ライフサイエンスコーパス: normobaric

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 Four-month old C56BL/6J mice were kept in a normobaric chamber at 50% O(2) for up to 3 weeks.

9 e to 10% O(2) for 4 h daily for 56 days in a normobaric chamber, developed pulmonary hypertension, ri

10 a for 3 weeks and then allowed to recover at normobaric conditions for 3 additional weeks.

11 Under normobaric conditions, 30 muM 24(S)-HC was required to p

12 Notably, raising the inspired oxygen (80%, normobaric) during the hypoxic period significantly redu

13 fference in change between the hypobaric and normobaric exposure was 0 ng/mL for thrombin-antithrombi

14 served in some hemostatic markers during the normobaric exposure, attributed to prolonged sitting and

15 between the changes in the hypobaric and the normobaric exposures.

16 Both Tg and Wt mice were exposed to normobaric hyperoxia (>99% oxygen) for 48, 72, and 84 ho

17 Normobaric hyperoxia (NBO) has been shown to be neuropro

18 Post-ischaemic normobaric hyperoxia caused an immediate and progressive

19 Normobaric hyperoxia did not increase cellular markers o

20 In this study, we show that normobaric hyperoxia extends the time window for effecti

21 adaptational changes during chronic moderate normobaric hyperoxia in mice.

22 ood O2 content; (ii) it is not known whether normobaric hyperoxia increases O2 delivery to the severe

23 Our data show that normobaric hyperoxia increases tissue O2 delivery, and t

24 unclear, but suggest that a short period of normobaric hyperoxia is not beneficial in this context.

25 Normobaric hyperoxia is under investigation as a treatme

26 Normobaric hyperoxia may be a clinically feasible adjunc

27 We have previously shown that normobaric hyperoxia may benefit peri-lesional brain and

28 y and non-invasively determine the impact of normobaric hyperoxia on CBF and oxygenation in ischaemic

29 To determine the effect of normobaric hyperoxia on cerebral metabolism in patients

30 In experimental models, normobaric hyperoxia reduces cerebral ischaemic injury a

31 xposed Madison strain Sprague-Dawley rats to normobaric hypoxia (10% oxygen) for 6 h or 3 d (short-te

32 ales age = (26 (sd 6)) years were exposed to normobaric hypoxia (12% O2 ) and normoxia (21% O2 ).

33 in multiple organs, and after subjection to normobaric hypoxia (8% O(2)), Cd73(-/-) mice manifested

34 aining performed during a 10-day exposure to normobaric hypoxia alters hormonal appetite regulation a

35 Normobaric hypoxia causes a rapid decrease in high-energ

36 he study was undertaken to determine whether normobaric hypoxia causes elevated brain volume and intr

37 moxia and after 5, 10, 20, and 30 minutes of normobaric hypoxia FI(O(2)) = 0.125.

38 eers (n=12, age 24 +/- 2 yr) were exposed to normobaric hypoxia in a purpose-built hypoxic chamber.

39 Here, we tested whether short-term normobaric hypoxia leads to changes in cardiac energetic

40 strated previously that in a murine model of normobaric hypoxia pulmonary fibrin deposition is a resu

41 ither increased, e.g. during exercise, acute normobaric hypoxia, and the intravenous infusion of cate

42 a-responsive elements, cells were exposed to normobaric hypoxia, and transcriptional activity was rec

43 When mice were kept under normobaric hypoxia, this caused a persistent suppression

44 ute (2 h) and prolonged (10 h) poikilocapnic normobaric hypoxia.

45 addition to laboratory studies which employ normobaric hypoxia.

46 d COX-2-deficient mice to a model of chronic normobaric hypoxia.

47 itude and whether training or sleeping under normobaric hypoxic conditions in the weeks before the as

48 eric pressure at an altitude of 2438 m), and normobaric normoxia (control condition; equivalent to at

49 0.67-1.83 m s(-1)) on a level gradient under normobaric normoxia (room air, 21% O2), moderate hypoxia

50 Our findings document that normobaric oxygen therapy administered during ischaemia

51 aken together with the available literature, normobaric oxygen therapy appears a promising therapy fo

52 rked and long-lasting sensorimotor deficits, normobaric oxygen therapy completely prevented sensorimo

53 only small increases in arterial O2 content, normobaric oxygen therapy experimentally induces signifi

54 trial published to date, early-administered normobaric oxygen therapy had no significant effect on c

55 Nevertheless, the effects of normobaric oxygen therapy on infarct volume in rodent mo

56 Here we tested the hypothesis that normobaric oxygen therapy prevents both selective neuron

57 Normobaric oxygen therapy was applied from the onset and

58 cts of brief (1 hour) and continued (7 days) normobaric oxygen treatment on function were evaluated i

59 9.31]; P=0.005) and was more frequent in the normobaric-oxygen group (15 percent vs. 4 percent, P=0.0

60 group (19 of 76 [25.0 percent]) than in the normobaric-oxygen group (35 of 76 [46.1 percent], P=0.00

61 er three hyperbaric-oxygen treatments or one normobaric-oxygen treatment plus two sessions of exposur

62 YP46A1 inhibitor, was severely toxic even at normobaric pressure.

63 n treatment plus two sessions of exposure to normobaric room air.