ABSTRACT
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.
ABSTRACT
OBJECTIVE: It is not yet clear how oxidative stress, free radicals, inflammatory cytokines and chemoattractants produced in the heart induce chronic heart failure. The myocardial damage caused by chronic diabetes results either from the persistence of inflammatory signaling directly in the heart or from the dysregulation of anti-inflammatory signaling systems. In the rat model of streptozotocin-induced diabetes (STZD) we investigated 1/ the concentration of free radicals (FR), 2/ reduced glutathione (GSH), 3/ lysozomal enzymes, 4/ inflammatory cytokines (tumor necrosis factor-? (TNF-?) and interleukin-6 (IL-6)), and monocyte chemoattractant protein-1 (mcp-1) in the myocardium. METHODS: Diabetes was induced in 12 male Wistar rats by injection of streptozotocin (STZ). The free radical scavenger and cardiac protectant SMe1EC2 (10 mg/kg/d.) was given orally for 5 days and 5 weeks and these animals were compared with the diabetic and non-diabetic controls. RESULTS: We found reduced heart rate and rate dependent functions of the rat heart, early release of free radicals triggering the release of cytotoxic inflammatory cytokines (like TNF-? and IL-6) and chemoattractants (mcp-1) as an example of this type of pathogens, resulting in the initiation and progression of cardiac pathology. The reduced myocardial contractility after STZD was accompanied with the increased reactive responsiveness of isolated aorta and mesenteric artery to phenylephrine, with increased production of chemoattractive proteins directly in the myocardium, with increased activity of peripheral beta-N-acetyl-glucosaminidase (NAGA), as representative of lysosomal activation processes. The pretreatment of SME1EC2 reduced increase in vascular reactivity, reduced myocardial depression and protected against myocardial toxicity. CONCLUSION: The newly identified and specific cardiac protectant SMe1EC2 could serve as a prospective target in the treatment of increased myocardial cytokine and chemoattractive proteins in diabetic cardiomyopathy.
