hyperoxic lung endothelial monolayer and attenuates eNOS
168  P450 (CYP)1A enzymes are protective against hyperoxic lung injury (HLI).
169 e-8/Bid pathway in signaling associated with hyperoxic lung injury and cell death in vivo and in vitr
170 mesenchymal stem cells (MSC) protect against hyperoxic lung injury at least in part by increasing the
171 l therapeutic window for mitigating neonatal hyperoxic lung injury by inhibiting senescence.
172 f GM-CSF in the lung would protect mice from hyperoxic lung injury by limiting alveolar epithelial ce
173 -6, which results in increased resistance to hyperoxic lung injury in Foxp1/HDAC2 compound mutant ani
174  remarkable effectiveness of MR1 in blunting hyperoxic lung injury in this preclinical model may be r
175 essing hEC-SOD in the airways attenuated the hyperoxic lung injury response, showed decreased morphol
176 s in the transcriptome and proteome of acute hyperoxic lung injury using the omics platforms: microar
177 ely, these results indicate that AM resolves hyperoxic lung injury via NOS3.
178                   Employing a mouse model of hyperoxic lung injury, a monoclonal anti-CD40 ligand (L)
179 sis may not significantly influence neonatal hyperoxic lung injury.
180 nes causes increased fluid resorption during hyperoxic lung injury.
181 zymes by hyperoxia may have implications for hyperoxic lung injury.
182 hrome P4501A enzymes have been implicated in hyperoxic lung injury.
183 s demonstrate that IL-11 markedly diminishes hyperoxic lung injury.
184 ight gain compared with wild-type pups after hyperoxic lung injury.
185 ath, resulting in enhanced susceptibility to hyperoxic lung injury.
186        In certain conditions, such as in the hyperoxic lung, this process may be deleterious.
187 sion in all segments of room air control and hyperoxic lungs infected with either dose of adbeta-gal.
188                  Net transgene expression in hyperoxic lungs was not different from room air controls
189 ion of Apo E and transferrin was observed in hyperoxic lungs.
190 inhaled O2, arterial pO2 134 +/- 9 mmHg), or hyperoxic mice (100% inhaled O2 starting 15 min after dM
191 sections demonstrated increased apoptosis in hyperoxic mice, predominantly in macrophages and alveola
192 l apoptosis, and pulmonary edema in lungs of hyperoxic mice.
193                                              Hyperoxic microenvironment created by an in vivo PMC imp
194 ffer potential for tumour biology studies in hyperoxic microenvironments and inspire the exploration
195                     Herein, a neonatal mouse hyperoxic model of coincident BPD and retinopathy was us
196                                      Using a hyperoxic model of premature brain injury, we have previ
197 ronic oxidative stress was applied using the hyperoxic model; acute oxidative stress was applied with
198 zation was associated with the change in the hyperoxic nadir in ventilation (as an index of carotid c
199                                          The hyperoxic nadir in ventilation was greater than sea leve
200 ere was a significant reduction of ROS in TG hyperoxic neonate group (156+/-14.2) compared to WT hype
201 Cs grown under physiologic ([O(2)](2.5)) and hyperoxic ([O(2)](A)) conditions.
202 ge significantly in response to apnea during hyperoxic or hypercapnic baseline conditions with both a
203 lated rat hepatocytes were incubated under a hyperoxic or hypoxic atmosphere for 60 min.
204 A4 cells also exhibited marked resistance to hyperoxic oxidant insult.
205 d-rank test was used to compare baseline and hyperoxic parameters.
206 e periods of hypoxia were followed by 8 h of hyperoxic perfusion.
207                                       At the hyperoxic phase, caffeine reduced oxygen-induced neural
208 ypoxic phase and negatively with that of the hyperoxic phase.
209 comprising a primary hypoxic and a secondary hyperoxic phase.
210 These data indicate that ET-1 contributes to hyperoxic pial artery vasoconstriction.
211  subnormal retinal oxygenation response to a hyperoxic provocation (DeltaPo2) is strongly associated
212  gene transfer techniques protects mice from hyperoxic pulmonary damage and delays death of mice.
213 athways may contribute to the development of hyperoxic pulmonary edema, lung injury, and respiratory
214 eceiving the same graft size, so the area in hyperoxic rats receiving 700 islets was not significantl
215                                     Lungs of hyperoxic rats showed increase in the expression of CYP1
216 islet area and number of islets engrafted in hyperoxic rats was significantly increased when compared
217 s, preserved alveolar and vascular growth in hyperoxic rats, and attenuated pulmonary hypertension.
218 of DA on active Na+ transport in control and hyperoxic rats, whereas the isomer beta-lumicolchicine,
219 via multi-wavelength irradiation in behaving hyperoxic rats.
220 ever, hypocalcemia acts synergistically with hyperoxic reoxygenation to produce more severe damage.
221                    During the ensuing 60-min hyperoxic reoxygenation, medium [Ca2+]ex was varied from
222                                          The hyperoxic response in rats (n = 9) injected with 10(-4)
223  a surrogate of blood flow, from physiologic hyperoxic responses (20% increase) to pathological hypox
224 tly decreased in blood vessels isolated from hyperoxic retinas compared with those from normoxic cont
225  used two sequential 3.5-minute normoxic and hyperoxic steady-state free-breathing UTE acquisitions.
226 tality in P. murina-infected mice exposed to hyperoxic stress by inhibition of inflammation and apopt
227 so exhibited increased survivability against hyperoxic stress when compared with rats receiving AdV-b
228 ility, locomotor activity, and resistance to hyperoxic stress, compared with wild-type controls.
229 ional culture conditions is a consequence of hyperoxic stress.
230  and heme oxygenase were induced by the same hyperoxic stress.
231 demonstrate the resilience of HCEnCs against hyperoxic stress.
232 tional role of secreted Cyr61 in response to hyperoxic stress.
233 iapoptotic effects of carbon monoxide during hyperoxic stress.
234                                              Hyperoxic subacute lung injury was induced by 95 % oxyge
235             Apnea was a frequent response to hyperoxic testing at earlier postmenstrual ages, suggest
236 ion and 28 weeks, 6 days gestation underwent hyperoxic testing at one to four time points between 32
237 easurements and Main Results: A total of 280 hyperoxic tests were analyzed (2.2 +/- 0.3 tests per inf
238 in Type I Diabetic (Akita) mice subjected to hyperoxic treatment.
239 ter 2 continuous cycles of hyperoxic-hypoxic-hyperoxic treatments compared with wild-type (WT) BM cel
240  in the mice tumor subjected to normoxic and hyperoxic treatments.
241 cantly reduced in sVlow subregions that were hyperoxic under 80% O2 conditions.
242 ogical responses of hypoxic vasodilation and hyperoxic vasconstriction in the human respiratory cycle
243  (CNS O2 toxicity) is preceded by release of hyperoxic vasoconstriction, which increases regional cer
244 HBO2 exposure is responsible for escape from hyperoxic vasoconstriction.
245              During 50% VO2max exercise, the hyperoxic ventilation nadir was also greater than sea le
246 dies are conducted in atmospheric O2 levels, hyperoxic with respect to the physiologic milieu.

 
Page Top