Intrinsic instability of flame–acoustic coupling

This paper shows that a flame can be an intrinsically unstable acoustic element. The finding is clarified in the framework of an acoustic network model, where the flame is described by an acoustic scattering matrix. The instability of the flame acoustic coupling is shown to become dominating in the limit of no acoustic reflections. This is in contrast to classical standing-wave thermoacoustic modes, which originate from the positive feedback loop between system acoustics and the flame. These findings imply that the effectiveness of passive thermoacoustic damping devices is limited by the intrinsic stability properties of the flame.     

Base excision repair deficient mice lacking the Aag alkyladenine DNA glycosylase

3-methyladenine (3MeA) DNA glycosylases remove 3MeAs from alkylated DNA to initiate the base excision repair pathway. Here we report the generation of mice deficient in the 3MeA DNA glycosylase encoded by the Aag (Mpg) gene. Alkyladenine DNA glycosylase turns out to be the major DNA glycosylase not only for the cytotoxic 3MeA DNA lesion, but also for the mutagenic 1,N6-ethenoadenine (epsilonA) and hypoxanthine lesions. Aag appears to be the only 3MeA and hypoxanthine DNA glycosylase in liver, testes, kidney, and lung, and the only epsilonA DNA glycosylase in liver, testes, and kidney; another epsilonA DNA glycosylase may be expressed in lung. Although alkyladenine DNA glycosylase has the capacity to remove 8-oxoguanine DNA lesions, it does not appear to be the major glycosylase for 8-oxoguanine repair. Fibroblasts derived from Aag -/- mice are alkylation sensitive, indicating that Aag -/- mice may be similarly sensitive.     

Modeling of a linear PM Machine including magnetic saturation and end effects: maximum force-to-current ratio

The use of linear permanent-magnet (PM) actuators increases in a wide variety of applications because of their high force density, robustness, and accuracy. These linear PM motors are often heavily loaded during short intervals of high acceleration, so that magnetic saturation occurs. This paper models saturation and end effects in linear PM motors using magnetic circuit models. The saturating parts of the magnetic circuit are modeled as nonlinear reluctances. Magnetomotive forces represent the currents and the magnets. This paper shows that when saturated, a negative d-axis current increases the force developed by the motor. Although the increase is not large, it is nevertheless useful, because a negative d-axis current also results in a decrease in the amplifier rating. Further, the trajectory for the maximum force-to-current ratio is derived. The correlation between the calculated and the measured force justifies the model.     

The electric variable transmission

First, an electromechanical converter with two mechanical ports and one electrical port (consisting of two concentric machines and two inverters) is considered. This converter works as a continuously variable transmission between the mechanical ports and may, e.g., replace the clutch, gearbox, generator, and starter motor in a motor vehicle. The working principle of this converter is explained. Next, a new converter, the electric variable transmission (EVT), is presented. This converter has similar properties, but is smaller and lighter. The EVT may be seen as built up from two concentric induction machines with a combined relatively thin yoke. Thus, we obtain one electromagnetic device instead of two magnetically separated devices. The working principle of the EVT is explained, and its losses are discussed.     

Xeroderma pigmentosum group F caused by a defect in a structure-specific DNA repair endonuclease

Rheumatoid arthritis (RA) is a chronic joint disease characterized by leukocyte invasion and synoviocyte activation followed by cartilage and bone destruction. Its etiology and pathogenesis are poorly understood. We describe a spontaneous mouse model of this syndrome, generated fortuitously by crossing a T cell receptor (TCR) transgenic line with the NOD strain. All offspring develop a joint disease highly reminiscent of RA in man. The trigger for the murine disorder is chance recognition of a NOD-derived major histocompatibility complex (MHC) class II molecule by the transgenic TCR; progression to arthritis involves CD4+ T, B, and probably myeloid cells. Thus, a joint-specific disease need not arise from response to a joint-specific antigen but can be precipitated by a breakdown in general mechanisms of self-tolerance resulting in systemic self-reactivity. We suggest that human RA develops by an analogous mechanism.