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The aim of this research was to study the wettability and solderability of SiC ceramics by the use of an active solder of the type Sn5Sb3Ti in a vacuum by electron beam heating. This solder exerts a narrow melting interval, and only one thermal effect, a peritectic reaction, was observed. The liquidus temperature of the solder is approximately 243 °C. The solder consists of a tin matrix where the Ti6(Sb,Sn)5 and TiSbSn phases are precipitated. The solder wettability on a SiC substrate decreases with decreasing soldering temperature. The best wetting angle of 33° was obtained in a vacuum at the temperature of 950 °C. The bond between the SiC ceramics and the solder was formed due to the interaction of Ti and Ni with silicon contained in the SiC ceramics. The formation of new TiSi2 and Ti3Ni5Si6 phases, which form the reaction layer and thus ensure the bond formation, was observed. The bond with Ni is formed due to the solubility of Ni in the tin solder. Two phases, namely the Ni3Sn2 and Ni3Sn phases, were identified in the transition zone of the Ni/Sn5Sb3Ti joint. The highest shear strength, around 40 MPa, was attained at the soldering temperature of 850 °C.

The proliferative peptide adrenomedullin (AM) has a wide distribution in a variety of tissues and cells. The mechanism how the AM gene is regulated in cells is not yet known. The renal cortex, renal vascular smooth muscles, glomeruli and tubular epithelial cells are very sensitive to hypoxia. Renal hypoxia produces acute renal tubular necrosis and markedly induces AM expression in damaged cells. However, little information is available regarding the possible pathophysiological production and release of renal tubular AM. Regulation of membrane-bound AM receptors in renal cells has not yet been systematically studied. To elucidate the potential pathological role of human AM we examined the production and release of AM, as well as the characteristics of surface membrane AM receptors in cultured monkey renal tubular epithelial cells (RC) exposed to hypoxia, induced with endothelin-1, and subjected to glucose deprivation. Exposure of RC to hypoxia (1 % O(2), 5 % CO(2) in N(2)), and to phorbol 12-myristate 13-acetate (PMA) increased production and secretion of AM and increased specific [(125)I]AM binding on RC. Metabolic stress (1 % glucose in the cultivation medium) and preincubation of RC with rival peptide endothelin-1 significantly reduced immunoreactive-AM in a conditioned medium and whole cell surface membrane AM binding on RC. Altogether, our data suggest that the AM is involved in the adaptation of renal tubular cells to hypoxia. Increased expression of AM mRNA and regulation of AM receptors in metabolic stress may function as an important autocrine/paracrine regulator(s) of renal tubular epithelial cells.