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1 viously reported that continuously breathing normobaric 11% O2 from an early age prevents neurologica
2              Finally, we show that breathing normobaric 11% O2 in mice with late-stage encephalopathy
3 rvative hypoxia regimens, such as continuous normobaric 17% O2 or intermittent hypoxia, are ineffecti
4 re removed from anesthetized rats kept under normobaric (640 Torr) and hypobaric conditions (380 Torr
5 OT treatment group (N=19) and a sham-treated normobaric air group (N=23).
6 ek 1.5 ATA/90-min HBOTs and the sham-treated normobaric air group the identical schedule of air treat
7           Conventional therapy is limited to normobaric and hyperbaric oxygen, with no available anti
8 eriodic breathing during acute and sustained normobaric and hypobaric hypoxia.
9  Four-month old C56BL/6J mice were kept in a normobaric chamber at 50% O(2) for up to 3 weeks.
10 e to 10% O(2) for 4 h daily for 56 days in a normobaric chamber, developed pulmonary hypertension, ri
11 a for 3 weeks and then allowed to recover at normobaric conditions for 3 additional weeks.
12                                        Under normobaric conditions, 30 muM 24(S)-HC was required to p
13   Notably, raising the inspired oxygen (80%, normobaric) during the hypoxic period significantly redu
14 fference in change between the hypobaric and normobaric exposure was 0 ng/mL for thrombin-antithrombi
15 served in some hemostatic markers during the normobaric exposure, attributed to prolonged sitting and
16 between the changes in the hypobaric and the normobaric exposures.
17          Both Tg and Wt mice were exposed to normobaric hyperoxia (>99% oxygen) for 48, 72, and 84 ho
18                                              Normobaric hyperoxia (NBO) has been shown to be neuropro
19                               Post-ischaemic normobaric hyperoxia caused an immediate and progressive
20 intravenous thrombolytics, to receive either normobaric hyperoxia combined with endovascular treatmen
21 combined with endovascular treatment or sham normobaric hyperoxia combined with endovascular treatmen
22           We aimed to evaluate the effect of normobaric hyperoxia combined with endovascular treatmen
23                                              Normobaric hyperoxia did not increase cellular markers o
24                  In this study, we show that normobaric hyperoxia extends the time window for effecti
25 s 2 (IQR 1-4) and it was 3 (1-4) in the sham normobaric hyperoxia group (adjusted common odds ratio 1
26  At 90 days, 14 (10%) of 140 patients in the normobaric hyperoxia group and 17 (12%) of 142 in the sh
27 eroxia group and 17 (12%) of 142 in the sham normobaric hyperoxia group died (adjusted risk differenc
28 90 days, the median score on the mRS for the normobaric hyperoxia group was 2 (IQR 1-4) and it was 3
29 adaptational changes during chronic moderate normobaric hyperoxia in mice.
30 ood O2 content; (ii) it is not known whether normobaric hyperoxia increases O2 delivery to the severe
31                           Our data show that normobaric hyperoxia increases tissue O2 delivery, and t
32  unclear, but suggest that a short period of normobaric hyperoxia is not beneficial in this context.
33                                              Normobaric hyperoxia is under investigation as a treatme
34                                              Normobaric hyperoxia may be a clinically feasible adjunc
35                We have previously shown that normobaric hyperoxia may benefit peri-lesional brain and
36 y and non-invasively determine the impact of normobaric hyperoxia on CBF and oxygenation in ischaemic
37                   To determine the effect of normobaric hyperoxia on cerebral metabolism in patients
38 of whom 282 were randomly assigned to either normobaric hyperoxia plus endovascular treatment (n=140)
39  plus endovascular treatment (n=140) or sham normobaric hyperoxia plus endovascular treatment (n=142;
40                      In experimental models, normobaric hyperoxia reduces cerebral ischaemic injury a
41                                              Normobaric hyperoxia treatment involved inhaling 100% ox
42  were candidates for endovascular treatment, normobaric hyperoxia yielded superior functional outcome
43 three independent neuroprotective approaches-normobaric hyperoxia, the free radical scavenger alpha-p
44 l outcomes at 90 days compared with the sham normobaric hyperoxia, without raising safety concerns.
45  underwent assessments at rest and following normobaric hypoxia ( FIO2 : 0.12), moderate intensity cy
46 xposed Madison strain Sprague-Dawley rats to normobaric hypoxia (10% oxygen) for 6 h or 3 d (short-te
47 rticular, we showed that chronic, continuous normobaric hypoxia (11% FIO2) prevents ataxia and neurol
48 ales age = (26 (sd 6)) years were exposed to normobaric hypoxia (12% O2 ) and normoxia (21% O2 ).
49  in multiple organs, and after subjection to normobaric hypoxia (8% O(2)), Cd73(-/-) mice manifested
50 r normoxia (F(I)O(2) = 0.209, RSN, n = 7) or normobaric hypoxia (F(I)O(2) = 0.136, RSH, n = 9).
51                                              Normobaric hypoxia (NH) and hypobaric hypoxia (HH) are b
52 aining performed during a 10-day exposure to normobaric hypoxia alters hormonal appetite regulation a
53                                              Normobaric hypoxia causes a rapid decrease in high-energ
54 he study was undertaken to determine whether normobaric hypoxia causes elevated brain volume and intr
55                     Hypoxia was induced in a normobaric hypoxia chamber by decreasing the partial pre
56 aphic signs of pulmonary hypertension during normobaric hypoxia correlated significantly with altered
57 moxia and after 5, 10, 20, and 30 minutes of normobaric hypoxia FI(O(2)) = 0.125.
58 eers (n=12, age 24 +/- 2 yr) were exposed to normobaric hypoxia in a purpose-built hypoxic chamber.
59 elopment of ionic edemas following prolonged normobaric hypoxia in agreement with cascadic models of
60           Here, we tested whether short-term normobaric hypoxia leads to changes in cardiac energetic
61 mprehensive analysis of the effects of acute normobaric hypoxia on human macro- and microcirculation.
62 P-8(-/-) and MMP-8(+/+) mice were exposed to normobaric hypoxia or normoxia for 4-8 weeks.
63 strated previously that in a murine model of normobaric hypoxia pulmonary fibrin deposition is a resu
64 id experiment including a 30-min interval of normobaric hypoxia with peripheral oxygen saturation bet
65 ither increased, e.g. during exercise, acute normobaric hypoxia, and the intravenous infusion of cate
66 a-responsive elements, cells were exposed to normobaric hypoxia, and transcriptional activity was rec
67        We examined the effects of prolonged, normobaric hypoxia, induced by 16 h of exposure to simul
68                    When mice were kept under normobaric hypoxia, this caused a persistent suppression
69  addition to laboratory studies which employ normobaric hypoxia.
70 d COX-2-deficient mice to a model of chronic normobaric hypoxia.
71 ute (2 h) and prolonged (10 h) poikilocapnic normobaric hypoxia.
72 itude and whether training or sleeping under normobaric hypoxic conditions in the weeks before the as
73 we examined the effect of repeated overnight normobaric hypoxic exposure on glycaemic control, appeti
74 ts were repeated under normoxic and hypoxic (normobaric (NH) and hypobaric (HH)) conditions, at real
75 is study was to examine the effects of acute normobaric (NH, decreased FiO(2)) and hypobaric (HH, 420
76 eric pressure at an altitude of 2438 m), and normobaric normoxia (control condition; equivalent to at
77 0.67-1.83 m s(-1)) on a level gradient under normobaric normoxia (room air, 21% O2), moderate hypoxia
78  performed an attention task during control (normobaric normoxia or NN), NH (fraction of inspired oxy
79 g treadmill walking under normal conditions (normobaric normoxia, 21% O(2)) and moderate hypoxia (13%
80 nt) hypoxia exposures compared to sea level (normobaric normoxia, NN).
81                   Our findings document that normobaric oxygen therapy administered during ischaemia
82 aken together with the available literature, normobaric oxygen therapy appears a promising therapy fo
83 rked and long-lasting sensorimotor deficits, normobaric oxygen therapy completely prevented sensorimo
84 only small increases in arterial O2 content, normobaric oxygen therapy experimentally induces signifi
85  trial published to date, early-administered normobaric oxygen therapy had no significant effect on c
86                 Nevertheless, the effects of normobaric oxygen therapy on infarct volume in rodent mo
87           Here we tested the hypothesis that normobaric oxygen therapy prevents both selective neuron
88                                              Normobaric oxygen therapy was applied from the onset and
89 cts of brief (1 hour) and continued (7 days) normobaric oxygen treatment on function were evaluated i
90 9.31]; P=0.005) and was more frequent in the normobaric-oxygen group (15 percent vs. 4 percent, P=0.0
91  group (19 of 76 [25.0 percent]) than in the normobaric-oxygen group (35 of 76 [46.1 percent], P=0.00
92 er three hyperbaric-oxygen treatments or one normobaric-oxygen treatment plus two sessions of exposur
93 YP46A1 inhibitor, was severely toxic even at normobaric pressure.
94 n treatment plus two sessions of exposure to normobaric room air.