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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  650 days old at death, were given 30 and 50 HBO treatments over 10- and 17-week periods, respectivel
15 ortality protection (control 14.7%, HPC 5.9% HBO-PC 5.7%, P=0.001).
16                                   Although a HBO derivative typically exhibits two rotamers with O...
17                                Additionally, HBO increased expression of Bcl-2 while decreasing cleav
18 changed after ischemic/reperfusion and after HBO treatment.
19 NOS activity and expression is changed after HBO(2) seizures.
20 2 days after seizures and protection against HBO(2) seizures by nNOS-specific inhibitor 7-nitroindazo
21 re not sufficient for protecting PRs against HBO-induced cell death.
22 05) compared to control (129+/-83 mm(3)) and HBO 1.5-ata (119+/-68 mm(3))-treated groups.
23 ds occurred during cerebral ischemia and and HBO regulated these striatal metabolites, which might co
24                               DDBO, DBO, and HBO are stable in aerated aqueous solution, in contrast
25 nlike the natural substrates, DDBO, DBO, and HBO do not change protonation state between pH's 4 and 9
26  triterpenes, the allylic isomers of HSQ and HBO, and an unidentified alcohol were produced in minor
27  HBO chamber at 3 atmospheres absolute (ATA) HBO for 1 h.
28             2-(2'-Hydroxyphenyl)benzoxazole (HBO) derivatives represent an important class of lumines
29 nt is started early after ischemia-onset but HBO dose appears important.
30 ructose-lysine, glucospane) were elevated by HBO, excluding significant lipid peroxidation and glucos
31 models and no studies have directly compared HBO-PC to hypoxic preconditioning (HPC).
32  HBO 1.5 ata, or HBO 2.5 ata in a customized HBO chamber allowing physiological monitoring and pericr
33 With rigorous temperature control, high dose HBO-PC and HPC showed comparable anatomic (mean hemisphe
34                                    High dose HBO-PC, but not HPC, suppressed aconitase activity by 65
35  after HPC (P=0.007) but not after high dose HBO-PC.
36  when temperature variability is eliminated, HBO-PC and HPC elicit similar preconditioning efficacy i
37 .0 atmosphere absolute (ata; control group), HBO 1.5 ata, or HBO 2.5 ata in a customized HBO chamber
38  product, (10S,13S)-10-hydroxybotryococcene (HBO), has a 1'-3 linkage between the farnesyl units.
39 tical infarction occurred less frequently in HBO 2.5-ata-treated than in control animals (44% vs. 71%
40                              INTERPRETATION: HBO was not effective in improving GMFM scores, and was
41 ale NIH Swiss mice were subjected to a 5-min HBO(2) treatment (100% oxygen at 3.5 absolute atmosphere
42 ily treatment: HBOT, N-acetylcysteine (NAC), HBO and NAC, and control (normoxia at sea level).
43 mg kg(-1) intraperitoneal); control (neither HBO nor NAC).
44 ge and cell death increased with duration of HBO exposure.
45 might contribute to the protective effect of HBO in cerebral ischemia.
46 udy was undertaken to evaluate the effect of HBO on ischemic striatal metabolites at different times
47                         The effectiveness of HBO in clinical and experimental cerebral ischemia, howe
48  data confirm the neuroprotective effects of HBO in cerebral ischemia and suggest that the mechanism
49 he nucleus (the central region) of lenses of HBO-treated animals was nearly twice that of the control
50 al palsy were randomized to 40 treatments of HBO (100% oxygen at 1.5atm) or hyperbaric air (HBA, 14%
51          These results do not support use of HBO as a therapy for cerebral palsy in young children wh
52                          However, the use of HBO with DOX potentiates the ROS-mediated cytotoxicity o
53                                  One week of HBO exposure was insufficient to cause PR death, but tis
54 ed by SD to 5-hydroxy-4H-1-benzopyran-4-one (HBO).
55 es (14+/-2; p<0.05) than control (10+/-3) or HBO 1.5-ata-treated animals (11+/-3).
56 solute (ata; control group), HBO 1.5 ata, or HBO 2.5 ata in a customized HBO chamber allowing physiol
57 olved in the mechanism of hyperbaric oxygen (HBO(2)) brain toxicity as nitric oxide synthase (NOS) in
58 s research has found that hyperbaric oxygen (HBO(2)) produces an acute antinociceptive effect that is
59  lenses were treated with hyperbaric oxygen (HBO) for 48 h, and proteins were analyzed by gas and liq
60 rial to determine whether hyperbaric oxygen (HBO) improves gross motor function in children with cere
61 ecular mechanisms whereby hyperbaric oxygen (HBO) improves ischemic wound healing remain elusive.
62                           Hyperbaric oxygen (HBO) is a potent means to increase the amount of oxygen
63        We have shown that hyperbaric oxygen (HBO) reduced cerebral infarction in rat middle cerebral
64                           Hyperbaric oxygen (HBO) reduces cerebral infarct size after middle cerebral
65                           Hyperbaric oxygen (HBO) therapy favorably improves oxygen transport to the
66 eduction in EPO levels by hyperbaric oxygen (HBO) used in a preclinical mouse model and in a pilot cl
67 s are more susceptible to hyperbaric oxygen (HBO)-induced cell death in vivo.
68 in aggregate formation in hyperbaric oxygen (HBO)-treated guinea pigs by using in vivo and in vitro
69 e (CO), and hyperbaric (pressurized) oxygen (HBO) alter vascular endothelium dysfunction and modulate
70  in cultured human fungiform taste papillae (HBO) cells with five arginyl dipeptides: Ala-Arg (AR), A
71  is a self-oscillating hindbrain population (HBO) that acts as a pacemaker for ocular saccades and co
72   The potency of hyperbaric preconditioning (HBO-PC) is uncertain compared to well-validated ischemic
73 an+/-S.D.) were smaller in animals receiving HBO at 2.5 ata (76+/-65 mm(3); p<0.05) compared to contr
74                       Of clinical relevance, HBO therapy before human UCB transplantation was well-to
75                             We conclude that HBO can improve outcome after temporary focal ischemia w
76 schemia was used to test the hypothesis that HBO enhances wound healing by modulating hypoxia-inducib
77                         We hypothesized that HBO given prior to or after MCAO reduces PMN infiltratio
78                  These results indicate that HBO improves ischemic wound healing by downregulation of
79                  These findings suggest that HBO(2)-induced acute antinociception might be due to act
80 ment was administered by putting rats in the HBO chamber at 3 atmospheres absolute (ATA) HBO for 1 h.
81  (mean 0.28, 95% C.I. 0.17-0.38) than in the HBO pretreatment group (0.12, 0.08-0.16), HBO posttreatm
82 tself in the phase-locked entrainment of the HBO by periodic stimuli.
83 nnel-inhibitor) all led to antagonism of the HBO(2)-induced acute antinociception in a dose-dependent
84                                        Three HBO-PC regimes (maximum 2.5 atmospheres for 150 min) wer
85 to convulsions during subsequent exposure to HBO(2) and to determine if NOS activity and expression i
86                             Upon exposure to HBO, rabbit lenses were swollen, and nuclei were yellow.
87 in the mechanism of increased sensitivity to HBO(2) in reexposures.
88      Three groups underwent daily treatment: HBO (90 minutes, 2.4 atm); systemic administration of th
89 was assessed over the next 6 min still under HBO(2) using the acetic acid abdominal constriction test
90                                     By using HBO derivative 4, the rotational energy barrier of 2- (2
91 ncreased lens nuclear opacity in the in vivo HBO model.
92 nt study was undertaken to determine whether HBO(2)-induced acute antinociception might involve a NO-
93 treated three times weekly for 7 months with HBO, and lens crystallin aggregation was investigated in
94 CAO and were randomized to pretreatment with HBO (3 ATA) immediately prior to (n=13), or posttreatmen
95 er forms of injury, cellular protection with HBO is associated with diminished infiltration of polymo
96                            Rats treated with HBO 2.5 ata had better mean+/-standard deviation (S.D.)
97 were reduced in ischemic wounds treated with HBO.
98 e sought to determine whether treatment with HBO initiated early after focal cerebral ischemia-onset

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