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We fabricated in situ powder-in-tube processed MgB 2 /Fe tapes using aromatic hydrocarbon of benzene, naphthalene, and thiophene as additives, and investigated the superconducting properties. We found that these aromatic hydrocarbons were very effective for increasing the Jc values. The Jc values of 20mol% benzene-added tapes reached 130A/mm 2 at 4.2K and 10T. This value was almost comparable to that of 10mol% SiC -added tapes and about four times higher than that of tapes with no additions.Microstructure analyses suggest that this Jc enhancement is due to both the substitution of carbon for boron in MgB 2 and the smaller MgB 2 grain size.The MgB 2 superconductor is expected to be applied to practical superconducting wires because its transition temperature, 39K, is much higher than those of conventional metallic superconductors.The lower cost of the raw materials, Mg and B, than that of Nb, is an additional advantage of MgB 2 .Recently, small coils using MgB 2 wires have been produced. In order to evaluate the potential of MgB 2 for power applications, wire processing techniques are now being actively developed throughout the world. The most popular method is the so-called in situ powder-in-tube (PIT) method,

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Sericin, a constituent of the silkworm cocoon, was added to the culture of four mammalian cell lines: murine hybridoma 2E3-O,human hepatoblastoma HepG2, human epithelial HeLa and human embryonal kidney 293 cells. The proliferation of all cell lineswas accelerated in the presence of sericin. The hybridoma cellline was further studied. The 2E3-O cell line was so well adapted to serum-free medium that both the proliferation rate and maximum cell density in serum-free ASF103 medium were higher than in RPMI medium supplemented with all lots of FBS tested, and this proliferation was stimulated by the addition of sericin in a dose-dependent manner. Stimulation was observed at sericin concentrations from 0.01 to 0.1 %, although 1% sericin was severely harmful to the culture. In comparison with bovine serum albumin (BSA), a widely used supplement in serum-free medium, sericin had an equivalent effect on the proliferation of the hybridomas and sericin additively stimulated the proliferation with BSA. Although heat easily denatures and inactivates most proteins, the activity of sericin was not affected by autoclaving. In a similar manner to the silkworm-derived sericin, recombinant sericin synthesized in E. coli also stimulated the hybridoma proliferation, irrespective of whether it was autoclaved or filtered. Since BSA is obtained from bovine serum and the risk of infections such as bovine spongiform encephalopathy cannot be eradicated, sericin derived from insects could be a preferable culture medium supplement for stimulating the proliferation of mammalian cells.

Reproductive and developmental disorders are the most sensitive toxic effects caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). TCDD is thought to produce many, if not all, of these toxic effects by impairing steroidogenesis and/or steroid action during the prenatal or early postnatal stages. However, the mechanism of the antisex steroid effect of TCDD is not well understood. This study revealed that steroidogenic acute-regulatory protein (StAR), a key transporter of cholesterol for steroidogenesis, in the testes of fetal rats are down-regulated by maternal exposure to TCDD. It was also shown that many mRNAs of steroidogenetic enzymes, including cytochromes P450 11A1, 17, and 11B1 and 3beta-hydroxysteroid dehydrogenase, are reduced in fetuses of TCDD-treated dams in a testis-specific manner. The same was also observed for the expression of estrogen-alpha receptors and androgen receptors. Whereas StAR expression was not affected by TCDD in cultured fetal testis, the fetal serum content of LH, a pituitary regulator of StAR, was significantly reduced by TCDD. In agreement with this, pituitary expression of LHbeta subunit mRNA in fetuses was reduced by maternal exposure to TCDD, whereas the alpha-subunit remained unchanged. The reduction in LHbeta is suggested to occur by a mechanism different from the reduction in the GnRH level. Direct supply of exogenous gonadotropin to TCDD-exposed fetuses completely abolished the reduction of StAR expression. Taken together, these results demonstrate that TCDD impairs steroidogenesis in the fetus by targeting pituitary gonadotropins.