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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
11 he HBO pretreatment group (0.12, 0.08-0.16), HBO posttreatment group (0.16, 0.13-0.19), and the sham
14 650 days old at death, were given 30 and 50 HBO treatments over 10- and 17-week periods, respectivel
20 2 days after seizures and protection against HBO(2) seizures by nNOS-specific inhibitor 7-nitroindazo
23 ds occurred during cerebral ischemia and and HBO regulated these striatal metabolites, which might co
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
30 ructose-lysine, glucospane) were elevated by HBO, excluding significant lipid peroxidation and glucos
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
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
39 tical infarction occurred less frequently in HBO 2.5-ata-treated than in control animals (44% vs. 71%
41 ale NIH Swiss mice were subjected to a 5-min HBO(2) treatment (100% oxygen at 3.5 absolute atmosphere
46 udy was undertaken to evaluate the effect of HBO on ischemic striatal metabolites at different times
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%
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.
66 eduction in EPO levels by hyperbaric oxygen (HBO) used in a preclinical mouse model and in a pilot cl
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
76 schemia was used to test the hypothesis that HBO enhances wound healing by modulating hypoxia-inducib
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
83 nnel-inhibitor) all led to antagonism of the HBO(2)-induced acute antinociception in a dose-dependent
85 to convulsions during subsequent exposure to HBO(2) and to determine if NOS activity and expression i
89 was assessed over the next 6 min still under HBO(2) using the acetic acid abdominal constriction test
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
98 e sought to determine whether treatment with HBO initiated early after focal cerebral ischemia-onset
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