[The protective effect of N-acetylcysteine on acute lung injury induced by PFIB inhalation].

Objective: To study the protective effect of N-acetylcysteine on acute lung injury induced by PFIB inhalation and its mechanism. Methods: Survival experiment: 48 male ICR (CD-1) mice were randomly divided into 4 groups, i. e., PFIB control group, NAC prevention group, NAC treatment group, and NAC prevention + treatment group, each group contains 12 animals. The mice of PFIB C group were exposed to PFIB without any treatment. The mice of NAC P group were exposed to PFIB 30min after NAC administration. The mice of NAC T group were exposed to PFIB 1h before NAC administration, The mice of NAC P+T group were administrated with NAC twice (30 min before and 1h after PFIB inhalation) . 150 mg/kg NAC was given by each time. The 7 days survival rate of mice after lethal dose PFIB exposure was observed. 18 male Wistar rats were randomly divided into 3 groups i.e., normal control group (N-C) , PFIB control group (PFIB-C) and NAC prevention group (NAC-P) , with each group contains 6 animals in the second experiment. The rats of N-C group received no treatment. The rats of NAC-P group and PFIB-C group were exposed to PFIB 30min after treatment of NAC (420 mg/Kg, i.p.) and saline, respectively. The respiratory functions of animals were tested before and 24 h after PFIB inhalation. The arterial blood gas was analyzed after rats were anesthetized 24 hours post sublethal dose PFIB exposure. Then samples of BALF, plasma and lung tissue were collected. Wet lung/body weight ratio, protein and phospholipid content in BALF, and T-SOD, GSH, GSH-Px in plasma and lung tissue were measured. The expression of Peroxiredoxin 2 was detected by Westernblot assay. Results: NAC prevention can significantly improve the survival of mice exposed to a lethal dose PFIB while NAC treatment is ineffective. Severe lung edema was observed in rats 24 h after PFIB exposure. Compared to N-C group, the wet lung/body weight ratio, protein and phospholipid content in BALF, and respiratory rate of PFIB control group all increased significantly (P<0.01) . The arterial oxygen partial pressure (PaO(2)) reduced significantly (P<0.05) . The GSH-Px activity in lung tissue reduced significantly (P<0.01) while the expression of Peroxiredoxin 2 increased significantly (P<0.01) . NAC prophylaxis significantly reduced the wet lung/body weight ratio, protein and phospholipid content in BALF, respiratory rate of rats exposed to PFIB (P<0.01) . Compared with PFIB-C group, the PaO(2) (P<0.05) and the activity of GSH-Px (P<0.01) and the expression of Peroxiredoxin 2 in lung tissue (P<0.01) were increased significantly. Conclusion: Acute lung injury induced by PFIB inhalation is related to oxidative stress caused by the stimulation to lung. induced and pulmonary subjected to stimulate the generation of exposure, NAC prevention can regulation of the redox system in lung tissue and protect target organ of the treated animals effectively.

Recent advances in the preparation and utilization of carbon nanotubes for hydrogen storage.

Recent progress in the production, purification, and experimental and theoretical investigations of carbon nanotubes for hydrogen storage are reviewed. From the industrial point of view, the chemical vapor deposition process has shown advantages over laser ablation and electric-arc-discharge methods. The ultimate goal in nanotube synthesis should be to gain control over geometrical aspects of nanotubes, such as location and orientation, and the atomic structure of nanotubes, including helicity and diameter. There is currently no effective and simple purification procedure that fulfills all requirements for processing carbon nanotubes. Purification is still the bottleneck for technical applications, especially where large amounts of material are required. Although the alkalimetal-doped carbon nanotubes showed high H2 weight uptake, further investigations indicated that some of this uptake was due to water rather than hydrogen. This discovery indicates a potential source of error in evaluation of the storage capacity of doped carbon nanotubes. Nevertheless, currently available single-wall nanotubes yield a hydrogen uptake value near 4 wt% under moderate pressure and room temperature. A further 50% increase is needed to meet U.S. Department of Energy targets for commercial exploitation. Meeting this target will require combining experimental and theoretical efforts to achieve a full understanding of the adsorption process, so that the uptake can be rationally optimized to commercially attractive levels. Large-scale production and purification of carbon nanotubes and remarkable improvement of H2 storage capacity in carbon nanotubes represent significant technological and theoretical challenges in the years to come.

Cleft palate and decreased brain gamma-aminobutyric acid in mice lacking the 67-kDa isoform of glutamic acid decarboxylase.

In addition to its role as an inhibitory neurotransmitter, gamma-aminobutyric acid (GABA) is presumed to be involved in the development and plasticity of the nervous system. GABA is synthesized by glutamic acid decarboxylase (GAD), but the respective roles of its two isoforms (GAD65 and 67) have not been determined. The selective elimination of each GAD isoform by gene targeting is expected to clarify these issues. Recently we have produced GAD65 -/- mice and demonstrated that lack of GAD65 does not change brain GABA contents or animal behavior, except for a slight increase in susceptibility to seizures. Here we report the production of GAD67 -/- mice. These mice were born at the expected frequency but died of severe cleft palate during the first morning after birth. GAD activities and GABA contents were reduced to 20% and 7%, respectively, in the cerebral cortex of the newborn GAD67 -/- mice. Their brain, however, did not show any discernible defects. Previous pharmacological and genetic investigations have suggested the involvement of GABA in palate formation, but this is the first demonstration of a role for GAD67-derived GABA in the development of nonneural tissue.

[Effect of xylazine on acetylcholine content of the hippocampal CA1 region in urethane anesthetized rats].

By using acetylcholine selective microelectrode technique, a biphasic effect of xylazine on acetylcholine content of the hippocampal CA1 region in urethane anesthetized rats was observed as evidenced by the fact that small doses of xylazine (2.0 and 6.0 mg.kg-1) significantly increased, while higher dose (10.0 mg.kg-1) decreased the acetylcholine content. Though idazoxan (0.6 mg.kg-1) significantly antagonized the effect of xylazine when used in combination, the acetylcholine content in the hippocampal CA1 region of urethane anesthetized rats was still much lower than that of the control group. In rats whose nucleus locus coeruleus was chemically lesioned, xylazine (2.0 and 6.0 mg.kg-1) significantly decreased the acetylcholine content, and idazoxan (0.6 mg.kg-1), which increased the acetylcholine content in the hippocampal CA1 region when used alone, completely antagonized the effect of xylazine. These results suggest that the biphasic effect of xylazine and the lower than normal acetylcholine content observed when idazoxan was used to antagonize xylazine induced changes in acetylcholine content of the hippocampal CA1 region in urethane anesthetized rats might be related to the effects of xylazine and idazoxan on the central noradrenergic neurotransmitter system.

[Antagonistic effects of cholinergic drugs on xylazine induced sedation].

Xylazine induced sedation in mice was observed as a kind of inhibition of exploratory activity. The reversible cholinesterase inhibitor cui xing ning (0.25-1.0 m.kg-1), the precursor of acetylcholine, choline bromide (100-300 mg.kg-1), and the M-receptor agonist arecoline (1.0-5.0 mg.kg-1) were shown to significantly antagonize xylazine (5.0 mg.kg-1) induced sedation. While cui xing ning (0.25 mg.kg-1) shifted the dose-response curve of xylazine induced sedation to the right, hemicholinum-3 (3 micrograms icv), which inhibits the synthesis of acetylcholine, shifted the dose-response curve to the left. These results suggest that the xylazine induced sedation may be partly due to a reduced central cholinergic function. Cui xing ning may have some value in the treatment of xylazine overdose and antagonize the anesthesia induced by anesthetics combined with xylazine.