Roof Loads for Reliability Analysis of Lumber Properties Data

With load information reported in previous studies, distributions of maximum lifetime roof loads are developed in a form suitable for use in reliability analyses of lumber properties data. A lognormal distribution is chosen as best representing normalized maximum lifetime roof snow load.Examples are given in which contrasting lumber data sets are compared using the calculated load distributions and assuming that each set must provide equal reliability (equal safety) in the final design. A factor, k, resulting from this reliability analysis is shown to be a logical adjustment parameter for use in engineering design codes

Floor Loads for Reliability Analysis of Lumber Properties Data

Utilizing load information reported in previous studies, we have developed distributions of maximum lifetime floor live loads in a form suitable for use in reliability analyses of lumber properties data. An extreme value type I distribution is chosen as best representing normalized maximum lifetime floor live loads.Examples are given in which contrasting lumber data sets are compared using the calculated load distributions and assuming that each set must provide equal reliability, or equal safety, in the final design. A factor, k, resulting from the reliability analysis is shown to be a logical adjustment parameter for use in engineering design codes.Combining these results with those of an earlier paper, the selection of load distributions for use in reliability analysis of lumber properties data is discussed

Increased expression of the SNARE accessory protein Munc18c in lipid-mediated insulin resistance

Fatty acids inhibit insulin-mediated glucose metabolism in skeletal muscle, an effect largely attributed to defects in insulin-mediated glucose transport. Insulin-resistant mice transgenic for the overexpression of lipoprotein lipase (LPL) in skeletal muscle were used to examine the molecular mechanism(s) in more detail. Using DNA gene chip array technology, and confirmation by RT-PCR and Western analysis, increases in the yeast Sec1p homolog Munc18c mRNA and protein were found in the gastrocnemius muscle of transgenic mice, but not other tissues. Munc18c has been previously demonstrated to impair insulin-mediated glucose transport in mammalian cells in vitro. Of interest, stably transfected C2C12 cells overexpressing LPL not only demonstrated increases in Munc18c mRNA and protein but also in transcription rates of the Munc18c gene. jlr To confirm the relevance of fatty acid metabolism and insulin resistance to the expression of Munc18c in vivo, a 2-fold increase in Munc18c protein was demonstrated in mice fed a high-fat diet for 4 weeks. Together, these data are the first to implicate in vivo increases in Munc18c as a potential contributing mechanism to fatty acid-induced insulin resistance