The optically active form of tritium-labeled A-factor (2-isocapryloyl-3R-hydroxymethyl-gamma-butyrolactone), a pleiotropic autoregulator responsible for streptomycin production, streptomycin resistance, and sporulation in Streptomyces griseus, was chemically synthesized. By using the radioactive A-factor, a binding protein for A-factor was detected in the cytoplasmic fraction of this organism. The binding protein had an apparent molecular weight of approximately 26,000, as determined by gel filtration. Scatchard analysis suggested that A-factor bound the protein in the molar ratio of 1:1 with a binding constant, Kd, of 0.7 nM. The number of the binding protein was roughly estimated to be 37 per genome. The "inducing material" virginiae butanolide C (VB-C), which has a structure very similar to that of A-factor and is essential for virginiamycin production in Streptomyces virginiae, did not inhibit binding. In addition, no protein capable of specifically binding 3H-labeled VB-C was found in S. griseus. Together with the observation that VB-C had almost no biological activity on the restoration of streptomycin production or sporulation in an A-factor-deficient mutant of S. griseus, these results indicated that the binding protein had a strict ligand specificity. Examination for an A-factor-binding protein in Streptomyces coelicolor A3(2) and Streptomyces lividans showed the absence of any specifically binding protein.

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Phosphorus is diffused into silicon at 900 'C from a phosphorus-doped silicon-dioxide layer. Since a profile of phosphorus concentration is expressed by a function of x 1yT,' where x is the distance from a surface and t the diffusion time, diffusion coefficients are determined by the Boltzmann-Matano method. They are larger than the intrinsic diffusion coefficient and are dependent not only on the concentration (the concentration effect) but also on some unknown condition at a surface (the surface effect). The surface effect extends more than 20 /J-deep into a bulk of silicon, and is stronger than the concentration effect. All of phosphorus atoms are located at substitutional sites. Diffusion-induced dislocations are not found. A new mechanism for the generation of excess vacancies is suggested. The new mechanism consists of the following: (i) Phosphorus diffuses by a vacancy mechanism. The diffusion of phosphorus occurs only through the diffusion of E centers. (ii) When phosphorus atoms enter from a surface into a bulk, they should be in a form of E centers. Affected by a surface, a large amount of E centers is formed per unit time at a surface. (iii) The E centers flow into a bulk. (iv) By their dissociations, excess vacancies are generated. The surface effect and the emitter dip effect are attributed to excess vacancies.

Several studies have reported the effects of vitamin C (L-ascorbic acid, AA) on ultraviolet B (UVB)-induced cell damage using cultured keratinocytes. However, the epidermis consists of multiple cell layers, and the effect of AA on UVB-induced damage to the human epidermis remains unclear. Therefore, we investigated the effect of AA on UVB-induced skin damage using reconstituted human epidermis. The reconstituted human epidermal surface was treated with 100 and 500 mM AA and cultured for 3 h before (pre-AA treatment) or after (post-AA treatment) 120 mJ/cm2 UVB irradiation. Pre- and post-AA treatments of the epidermal surface suppressed UVB-induced cell death, apoptosis, DNA damage, reactive oxygen species (ROS) production, and the inflammatory response by downregulating tumour necrosis factor-α (TNF-α) expression and release. Moreover, the pre-AA treatment was more effective at preventing UVB-induced skin damage than the post-AA treatment. In summary, pre- and post-AA treatments of the epidermis prevent UVB-induced damage.