ライフサイエンスコーパス: HBO

1 HBO exposure produced a major loss of PR cells in the ce

2 HBO treated animals also had better neurologic outcomes

3 HBO treatment decreased glucose, pyruvate, and glutamate

4 HBO treatment improved healing of the ischemic wounds.

5 HBO treatment in vivo appeared to accelerate age-related

6 HBO treatment in vivo has been shown to produce increase

7 HBO treatment was administered by putting rats in the HB

8 HBO-treated ischemic wounds also manifested reduced phos

9 ght decrease: control 42%, HPC 25% (P=0.01), HBO-PC 26% (P=0.01) and mortality protection (control 14

10 Small quantities of (S)-HSQ and (10R,13S)-HBO were also formed.

11 he HBO pretreatment group (0.12, 0.08-0.16), HBO posttreatment group (0.16, 0.13-0.19), and the sham

12 Forty-six children (24 HBO, 22 HBA) were analyzed at the second interim analysi

13 nly in the nuclear region of lenses after 30 HBO treatments, compared with control lenses.

14 With an additional 40 HBO(2) sessions, the original HBO(2) group reported addi

15 650 days old at death, were given 30 and 50 HBO treatments over 10- and 17-week periods, respectivel

16 an 13-week change scores were 10.6 +/- 10.6 (HBO(2) group) and 3.6 +/- 5.9 (sham group) (mean differe

17 ortality protection (control 14.7%, HPC 5.9% HBO-PC 5.7%, P=0.001).

18 Although a HBO derivative typically exhibits two rotamers with O...

19 Additionally, HBO increased expression of Bcl-2 while decreasing cleav

20 changed after ischemic/reperfusion and after HBO treatment.

21 NOS activity and expression is changed after HBO(2) seizures.

22 2 days after seizures and protection against HBO(2) seizures by nNOS-specific inhibitor 7-nitroindazo

23 re not sufficient for protecting PRs against HBO-induced cell death.

24 cted by reviewing the medical records of all HBO-treated RAO patients in our department and comparing

25 05) compared to control (129+/-83 mm(3)) and HBO 1.5-ata (119+/-68 mm(3))-treated groups.

26 ds occurred during cerebral ischemia and and HBO regulated these striatal metabolites, which might co

27 DDBO, DBO, and HBO are stable in aerated aqueous solution, in contrast

28 nlike the natural substrates, DDBO, DBO, and HBO do not change protonation state between pH's 4 and 9

29 triterpenes, the allylic isomers of HSQ and HBO, and an unidentified alcohol were produced in minor

30 HBO chamber at 3 atmospheres absolute (ATA) HBO for 1 h.

31 2-(2'-Hydroxyphenyl)benzoxazole (HBO) derivatives represent an important class of lumines

32 nt is started early after ischemia-onset but HBO dose appears important.

33 ructose-lysine, glucospane) were elevated by HBO, excluding significant lipid peroxidation and glucos

34 models and no studies have directly compared HBO-PC to hypoxic preconditioning (HPC).

35 HBO 1.5 ata, or HBO 2.5 ata in a customized HBO chamber allowing physiological monitoring and pericr

36 With rigorous temperature control, high dose HBO-PC and HPC showed comparable anatomic (mean hemisphe

37 High dose HBO-PC, but not HPC, suppressed aconitase activity by 65

38 after HPC (P=0.007) but not after high dose HBO-PC.

39 when temperature variability is eliminated, HBO-PC and HPC elicit similar preconditioning efficacy i

40 .0 atmosphere absolute (ata; control group), HBO 1.5 ata, or HBO 2.5 ata in a customized HBO chamber

41 product, (10S,13S)-10-hydroxybotryococcene (HBO), has a 1'-3 linkage between the farnesyl units.

42 Immediate HBO significantly reduced the lesions in rats that recei

43 tical infarction occurred less frequently in HBO 2.5-ata-treated than in control animals (44% vs. 71%

44 INTERPRETATION: HBO was not effective in improving GMFM scores, and was

45 ale NIH Swiss mice were subjected to a 5-min HBO(2) treatment (100% oxygen at 3.5 absolute atmosphere

46 ily treatment: HBOT, N-acetylcysteine (NAC), HBO and NAC, and control (normoxia at sea level).

47 mg kg(-1) intraperitoneal); control (neither HBO nor NAC).

48 ge and cell death increased with duration of HBO exposure.

49 might contribute to the protective effect of HBO in cerebral ischemia.

50 udy was undertaken to evaluate the effect of HBO on ischemic striatal metabolites at different times

51 Effect of HBO, pressurized to 2.5 atmospheres absolute (ATA) at ra

52 The effectiveness of HBO in clinical and experimental cerebral ischemia, howe

53 data confirm the neuroprotective effects of HBO in cerebral ischemia and suggest that the mechanism

54 he nucleus (the central region) of lenses of HBO-treated animals was nearly twice that of the control

55 al palsy were randomized to 40 treatments of HBO (100% oxygen at 1.5atm) or hyperbaric air (HBA, 14%

56 These results do not support use of HBO as a therapy for cerebral palsy in young children wh

57 However, the use of HBO with DOX potentiates the ROS-mediated cytotoxicity o

58 One week of HBO exposure was insufficient to cause PR death, but tis

59 ed by SD to 5-hydroxy-4H-1-benzopyran-4-one (HBO).

60 es (14+/-2; p<0.05) than control (10+/-3) or HBO 1.5-ata-treated animals (11+/-3).

61 solute (ata; control group), HBO 1.5 ata, or HBO 2.5 ata in a customized HBO chamber allowing physiol

62 additional 40 HBO(2) sessions, the original HBO(2) group reported additional improvements on NSI at

63 olved in the mechanism of hyperbaric oxygen (HBO(2)) brain toxicity as nitric oxide synthase (NOS) in

64 s research has found that hyperbaric oxygen (HBO(2)) produces an acute antinociceptive effect that is

65 brain injury received 40 hyperbaric oxygen (HBO(2)) sessions or 40 sham sessions over 12 weeks.

66 dy aims to assess whether hyperbaric oxygen (HBO) applied immediately after tooth extraction could am

67 lenses were treated with hyperbaric oxygen (HBO) for 48 h, and proteins were analyzed by gas and liq

68 rial to determine whether hyperbaric oxygen (HBO) improves gross motor function in children with cere

69 ecular mechanisms whereby hyperbaric oxygen (HBO) improves ischemic wound healing remain elusive.

70 Hyperbaric oxygen (HBO) is a potent means to increase the amount of oxygen

71 We have shown that hyperbaric oxygen (HBO) reduced cerebral infarction in rat middle cerebral

72 Hyperbaric oxygen (HBO) reduces cerebral infarct size after middle cerebral

73 Hyperbaric oxygen (HBO) therapy favorably improves oxygen transport to the

74 eduction in EPO levels by hyperbaric oxygen (HBO) used in a preclinical mouse model and in a pilot cl

75 s are more susceptible to hyperbaric oxygen (HBO)-induced cell death in vivo.

76 in aggregate formation in hyperbaric oxygen (HBO)-treated guinea pigs by using in vivo and in vitro

77 e (CO), and hyperbaric (pressurized) oxygen (HBO) alter vascular endothelium dysfunction and modulate

78 in cultured human fungiform taste papillae (HBO) cells with five arginyl dipeptides: Ala-Arg (AR), A

79 is a self-oscillating hindbrain population (HBO) that acts as a pacemaker for ocular saccades and co

80 The potency of hyperbaric preconditioning (HBO-PC) is uncertain compared to well-validated ischemic

81 ith matched RAO patients who did not receive HBO treatment.

82 an+/-S.D.) were smaller in animals receiving HBO at 2.5 ata (76+/-65 mm(3); p<0.05) compared to contr

83 Of clinical relevance, HBO therapy before human UCB transplantation was well-to

84 We conclude that HBO can improve outcome after temporary focal ischemia w

85 schemia was used to test the hypothesis that HBO enhances wound healing by modulating hypoxia-inducib

86 We hypothesized that HBO given prior to or after MCAO reduces PMN infiltratio

87 These results indicate that HBO improves ischemic wound healing by downregulation of

88 These findings suggest that HBO(2)-induced acute antinociception might be due to act

89 The HBO(2) group improved on measures of olfaction, anxiety,

90 is the first in vivo study demonstrating the HBO applied immediately after tooth extraction effective

91 ment was administered by putting rats in the HBO chamber at 3 atmospheres absolute (ATA) HBO for 1 h.

92 (mean 0.28, 95% C.I. 0.17-0.38) than in the HBO pretreatment group (0.12, 0.08-0.16), HBO posttreatm

93 Baseline NSI was 35.9 +/- 15.8 in the HBO(2) group (n = 26) and 30.7 +/- 16.9 in the sham grou

94 tself in the phase-locked entrainment of the HBO by periodic stimuli.

95 nnel-inhibitor) all led to antagonism of the HBO(2)-induced acute antinociception in a dose-dependent

96 Three HBO-PC regimes (maximum 2.5 atmospheres for 150 min) wer

97 to convulsions during subsequent exposure to HBO(2) and to determine if NOS activity and expression i

98 Upon exposure to HBO, rabbit lenses were swollen, and nuclei were yellow.

99 in the mechanism of increased sensitivity to HBO(2) in reexposures.

100 Three groups underwent daily treatment: HBO (90 minutes, 2.4 atm); systemic administration of th

101 months later, all were offered 40 unblinded HBO(2) sessions.

102 was assessed over the next 6 min still under HBO(2) using the acetic acid abdominal constriction test

103 By using HBO derivative 4, the rotational energy barrier of 2- (2

104 ncreased lens nuclear opacity in the in vivo HBO model.

105 nt study was undertaken to determine whether HBO(2)-induced acute antinociception might involve a NO-

106 treated three times weekly for 7 months with HBO, and lens crystallin aggregation was investigated in

107 CAO and were randomized to pretreatment with HBO (3 ATA) immediately prior to (n=13), or posttreatmen

108 er forms of injury, cellular protection with HBO is associated with diminished infiltration of polymo

109 Rats treated with HBO 2.5 ata had better mean+/-standard deviation (S.D.)

110 All patients treated with HBO received treatment within 7 days of the onset of vis

111 were reduced in ischemic wounds treated with HBO.

112 e sought to determine whether treatment with HBO initiated early after focal cerebral ischemia-onset