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In the case of cyclically loaded brazed joints, especially in safety-relevant components like common rail systems for common rail direct fuel injection, it is necessary to reliably estimate the fatigue strength, considering the influence of different manufacturing processes, manufacturing parameters, and failure behavior. In this paper, induction-brazed, vacuum-brazed, and continuous furnace-brazed joints are used to develop a reliable approach to assess the fatigue life. Therefore, the specimens were characterized and tested under load control using constant amplitudes. It is found that the local brazing geometry in conjunction with the surface condition, which differs by different topography values and by the position and number of initial defects, have the most influence on the failure behavior and consequently on the fatigue strength. Irrespective of this, however, it is shown that the fatigue strength can be estimated sufficiently well even with a simplified finite element modeling that uses idealized fillet radii and by taking support effects into account.

Brazing is a joining technique used in many industries for components that consist of many individual parts. Many of these components are cyclically loaded during service. For this reason, reliable approaches to assess the service life must be developed. For this purpose, it is necessary to gain knowledge about factors influencing the fatigue strength and the damage behavior. In this paper induction, vacuum- and continuous furnace brazed shear and peel specimen with different brazing gap widths are analyzed. Therefore, the specimens were characterized, measuring the geometry of the specimens and surface condition of the brazing radii, and tested under load control using constant amplitudes. It is found that the manufacturing process and the parameters used have a significant influence on the mechanical properties of the brazing material, the surface condition and the profile of the fillet radii. These properties have again an influence on the damage behavior and the fatigue strength. In particular crack-like defects of varying severity, which can extend deep into the brazing material, that are located in highly stressed areas of the fillet radii have a significant influence on the fatigue strength. It is also found that, regardless of the brazing process used, there is a tendency in the area of the brazing gap width for the number and size of defects to increase with increasing gap size, which can negatively affect fatigue strength depending on the damage behavior.

The induction of experimental arthritis in rhesus monkeys was studied by intradermal immunization of bovine type II collagen and antigens derived fromMycobacterium tuberculosis, Streptococcus pyogenes, andEubacterium aerofaciens. The tested bacterial antigens proved to be not arthritogenic. Bovine type II collagen induced clinical arthritis in 50% of the rhesus monkeys. Type II collagen induced arthritis in rhesus monkeys proved to be a potential model to study clinical, serological, histological, genetic, and immunologic features associated with human RA.

Type II collagen-induced arthritis (CIA) is an experimentally inducible autoimmune disorder that is, just like several forms of human arthritis, influenced by a genetic background. Immunization of young rhesus monkeys (Macaca mulatta) with type II collagen (CII) induced CIA in about 70% of the animals. One major histocompatibility complex (MHC) class I allele was present only in young animals resistant to CIA and absent in arthritic animals. This strong association suggests that the MHC class I allele itself, or a closely linked gene, determines resistance to CIA. The mechanism controlling the resistance to CIA becomes less efficient in aged animals since older rhesus monkeys, which were positive for the resistance marker, developed a mild form of arthritis. At the cellular level it is demonstrated that resistance to CIA is reflected by a low responsiveness of T cells to CII. This association between a specified MHC class I allele and resistance to an autoimmune disease points at the importance of the MHC class I region in the regulation of the immune response to an autoantigen.