Toru Itoh

Indomethacin (IND) inhibits an enhanced renin release following the captopril, SQ 14225, administration.

Abstract The present study was done to investigate the role of endogenous prostaglandins in the mechanism of renin release stimulated by angio-tensin I-converting enzyme inhibitor, SQ 14225 in 9 hypertensive patients and 3 normotensive subjects. Plasma renin activity was significantly i increased after the administration of SQ 14225 and decreased to control levels after the addition of indomethacin. Pre-treatment with indomethacin also inhibited the augmentation of renin release following the SQ 14225 administration. Urinary excretion of prostaglandin E was not significantly increased after the SQ 14225 administration but significantly decreased after the administration of indomethacin. The present data that the augmented renin release due to the suppression of the negative short feedback mechanism of renin release by SQ 14225 was inhibited by indomethacin suggest that endogenous prostaglandin system may contribute to the short feedback mechanism of renin release.

Estimation of Urinary Kininogenase Activity Using Bovine Serum Low Molecular Weight Kininogen

Estimation of urinary kininogenase activity by radioimmunoassay of generated kinin was studied. Bovine serum low molecular weight kininogen was proved not to cross-react with kallidin antibody and also bradykinin antibody. This kininogen was used as substrate measuring urinary kininogenase activity. Separation of released kinin from the kininogen was not required in the present method. Urinary kallikrein activity was found to be significantly decreased in essential hypertension, in chronic glomerulonephritis and in patients who had received renal transplantation. On the contrary, an increase in urinary kallikrein was found in primary aldosteronism and in Bartters syndrome. The present method was very useful for measuring kininogenase activity.

T Lymphocyte Precursors Migrate Towards Chemotactic Peptides Secreted by Embryonic or Juvenile Thymus

During embryonic life the thymic rudiment is extensively seeded by invading hemopoietic precursors that give rise to mature T cells (1). In birds thymus, colonization by precursor cells is limited to two defined time periods of embryonic development (2). The first hemopoietic precursor cells appear at day 5 in the thymus of quail embryos. At this stage of development the precursors were enriched in the perithymic region. These precursors are often in contact with endothelial cells of the jugular vein, a prefered site of extravasation; they are also dispersed within the mesenchymal tissue around the thymus, and adhere to the basal lamina that separates the thymus from the mesenchyme (3).

Silicon carbide microfabrication by silicon lost molding for glass press molds

This paper describes two silicon carbide (SiC) microfabrication processes for SiC glass-press molds. One is silicon lost molding combined with SiC chemical-vapor deposition (CVD) and SiC reaction sintering (RS). The other is silicon lost molding combined with SiC CVD and SiC solid-state reaction bonding (SSRB). In both of these processes, an original pattern on a silicon substrate is transferred to a CVD SiC film, and then the film is backed by bulk SiC to obtain rigidity and robustness against pressing force. Finally, the silicon substrate is etched away to release a SiC mold. In the process using SiC CVD and RS, an original pattern on a silicon substrate was transferred to a SiC mold, but the surface roughness of the SiC mold was 0.05-0.08 mum Ra, and worse than required by the glass-press mold. This was caused by the transformation of amorphous SiC to polycrystalline SiC in RS, which was confirmed by the X-ray diffraction (XRD) data of the CVD SiC film before and after RS. In the process using SiC CVD and SSRB, the surface of the SiC mold was smooth (0.004-0.008 mum Ra) without the crystallization of the amorphous CVD SiC film. The SiC mold was pressed to Pyrex glass to demonstrate its high-temperature strength. The Pyrex glass was deformed by the SiC mold at 850 degC without a void, and no significant deformation of the SiC mold was observed