We examined recent volcanic cloud events in the Western Pacific and Indonesian area, to validate the performance of remote sensing techniques used to support the International Airways Volcano Watch (IAVW). Five events were considered, during which eruptions from eight volcanoes injected ash into the upper troposphere or lower stratosphere. For one of the eruptions, at Miyakejima, Japan, at least five aircraft encountered volcanic ash clouds, and the cost to three operators alone exceeded US $12,000,000 in aircraft repairs, diversions, and lost operating time. We performed 'reverse' absorption and 'pattern analysis' using GMS-5/VISSR, MODIS and AVHRR data, and we examined TOMS SO 2 and Aerosol Index data, surface-based observations, pilot reports, and dispersion model output. Our results verify that the introduction of 'reverse' absorption using the geostationary GMS-5 platform significantly enhanced our capacity to monitor volcanic ash clouds in the region. In one case, we tracked an eruption cloud for approximately 80 hours. The primary impediment to remote monitoring is the presence of overlying cloud, or substantial amounts of ice within the volcanic clouds. TOMS data showed success in identifying volcanic clouds during these conditions, but was limited by the infrequency of observations. More effective future operation of the IAVW relies on developing complementary methods of volcanic cloud remote sensing, and greatly increasing the amount and quality of available surface and air observations, including observations of precursor activity. An understanding of the likely future limitations of remote sensing techniques will aid in the refining of IAVW procedures.

No abstract

The Cytochrome P450 is the major enzyme involved in drug metabolism. CYP enzymes are responsible for the metabolism of most clinically used drugs. Individual variability in CYP activity is one important factor that contributes to drug therapy failure. We have developed a new straightforward TaqMan PCR genotyping assay to investigate the prevalence of the most common allelic variants of polymorphic CYP enzymes CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A5 in the Japanese population. Moreover, we focused on the combination of each genotype for clinical treatment. The genotype analysis identified a total of 139 out of 483 genotype combinations of five genes in the 1,003 Japanese subjects. According to our results, most of subjects seemed to require dose modification during clinical treatment. In the near future, modifications should be considered based on the individual patient genotype of each treatment.

We have evaluated the chemopreventive effects of curcumin on diethylstilbestrol (DES)-induced tumor promotion of rat mammary glands initiated with radiation. Sixty-four pregnant rats received whole body irradiation with 2.6 Gy γ-rays from a 60 Co source at day 20 of pregnancy and were divided into two groups after weaning. In the control group of 39 rats fed a basal diet and then implanted with a DES pellet for 1 year, 33 (84.6%) developed mammary tumors. Twenty-five rats were fed diet containing 1% curcumin immediately after weaning and received a DES pellet, as for the control. The administration of dietary curcumin significantly reduced the incidence (28.0%) of mammary tumors. Multiplicity and Iball's index of mammary tumors were also decreased by curcumin. Rats fed the curcumin diet showed a reduced incidence of the development of both mammary adenocarcinoma and ER(⍣)PgR(⍣) tumors in comparison with the control group. On long-term treatment with curcumin, body weight and ovarian weight were reduced, but liver weight was increased. Compared with the control rats, the curcumin-fed rats showed a significant reduction in serum prolactin, whereas estradiol-17β and progesterone concentrations were not significantly different between the two groups. Curcumin did not have any effect on the concentration of free cholesterol, cholesterol ester and triglyceride. Feeding of the curcumin diet caused a significant increase in the concentrations of tetrahydrocurcumin, arachidonic acid and eicosapentaenoic acid and a significant decrease in thiobarbituric acid-reactive substance concentration in serum. Whole mounts of the mammary glands showed that curcumin yielded morphologically indistinguishable proliferation and differentiation from the glands of the control rats. These findings suggest that curcumin has a potent preventive activity during the DESdependent promotion stage of radiation-induced mammary tumorigenesis.

The existence of the T-type VDC in bronchial smooth muscle and the high sensitivity of this channel to volatile anesthetics seem to be, at least in part, responsible for the different reactivities to the anesthetics in tracheal and bronchial smooth muscles.

Purpose: The present study was designed to clarify the direct effects of the volatile anesthetics halothane, isoflurane and sevoflurane on oxytocin-induced uterine smooth muscle contraction from pregnant rats.Methods: Longitudinal smooth muscle layers were obtained from pregnant rats. Intracellular concentration of free Ca ++ ([Ca ++ ] i ) was measured, using a fluorescence technique, simultaneously with muscle tension. Inward Ba ++ current (I Ba ) through voltage-dependent Ca ++ channels (VDCCs) was measured using a whole cell patch clamp technique. After incubation with 20 nM oxytocin, halothane, isoflurane or sevoflurane (1, 2, and 3%) was introduced into the tissue bath.Results: All volatile anesthetics significantly inhibited muscle contraction concomitant with a decrease in [Ca ++ ] i . Volatile anesthetics also inhibited the peak I Ba . When the anesthetic concentrations were expressed as multiples of minimum alveolar concentrations, there were no differences in the inhibitory potencies of the three volatile agents tested for muscle tension and VDCC.Conclusions: Volatile anesthetics halothane, isoflurane and sevoflurane reduce the oxytocin-induced contraction of pregnant uterine smooth muscle. Inhibition of the contraction by the volatile anesthetics is due, at least in part, to the decrease in [Ca ++ ] i , and the decrease in [Ca ++ ] i may be mediated by inhibition of VDCC activity.

The data suggested that dihydronitidine toxicity targeted a particular intracellular organelle in the tumor cells.

No abstract