Our results suggest that pneumoperitoneum increases sympathetic cardiac activity. The choice of general anesthetic did not seem to have a major influence on the change in the cardiac autonomic nervous system after induction of pneumoperitoneum for laparoscopic cholecystectomy.

A growing body of evidence has shown that oxidative stress may be involved in the development of vascular complications associated with diabetes. However, the molecular mechanism for increased reactive oxygen species (ROS) production in diabetes remains uncertain. Among various possible mechanisms, attention have increasingly been paid to NAD(P)H oxidase as the most important source of ROS production in vascular cells. High glucose level stimulates ROS production through protein kinase C (PKC)-dependent activation of vascular NAD(P)H oxidase. Furthermore, the expression of NAD(P)H oxidase components is increased in micro- and macrovascular tissues of diabetic animals in association with various functional disorders and histochemical abnormalities. These results suggest that vascular NAD(P)H oxidase-driven ROS production may contribute to the onset or development of diabetic micro- or macrovascular complications. In this point of view, the possible new strategy of antioxidative therapy for diabetic vascular complications is discussed in this review.

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The photoreactions of 2,4,6-triphenyl- (TPP), 2-t-butyl-4,6-diphenylpyrylium (2BDPP) and 2,4,6-triphenylthiopyrylium (TPTP) salts in tetrahydrofuran (THF) and/or 1,2-dimethoxyethane were investigated. Photoproducts were identified to be pyranyl radicals on the basis of photochemical behavior and ESR spectra. Quantum yields of one-electron reduction reactions of TPP, 2BDPP, and TPTP were obtained to be 0.21, 0.047, and 0.53, respectively. The hf coupling constants of protons in the radicals were determined by simulation. The photoillumination of TPP in THF at low temperatures revealed that a certain intermediate radical species was involved in this one-electron photoreduction.

We have observed that a polyvinyl alcohol (PVA) brush-process generates many particles when there is a large friction force between the brush and a Si wafer surface terminated by hydrogen. PVA brush-based processes are widely used as a post chemical mechanical polishing (CMP) clean. We noted that the particles increase with the friction force between the brush and the surface. In addition, the particle size varies with the friction force. Raman spectroscopy detected a CH 2 stretching band at 2900 cm −1 , and C-C bands at 1330 cm −1 (D band) and 1600 cm −1 (G band). We infer that these C-C bands indicate the presence of amorphous carbon. In order to prevent a PVA brush cleaning process from producing particles, there must be a careful consideration of the scrub process parameters and the underlying surface conditions. We suggest a mechanism for the large particle generation observed by considering the zeta potential between the PVA brush bristles and the Si wafer surface. From a practical perspective, we tested the removal efficiency of the particles generated by the scrubbing process in a wet sink instead of using poly styrene latex (PSL) particles because of quick turn-around and low cost.

We previously reported that organic solvent (ethanol) treatment of a film formed by plasma enhanced chemical vapor deposition (PE-CVD) remarkably improved the gap-filling property of O3-tetraethylorthosilicate (O3-TEOS) atmospheric pressure chemical vapor deposition (AP-CVD) film. Based on these results, we concluded that alkoxy (ethoxy) groups, which are generated by ethanol treatment, reduced the adsorptive activities of the sites distributed on the surface, causing a decrease in the sticking probability of vapor-phase species responsible for the deposition. However, an opposite hypothesis has been reported, which proposes that ethoxy groups become adsorption sites. In this study, we offer a counterargument and clarify that ethoxy groups, which were generated by ethanol treatment following light etching using dilute hydrofluoric acid (HF), do not become adsorption sites on the surface of thermally grown silicon dioxide (thermal SiO2) during O3-TEOS film deposition, since the O3-TEOS film was formed at a low deposition rate (DR). A smooth surface and excellent gap-filling into the patterns covered with thermal SiO2 were observed on the O3-TEOS film formation by ethanol treatment. We propose that a degasification step during O3-TEOS film formation or during annealing after the deposition could be closely related to improved surface roughness and gap-filling.

Sevoflurane is a recently introduced volatile inhalation anaesthetic and is already used commonly in Japan. We investigated the potential of sevoflurane to cause lipid peroxidation in vivo and in vitro. For the in vitro study, pentane formation in a mixture of guinea pig liver microsomes and sevoflurane in the presence of nicotinamide adenine dinucleotide phosphate (NADPH) was analyzed by gas chromatography. Under anaerobic conditions, pentane formed without sevoflurane, but sevoflurane potentiated this anaerobic pentane formation. Two antioxidant agents, vitamine E and glutathione, reduced the pentane formation induced by sevoflurane. In the in vivo study, 18 guinea pigs were exposed to air (control), 0.5% halothane, or 1.2% sevoflurane. The extent of lipid peroxidation and liver damage was investigated by measuring the level of thiobarbituric acid reactive products and serum transaminase (alanine-aminotransferase: ALAT and aspartate-aminotransferase: ASAT) activity 12 hr after exposure. Both halothane and sevoflurane significantly increased thiobarbituric acid-reactive products. The increase in thiobarbituric acid-reactive products seen with sevoflurane administration was half that seen with halothane. Sevoflurane increased the ALAT activity to the same extent as did halothane but did not increase the ASAT activity. We conclude that sevoflurane potentiates lipid peroxidation in guinea pig liver microsomes in vivo and in vitro. However, because the degree of liver damage as measured by transaminase activity was minimal and the mechanism of sevoflurane-induced lipid peroxidation is still unknown, we must be cautious in applying these results to humans.