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This paper presents a method for enhancing the ablation plasma production and the flyer velocity for flyer acceleration. A significant approach introduced is to optimize the interaction field of the ablation plasma and the Al target. To do so, it is acceptable to adjust the distance of ion beam irradiation. A one-dimensional hydrodynamic model is used in the calculations. The cube-interpolated propagation (CIP) method is used to describe the ablation plasma production and the acceleration mechanism. In the calculations, a single-pulsed ion beam with a total energy density of 120 J/cm2 is used. The interaction field (ion beam irradiation distance) that varies from 50 to 1000 µm is fixed for the calculations. At the interaction field of 50 µm, the flyer velocity of 2 km/s is calculated, while the value of 1.3 km/s is obtained at the distance of 400 µm. The results show that the closer the interaction field (distance of ion beam irradiation), the higher the flyer velocity obtained. In addition, the results reveal that the interaction field directly affects the amount of the ablation plasma produced and the flyer momentum.

In situ synthesis of estrogens by breast cancer tissue provides a potential explanation for the high concentrations of estradiol in mammary neoplasms in postmenopausal women. A major metabolic pathway for estrogen biosynthesis is the conversion of androstenedione to estrone via the enzyme aromatase. Biochemical studies have demonstrated aromatase in tumor tissue, but at relatively low and not clearly biologically significant levels. The present study tested the hypothesis that tumor levels of aromatase, albeit low, could be biologically important if present in high concentrations in focal clusters of specific cell types. A pilot study used an immunohistochemical method in frozen sections of fresh breast tumors as an optimal means to detect aromatase. Twelve of 18 tumors contained aromatase-positive cells, some with highly intense staining. A follow-up study then attempted to precisely define the types of cells containing aromatase and correlate the immunohistochemical findings with biochemical aromatase activity. A modified H-score (histological scoring system) was used to semiquantitate the amount of aromatase staining in tumor epithelial, stromal spindle, stromal inflammatory, and normal breast epithelial cells. We found that immunohistochemical staining for aromatase predominated in stromal spindle cells with a median H-score of 13, whereas tumor epithelial, stromal inflammatory, and normal breast elements contained lesser amounts (median H-scores of 4.8, 0.03, and 0.5, respectively). The H-score for stromal spindle cells, but not those for other cell types, correlated highly with the biochemical aromatase assay (P0.01). Using a cut-off parameter estimated by a sensitivity/specificity (receiver operating curve) analysis, 62% of tumors were classified as aromatase positive based on stromal spindle cell staining. A similar number were also positive by biochemical assay, with concordance between the two methods of 77%. These observations provide substantial evidence for the presence of aromatase in human breast tumors, particularly in stromal spindle cells, and support the biological importance of aromatase for in situ production of estradiol.

The expression of aromatase mRNA in cultured mouse brain cells was measured by a quantitative reverse transcription-PCR method using an internal standard. Aromatase mRNA was expressed in the cultured neurons prepared from diencephalon at 0.037 ± 0.005attomol/μg total RNA. However, the mRNA was detected in neither the neurons from cerebral cortex nor astrocytes. These results demonstrate that expression of aromatase mRNA is regulated in cell type- and region-specific manners in cultured brain cells. The aromatase mRNA levels in neurons obtained from diencephalon were not affected by administration of testosterone, estradiol, dexamethasone, forskolin, or 12-O-tetradecanoyl 13-acetate. The results are in apparent disagreement with previous reports concerning regulation by androgens of brain aromatase activity in vivo and may suggest that aromatase expression in brain neurons is not directly induced by androgens. Androgen induction of brain aromatase may be mediated by several steps including cell-cell (neuron-neuron and/or neuron-glia) interaction.

An efficient expression system for a cDNA clone of human placental aromatase has been developed using the baculovirus expression system in TN5 ( Tricoplusia ni ) cells. The protein was expressed at high levels, with specific aromatase activity and specific P450 content comparable to that found in human placental microsomes. To achieve these high levels of activity, hemin had to be added to the cultures of infected cells and NADPH-cytochrome P450 reductase had to be included in the assay buffer. The spectral properties of ligand bound forms of the baculovirus expressed aromatase were very similar to those exhibited by the same ligand bound forms of the enzyme purified from placental microsomes. This expression system appears to be a suitable source for the purification of milligram quantifies of recombinant aromatase.

The volume and cytoarchitectonic organization of the sexually dimorphic medial preoptic nucleus (POM) of the quail are sensitive to plasma levels of testosterone (T). We previously showed that, in castrated quail, T or its estrogenic metabolite, estradiol (E2), increases the size of the large neurons located in the lateral part of POM. Embryonic treatments with estrogens are also known to affect permanently the size of these large neurons. Since the lateral POM also contains a dense population of aromatase-immunoreactive (ARO-ir) cells, and these are known to be a target for steroids, we hypothesized that the effects of steroids identified in previous experiments were primarily directed to these ARO-ir cells. This idea was tested in two experiments in which the size of these cells was measured in male quail under various endocrine conditions. In experiment 1, a detailed analysis of ARO-ir and of non-immunoreactive cells in the POM of adult, sexually mature males revealed that the immunoreactive perikarya are larger than the non-immunoreactive cells and that they constitute the vast majority of the large cells (area50 microns 2) in the POM. In experiment 2, it was shown that T and E2 actually increase the size of ARO-ir cells in the POM while the androgenic metabolite of T, dihydrotestosterone has no effect at this level. Taken together, these data suggest that the sex differences and the steroid-induced changes in cell size previously described in the study of POM sections stained for Nissl material largely concern aromatase-containing cells. Since aromatization of T plays a limiting role in the activation of male copulatory behavior, these changes may represent the morphological signature of the mechanisms causally involved in the control of this behavior.

In this study, the temperature characteristic of the thin copper wire annealed in atmospheric pressure dielectric barrier discharge (APDBD) system is studied. An equivalent circuit model was used to analyze the wire surface temperature in APDBD. The analysis model showed that the ion bombardment on the wire surface was the main factor that determined wire surface temperature. The average temperature of the thin copper wire in APDBD reactor was calculated as a function of reactor diameter, dielectric material type, applied voltage, ion mass, and gas thermal conductivity. It was, however, shown that applied voltage was the most important parameter to elevate the thin wire temperature up to appropriate annealing temperature. Also, reactor length and carrier speed were crucial for controlling annealing temperature.

The objective of the current MHD acceleration study is to thoroughly explain the compact experimental demo of MHD accelerator and to clarify some significant plasma variables both within and at the exit of the newly introduced mullite ceramic compact channel. The significant challenge of the current study is to use the 0.4-tesla neodymium magnetic as an MHD source, while the model rocket engine (C6-0, ESTES) is introduced and employed as a gas (plasma) source. The results of present demonstrations reveal that the highest gas velocity was calculated at 117.2 m/s using the gas pressure measurement through the pitot tube. The TOF method using two photo diodes showed the slowest speed of 50 m/s.

Extensive screening of aromatase cDNA was carried out in cDNA libraries from various human tissues. The DNA sequences of all the isolated cDNA clones were identical in the region encoded by exons 2-10 of the aromatase gene. However, tissue-specific sequences, which were classified into four groups, were observed in the 5' portions of the clones corresponding to the region encoded by exon 1. All of them were also found in clones isolated from a human genomic library and mapped between exons 1 and 2 of the human aromatase gene reported previously, suggesting the presence of multiple exons 1 and promoters in the gene. Reverse transcription-PCR analyses of aromatase mRNAs in various tissues revealed that aromatase transcripts are tissue-specifically spliced by alternative use of multiple exons 1, although minor forms of the transcripts were also present in each tissue. Aromatase mRNA is spliced from 10 exons in most tissues, but from 9 exons in the prostate and from 10 or 11 exons in the placenta. This suggests that tissue-specific regulation of the aromatase gene in various tissues may be explained by alternative use of multiple exons 1 flanked with tissue-specific promoters. The alternative use of multiple exons 1 for liver transcripts was found to change developmentally. Furthermore, switch from an adipose-specific exon 1 to another type of exon 1 was observed in aromatase transcripts of adipose tissues of three of five breast cancer patients.

It is established that testosterone (T) increases aromatase activity (AA) in the quail brain and that this induction of AA represents a limiting factor in the activation of male copulatory behavior. This action of T presumably results from an induction of aromatase synthesis since the number of aromatase-immunoreactive (ARO-ir) cells increases and, in parallel, there is an increase in aromatase mRNA as measured by reverse transcriptase-polymerase chain reaction (RT-PCR) technology. The specific role of androgenic and estrogenic metabolites of T in this induction is not yet clear but product-formation assays suggest that both types of compounds synergize to increase AA. The exact role of androgens and estrogens in the induction of aromatase was examined by studying both the aromatase protein by immunocytochemistry and the aromatase mRNA by RT-PCR in castrated quail that had been treated with T or its androgenic metabolite, 5 alpha-dihydrotestosterone (DHT) or its estrogenic metabolite, estradiol-17 beta (E2) or both DHT and E2 simultaneously. A specific quantitative PCR technique using a modified aromatase as internal standard was developed for this purpose. T increased the number of ARO-ir cells in all brain areas and increased the concentration of ARO mRNA in the preoptic area-anterior hypothalamus (POA-aHYP) and in the posterior hypothalamus (pHYP). E2-treated birds had more ARO-ir cells than castrates in the posterior part of the medial preoptic nucleus (POM), in the bed nucleus stria terminalis (BNST) and tuber. Their aromatase mRNA concentration was significantly increased in the POA-aHYP but this effect did not reach significance in the pHYP. DHT by itself had no effect on either the number of ARO-ir cells (all brain regions considered) or the concentration of aromatase mRNA. DHT, however, synergized with E2, both in inducing ARO-ir neurons and in increasing aromatase mRNA concentration. This synergism was shown to be statistically significant in several brain areas. These data demonstrate that both androgens and estrogens regulate aromatase at the pretranslational level. Because the percentage increase in the number of ARO-iR cells was in general very similar to the increase in aromatase mRNA concentration, these data also suggest that these steroids regulate aromatase mostly by changing its mRNA synthesis or catabolism.

Aromatase mRNA in human skin fibroblasts was greatly increased in the presence of dexamethasone. Aromatase cDNA was prepared depending on mRNA of dexamethasone-treated fibroblasts by the PCR method including the rapid amplification of cDNA ends (RACE) protocol. The isolated cDNA had the same sequences as placental aromatase cDNA in the region encoded by exons 2–10. However, all 5'-fragments obtained from fibroblast aromatase cDNA contained a unique sequence in the region encoded by exon 1. A unique sequence was also deduced for the region between exons 1 and 2 of the placental aromatase gene from its cDNA, indicating that this region is used as an exon 1 by alternative splicing in skin fibroblasts. Tissue-specific use of multiple exons 1 in the splicing of aromatase transcripts was demonstrated by the mRNAs obtained from various tissues.

A sensitive method was developed for the determination of trace amounts of aromatase mRNA in various tissues. Aromatase mRNA was quantitated by subjecting it to reverse transcription in the presence of an internal standard RNA and then amplifying the resulting cDNA by polymerase chain reaction with a fluorescent primer. The tissue distribution of aromatase mRNA in mice was examined by this polymerase chain reaction method. Results showed that aromatase mRNA is expressed in the brain, testis, and ovary, but scarcely at all in other tissues, including the placenta. In mouse brain, aromatase is mainly located in the forebrain, especially the diencephalon. In adult male and female diencephala, aromatase mRNA levels were 0.022 +/- 0.004 and 0.014 +/- 0.003 attomoles/micrograms total RNA, respectively. Aromatase in the diencephalon is known to participate in brain differentiation and sexual behavior, so changes in its mRNA levels in the brain during development were examined. Aromatase mRNA was first detected in the 12-day-old fetus and was found to increase rapidly during the fetal and neonatal periods. Its mRNA levels in male and female brains reached maxima of 0.068 +/- 0.008 and 0.059 +/- 0.006 attomoles/micrograms total RNA, respectively, 3-4 days after birth and then gradually decreased to adult levels. These observations are consistent with previous data indicating that the marginal period of neonatal imprinting of sexual differences is within a week after birth and suggest that brain aromatase may be important in sexual differentiation and behavior.

The aromatase cytochrome P-450 (P-450AROM) cDNA, which was identified by homologies in the DNA and in the deduced amino acid sequences with human P-450AROM cDNA, was isolated from a brain cDNA library of Japanese quail, demonstrating the presence of RNA transcripts of P-450AROM in the quail brain. To determine trace amounts of P-450AROM mRNA in the brain and to examine the effects of testosterone on its expression, a quantitative PCR method of RNA transcripts was developed. Brain total RNA was subjected to reverse transcription reaction and then quantitated by PCR from cDNA with a fluorescent dye-labeled primer. The quantity of P-450AROM mRNA was calculated by using an internal standard of modified P-450AROM (m-P-450AROM) RNA. The brain P-450AROM was primarily transcribed in the hypothalamus area (1.15 +/- 0.14 amol/micrograms of RNA) and traces of transcripts only were detected in the cerebellum (0.038 +/- 0.005 amol/micrograms of RNA). The P-450AROM mRNA in the hypothalamus of castrated quail was low (0.270 +/- 0.078 amol/micrograms of RNA) and increased 4- to 5-fold following treatment with testosterone. These results demonstrate, for the first time, that the increase in P-450AROM activity that is observed in the brain following treatment with testosterone results from a pretranslational regulation of the P-450AROM by androgens.

Bovine cytochrome P-450(SCC) introduced with the baculovirus host vector system was found to be expressed in Spodoptera frugiperda cells. Cell fractionation analysis indicated that the P-450(SCC) expressed as the precursor form was transported into mitochondria and converted to a mature form. However, this form did not exhibit definite activity for cholesterol side chain cleavage. These findings suggest that most of the P-450(SCC) expressed by this system is an inactive protein within mitochondria that is not folded to the conformation of the active enzyme and/or does not incorporate heme appropriately.

Introduction Peripherally localized aromatase, which converts circulating androgens into estrogens, is important in the pathogenesis of postmenopausal breast carcinomas. We have previously shown that aromatase mRNA levels are higher in elderly breast carcinomas (EldCa) than breast carcinomas of the control group (ContCa) or normal breast tissues. Aromatase expression has been reported to be regulated through the alternative use of multiple exons 1 (exons 1a-1f and so on); however, the preferential usage of exons 1 in elderly breast tissue has never been systematically examined. In order to properly treat and protect against EldCa, the regulation mechanism of aromatase expression in elderly breast tissues should be elucidated. The aim of the present study is to elucidate whether there are any specific patterns in use of multiple exons 1 in elderly breast tissue. Methods Usage of multiple exons 1 of the aromatase gene and mRNA levels of aromatase were examined by reverse transcription-polymerase chain reaction analysis in breast tissues of 38 elderly patients with breast cancer (age 80–99), and the results were compared with those in 35 patients of the control group (age 37–70). One-factor analysis of variance and the Scheffé test were used for the comparison of aromatase mRNA levels. Patterns of preferential utilization of multiple exons 1 of the aromatase gene were compared by χ2 test for independence or Fisher exact test for independence using a contingency table. Results Exon 1d was utilized much more frequently in elderly tissue than in the control group irrespective of cancerous or normal tissue (EldCa, 36/38, 95% versus ContCa, 7/35, 20%, P < 0.0001; normal tissue of the elderly, EldNorm, 30/34, 88% versus normal tissue of controls, ContNorm, 2/29, 7%, P < 0.0001). Twenty EldCa (53%) and 12 EldNorm (35%) used both exons 1c and 1d; however, their dominance was reversed (EldCa, all 1d > 1c; EldNorm, all 1c > 1d). Conclusions Elderly breast tissues exhibited specific patterns in use of multiple exons 1, which at least partly explained the higher aromatase levels in EldCa. The mechanisms of how these specific patterns occur during aging and carcinogenesis should be further examined.

Females gender itself is a risk factor for drug-induced torsades de pointes (TdP) arrhythmia which is associated with QT prolongation caused by blockade of human ether-a-go-go related gene (hERG) currents. Some clinical evidence suggests that estrogen is a determinant of the gender-differences in drug-induced QT prolongation and baseline QTC intervals. Although the chronic effects of estrogen have been studied, it remains unclear whether the gender differences are due entirely to transcriptional regulations through estrogen receptors. We here found that the most bioactive estrogen, 17beta-estradiol (E2), acutely delayed cardiac repolarization within the physiological serum level (0.1-1 nM). E2 slightly but significantly suppressed hERG currents (Kd = 0.6 nM) by modifying channel gating kinetics. Mutagenesis study showed the interaction of E2 with F656, a common drug-binding site at the inner pore-cavity of hERG. E2 enhanced both hERG suppression and QTC prolongation by its blocker, E4031. The lack of effects of testosterone on hERG currents and E4031-sensitivity implicates the critical role of aromatic centroid present in E2 but not in testosterone, which is supported by data from aromatase-null mice that cannot produce estrogen. The aromatase-null mice showed lower sensitivity to E4031-induced QT prolongation compared with those of wild type mice, and i.v. application of exogenous E2 (0.1 μg/kg) subsequent to E4031 administration rapidly prolonged QT intervals, indicating that aromatized estrogen emphasize the effect of E4031 on cardiac repolarization in vivo. Our data indicate that E2 acutely affects the hERG channel gating and the E4031-induced QTC prolongation, and may provide a novel mechanism for the higher susceptibility to drug-induced arrhythmia in women.

The distribution of aromatase-immunoreactive cells was studied by immunocytochemistry in the mouse forebrain using a purified polyclonal antibody raised against human placental aromatase. Labeled perikarya were found in the dorso-lateral parts of the medial and tuberal hypothalamus. Positive cells filled an area extending between the subincertal nucleus in the dorsal part, the ventromedial hypothalamic nucleus in the ventral part, and the internal capsule and the magnocellular nucleus of the lateral hypothalamus in the lateral part. The same distribution was seen in the two strains of mice that were studied (Jackson and Swiss), and the number of immunoreactive perikarya did not seem to be affected by castration or testosterone treatment. No immunoreactivity could be detected in the medial regions of the preoptic area and hypothalamus; these were expected to contain the enzyme based on assays of aromatase activity performed in rats and on indirect autoradiographic evidence in mice. Our data raise questions concerning the distribution of aromatase in the brain and the mode of action of the centrally produced estrogens.

To clarify the mechanism of phenobarbital-mediated increase in the CYP2B subfamily, we tried to detect target(s) of the inducer using azido-PB (AZPB), a photoaffinity ligand, as the probe. Immunoblot experiments with anti-AZPB antibody showed that binding of AZPB to proteins in rat liver microsomes the molecular weight of which is around 50 kDa is specifically competed by PB. Liver cytosol did not have any such proteins. When purified P450s were used as the target for AZPB, the binding was competed by PB most markedly in the CYP2B subfamily. The binding of AZPB to purified CYP2B2 was effectively lowered by 2, 2', 4, 4', 5, 5'-hexachlorobiphenyl, one of the potent inducers of the CYP2B subfamily, as well as PB. The other inducers for other subfamilies such as dexamethasone and β-naphthotlavone were without the effect. These results support the idea that the target of inducers mediating CYP2B induction is the CYP2B itself. To search the endogenous mediators which play a role in the CYP2B induction, we examined the role of steroid hormones and certain sterols in cultured rat hepatocytes. As the results, testosterone and the metabolites did not have ability to induce CYP2B proteins and to suppress PB-mediated induction. On the other hand, estradiol caused marked induction of the CYP2B 1/2. The role of estradiol was partially supported by experiments using aromatase-deficient mice: constitutive expression of the Cyp2b 10 in the knockout mice is less than the wild-type mice. The role of cholesterol and androstenol in the regulation of the rat CYP2B will also be presented.

This paper studies the performance of a diagonal channel Magnetohydrodynamic (MHD) power generation. This system includes a diagonal conducting wall MHD generator. As a model of channel, we use a scramjet-driven MHD generator where the MHD generator is directly integrated into the propulsion system. The channel specification is 59.28 cm in length. The working plasma for the power system is generated from freestream air and conventional scramjet fuels combustor. As a result, we present the flow velocity, current density distribution and power generated. And in this case, it can be found that the combustion efficiency of 95% has better power generation than 85 and 75% combustion efficiencies.

An immunocytochemical peroxidase-antiperoxidase procedure using a purified polyclonal antibody raised against human placental aromatase was used to localize aromatase-containing cells in the Japanese quail brain. Immunoreactive cells were found only in the preoptic area and hypothalamus, with a high density of positive cells being present in the sexually dimorphic medial preoptic nucleus, in the ventromedial nucleus of the hypothalamus and in the infundibulum. The positive material was localized in the perikarya and in adjacent cytoplasmic processes. Aromatase-containing cells were a specific marker for the sexually dimorphic preoptic nucleus. Treatment with testosterone produced a 6-fold increase in the aromatase activity of the preoptic area and a 4-fold increase in the number of immunoreactive cells in the medial preoptic nucleus. Thus, the increase in aromatase activity observed after testosterone administration is caused by a change in enzyme concentration.

Objective To assess the effect of aromatase inhibitors with GnRH agonist for a severe symptomatic adenomyosis that is refractory to GnRH agonist and danazol with GnRH agonist. Design Case report. Setting Clinical practice in university hospital. Patient(s) A 34-year-old woman with a complaint of severe dysmenorrheal, symptomatic anemia, and a desire to retain fertility. Intervention(s) Aromatase inhibitor anastrozole given orally (1.0 mg or 2.0 mg daily) for 16 weeks and GnRH agonist given monthly (injected SC, 1.8 mg) for 4 months. Main Outcome Measure(s) Measurements of uterine volume and levels of serum E 2 , estrone, A, dehydroepiandrosterone sulfate, LH, FSH, and CA125. Result(s) Uterine volume was reduced. The reduction rate of uterine volume estimated by magnetic resonance imaging and ultrasonography was 60% after 8 weeks of treatment. Conclusion(s) Aromatase inhibitor with GnRH agonist therapy was useful for the management of a severely adenomyotic woman whose desire was for conservative treatment.

This paper presents the hydrodynamie efficiency of ablation plasma produced by a pulsed ion beam, as obtained on the basis of the ion beam target interaction concept. We used a one-dimensional hydrodynamie model to explain the ablation acceleration behavior. Hydrodynamic variables are evaluated in terms of ablation velocity conversion efficiency and ablation efficiency. We obtained 18% value for the energy conversion efficiency, while an ablation efficiency of about 70% is achieved at an ion-beam energy density of 60 J cm -2 (beam power density of ≈1GWcm -2 ). A thrust producing capability is also investigated.

Introduction The expression of the oestrogen receptor (ER) is one of the more important clinical parameters of breast cancer. However, the relationship between the ER and its ligand, oestradiol, and the enzymes that synthesise it are not well understood. The expression of mRNA transcripts of members of the oestradiol metabolic and signalling pathways including the ER was studied in detail.

The 17 beta-hydroxysteroid dehydrogenases (17 beta HSDs) play an important role in the regulation of intracellular levels of biologically active sex steroid hormones in various human tissues. To date, eight distinctive 17 beta HSD enzymes have been cloned and characterized in humans. Among these isoenzymes, 17 beta HSD type 2 (17 beta HSD2) catalyses the conversion of testosterone into androstenedione and/or oestradiol into oestrone in various tissues, and it has thus been suggested to be involved in the biological inactivation of these sex steroids. The human gastrointestinal tract and liver are considered as the principle sites of inactivation and metabolism of various forms of orally administered sex steroids. We therefore examined 17 beta HSD2 expression and activity in human adult non-pathological gastrointestinal tract in order to clarify further the biological significance of this enzyme. A total of 80 specimens (40 from males and 40 from females) of normal oesophageal, stomach, duodenal, ileal, colonic and rectal tissues were examined for immunohistochemistry. Altogether, 17 tissue specimens were used for enzyme assay, and eight for RNA analysis. 17 beta HSD2 activity was detected in the stomach, duodenum, ileum, colon and rectum. 17 beta HSD2 mRNA was most abundant in the small intestine. 17 beta HSD2 immunoreactivity was localized almost exclusively to the absorptive epithelium, which may be involved in the inactivation of excessive endogenous and exogenous active sex steroids. Results from the present study thus suggest that the human gastrointestinal tract is an important sex steroid metabolizing organ in humans.

When we irradiate a foil with an intense pulsed ion beam, ablation plasma is created, and the foil is accelerated. In this study, we developed a numerical model of this phenomenon. We analyze the temperature and pressure of the ablation plasma, and the velocity of the accelerated foil by numerical simulation. It was possible for us to analyze the behavior and detailed results of the ablation plasma expansion and acceleration of the foil. We could also observe the processes of ablation plasma expansion and foil acceleration by back-lighting high-speed photography. The numerical results of foil velocity agree well with the experimental ones over a wide range of energy density values of an ion beam. We analyzed the time trend of the foil velocity, and we could observe that the foil is rapidly accelerated immediately after a delay.

Recent activities conserning pulsed power technology and its applications are reviewed. Using high-density ablation plasma produced due to the short range of an ion beam in targets, we have successfully prepared crystallized B4C thin films by ion-beam evaporation, which are characterized by hardness, wear resistance, and stability at high temperatures. Fullerenes have been prepared as well. Ultrafine nanosize powders were synthesized by pulsed wire discharge. Flue gas treatment of NO x was achieved by intense pulsed relativistic electron beam. Foil acceleration was observed to be ∼8 km/s at the ablation pressure of 13 GPa. Pulsed laser deposition was used to prepare (Cr1-x , Al x )N films. The AlN solubility limit was found to be 77 at.% AlN. The hardness of the films increases with x up to 0.75, and decreases rapidly due to their being amorphous in structure. A highly repetitive, new pulsed power generator is operational, with the specifications of 400 kV, 13 kA, 120 ns, and 1 pps.

Aromatase has been purified to homogeneity from human placental microsomes based on detection of its catalytic activities in the eluates from columns of octylamino-Sepharose 4B, hydroxylapatite, Mono S, hydroxylapatite HCA, and Mono Q. The purified preparation shows only one band corresponding to the apparent subunit molecular weight of 51,000 daltons on sodium dodecyl sulfate-polyacrylamide gel. The aromatase in the presence of NADPH and NADPH-cytochrome P-450 reductase converts testosterone to 17 beta-estradiol with the high specific activity of 103 nmol/min/mg of protein. However, whether the preparation is reduced by sodium dithionate chemically or by NADPH and the reductase enzymatically, its reduced, CO-difference spectrum has no peak at about 450 nm and has only a small peak at about 420 nm, probably due to its inactivation in spite of the catalytically full activity in the same preparation. The absolute spectrum of the aromatase exhibits a Soret peak at 423 nm in the absence of testosterone and addition of testosterone to the aromatase sample makes its absorption peak shift gradually from 423 to 393 nm (high spin type peak), which is a usual characteristic in the spectrum of cytochrome P-450. The reconstituted aromatase system efficiently catalyzes aromatization of 4-androstenedione, 19-hydroxy-4-androstenedione as well as testosterone. 16 alpha-Hydroxy-4-androstenedione and 16 alpha-hydroxytestosterone are also aromatized less efficiently and 19-nortestosterone is aromatized least efficiently. The reconstituted aromatase could scarcely oxidize various xenobiotics examined, suggesting a strict and narrow substrate specificity of this enzyme.(ABSTRACT TRUNCATED AT 250 WORDS)

A power-generation experiment with a disk MHD generator driven by potassium-seeded helium was made. High values of the output power density and of the enthalpy extraction have been obtained. For helium temperatures between 2200 and 2400 K, an output power density of 120 MW/cu m and an enthalpy extraction of 20.4 percent have been measured. The measured static pressure distribution has shown that strong gasdynamical shock has not been observed in the MHD channel under this high enthalpy extraction. It has been suggested that the disk generator performances can be predicted by one-dimensional calculations with ideal plasma parameters for the case of no negative potential region at the channel inlet and no shock formation in the disk generator. 11 refs.

By using both double-colony hybridization and an in situ immunostaining assay for transformants, 39 cDNA clones (clone p-16 alpha) encoding mouse liver microsomal testosterone 16 alpha-hydroxylase (cytochrome P-450(16) alpha) were isolated from a cDNA library constructed in the cloning vector pUC-9 with poly(A)+ RNA immunoenriched from total liver polysomes of male 129/J mice. mRNA selected by hybridization with clone p-16 alpha translated the P-450(16) alpha apoprotein in vitro. Total cellular proteins, which were prepared from immunopositive transformant Escherichia coli cells, were conjugated with Sepharose 4B. Antibody purified with the Sepharose 4B conjugate from mixed antiserum to P-450(16) alpha and P-450(15) alpha specifically inhibited testosterone 16 alpha-hydroxylase activity in microsomes. The cDNA insert of one recombinant plasmid (clone P-16 alpha-1) was 1.75 kilobases in size and contained one or more internal restriction sites for HindIII, BamHI, Bgl I, Pst I, Alu I, HinpI, and Rsa I. 32P-labeled clone p-16 alpha-1 hybridized with a single mRNA (2000 bases) that was 10 times more concentrated in liver cells from male 129/J mice than in female mice. This result was consistent with the finding that poly(A)+ RNA from male mice translated 10 times as much P-450(16) alpha in vitro as did the poly(A)+ RNA from females. Thus, the predominant expression of testosterone 16 alpha-hydroxylase in male 129/J mice is regulated pretranslationally, presumably at the transcriptional level of the P-450(16) alpha gene.

1. The subcellular distribution of nitrobenzene reduction activity in rat liver cells indicated the existence of two different enzyme systems, one localized in microsomes and the other localized in cytosol. The activity in the cytosol was mainly attributable to xanthine oxidase, judging from its substrate specificity and the inhibition by allopurinol. 2. The participation of the microsomal electron transport system in nitrobenzene reduction was examined by using antibodies against four components of the system, NADPH-cytochrome c reductase (fpT), NADH-cytochrome b5 reductase (fpD), cytochrome b5, and cytochrome P-450. Both NADH- and NADPH-dependent nitrobenzene reduction activities were strongly inhibited by anti-fpT IG and also by anti-P450 IG, but not inhibited by anti-fpD IG or anti-b5 IG. The reduction of nitrosobenzene and phenylhydroxylamine, which are supposed to be the intermediates of nitrobenzene reduction, was also examined, and it was found that NADH- and NADPH-dependent reduction of both compounds were strongly inhibited by anti-fpT IG and anti-P450 IG, but not by anti-fpD IG or anti-b5 IG. 3. Reconstruction experiments using purified NADPH-cytochrome P-450 reductase and cytochrome P-450 were also carried out and it was confirmed that the reduction of nitrobenzene, nitrosobenzene, and phenylhydroxylamine to aniline could be effected by these two components. 4. Nitrobenzene reduction by microsomes exhibited a short initial time lag and was activated by the addition of purified NADPH-cytochrome c reductase, whereas nitrosobenzene and phenylhydroxylamine reductions did not show any initial time lag and were not activated by the reductase. These observations suggest that the reduction of nitrobenzene to an intermediate, possibly nitrosobenzene or phenylhydroxylamine, limits the rate of aniline formation, and such an initial step of nitrobenzene reduction can be catalyzed by NADPH-cytochrome c reductase alone. Cytochrome P-450 is essential at least in the final step of nitrobenzene reduction to aniline. This conclusion was further confirmed by determination of these intermediates in nitrobenzene reduction.