ETARA PC version 3.3 user's guide: Reliability, availability, maintainability simulation model

A user's manual describing an interactive, menu-driven, personal computer based Monte Carlo reliability, availability, and maintainability simulation program called event time availability reliability (ETARA) is discussed. Given a reliability block diagram representation of a system, ETARA simulates the behavior of the system over a specified period of time using Monte Carlo methods to generate block failure and repair intervals as a function of exponential and/or Weibull distributions. Availability parameters such as equivalent availability, state availability (percentage of time as a particular output state capability), continuous state duration and number of state occurrences can be calculated. Initial spares allotment and spares replenishment on a resupply cycle can be simulated. The number of block failures are tabulated both individually and by block type, as well as total downtime, repair time, and time waiting for spares. Also, maintenance man-hours per year and system reliability, with or without repair, at or above a particular output capability can be calculated over a cumulative period of time or at specific points in time

Design, fabrication, and test of a steel spar wind turbine blade

The design and fabrication of wind turbine blades based on 60 foot steel spars are discussed. Performance and blade load information is given and compared to analytical prediction. In addition, performance is compared to that of the original MOD-O aluminum blades. Costs for building the two blades are given, and a projection is made for the cost in mass production. Design improvements to reduce weight and improve fatigue life are suggested

CD36 and Na/K-ATPase- α 1 Form a Proinflammatory Signaling Loop in Kidney

Proatherogenic, hyperlipidemic states demonstrate increases in circulating ligands for scavenger receptor CD36 (eg, oxidized low-density lipoprotein [oxLDL]) and the Na/K-ATPase (eg, cardiotonic steroids). These factors increase inflammation, oxidative stress, and progression of chronic kidney disease. We hypothesized that diet-induced obesity and hyperlipidemia potentiate a CD36/Na/K-ATPase–dependent inflammatory paracrine loop between proximal tubule cells (PTCs) and their associated macrophages and thereby facilitate development of chronic inflammation and tubulointerstitial fibrosis. ApoE-/- and apoE-/-/cd36-/- mice were fed a high-fat diet for ≤32 weeks and examined for physiologic and histologic changes in renal function. Compared with apoE-/-, apoE-/-/cd36-/- mice had improved creatinine clearance and blood pressure which corresponded histologically with less glomerular and tubulointerstitial macrophage accumulation, foam cell formation, oxidant stress, and interstitial fibrosis. Coimmunopreciptation and a cell surface fluorescence-based crosslinking assay showed that CD36 and Na/K-ATPase α-1 colocalized in PTCs and macrophages, and this association was increased by oxLDL or the cardiotonic steroid ouabain. OxLDL and ouabain also increased activation of Src and Lyn in PTCs. Cell-free conditioned medium from PTCs treated with oxLDL or ouabain increased macrophage migration. OxLDL, ouabain, or plasma isolated from high-fat diet–fed mice stimulated reactive oxygen species production in PTCs, which was inhibited by N-acetyl-cysteine, apocynin, or Na/K-ATPase α-1 knockdown. These data suggest that ligands generated in hyperlipidemic states activate CD36 and the Na/K-ATPase and potentiate an inflammatory signaling loop involving PTCs and their associated macrophages, which facilitates the development of chronic inflammation, oxidantstress, and fibrosis underlying the renal dysfunction common to proatherogenic, hyperlipidemic states