Effects of vitamin E and flaxseed on rumen-derived fatty acid intermediates in beef intramuscular fat

To elucidate the effects of dietary vitamin E with or without flaxseed on beef fatty acid composition, 80 feedlot steers were fed 4 diets: Control-E (451 IU dl-α-tocopheryl acetate/head/day), Control+E (1051 IU dl-α-tocopheryl acetate/head/day), Flax-E (10% ground) and Flax+E. Vitamin E had no effect on animal growth or carcass weight (p>0.05), while flaxseed-fed steers had greater average daily gain (p=0.007), final live weight (p=0.005) and heavier carcasses (p=0.012). Feeding flaxseed increased the total n-3 fatty acid content of beef and this response was further accentuated by the inclusion of high levels of vitamin E in the diet. Feeding flax increased levels of some 18:3n-3 partial hydrogenation products including c15- and t13/14-18:1 and several 18:2 isomers (p<0.001) but decreased t10-18:1 (p<0.001). Vitamin E enhanced intramuscular levels of 18:3n-3 and its biohydrogenation products leading to greater accumulations of total n-3 fatty acids in lean ground beef. The consequences of increasing the concentrations of partially hydrogenated products on human health have yet to be investigated.     

Norepinephrine inhibits a toxin resistant Ca2+ current in carotid body glomus cells: evidence for a direct G protein mechanism

The rabies virus glycoprotein molecule (G) can be divided into two parts separated by a flexible hinge: the NH2 half (site II part) containing antigenic site II up to the linear region (amino acids [aa] 253 to 275 encompassing epitope VI [aa 264]) and the COOH half (site III part) containing antigenic site III and the transmembrane and cytoplasmic domains. The structural and immunological roles of each part were investigated by cell transfection and mouse DNA-based immunization with homogeneous and chimeric G genes formed by fusion of the site II part of one genotype (GT) with the site III part of the same or another GT. Various site II-site III combinations between G genes of PV (Pasteur virus strain) rabies (GT1), Mokola (GT3), and EBL1 (European bat lyssavirus 1 [GT5]) viruses were tested. Plasmids pGPV-PV, pGMok-Mok, pGMok-PV, and pGEBL1-PV induced transient expression of correctly transported and folded antigens in neuroblastoma cells and virus-neutralizing antibodies against parental viruses in mice, whereas, pG-PVIII (site III part only) and pGPV-Mok did not. The site III part of PV (GT1) was a strong inducer of T helper cells and was very effective at presenting the site II part of various GTs. Both parts are required for correct folding and transport of chimeric G proteins which have a strong potential value for immunological studies and development of multivalent vaccines. Chimeric plasmid pGEBL1-PV broadens the spectrum of protection against European lyssavirus genotypes (GT1, GT5, and GT6).     

Protein kinase calpha regulates human monocyte O-2 production and low density lipoprotein lipid oxidation

Our previous studies have shown that human native low density lipoprotein (LDL) can be oxidized by activated human monocytes. In this process, both activation of protein kinase C (PKC) and induction of superoxide anion (O-2) production are required. PKC is a family of isoenzymes, and the functional roles of individual PKC isoenzymes are believed to differ based on subcellular location and distinct responses to regulatory signals. We have shown that the PKC isoenzyme that is required for both monocyte O-2 production and oxidation of LDL is a member of the conventional PKC group of PKC isoenzymes (Li, Q., and Cathcart, M. K. (1994) J. Biol. Chem. 269, 17508-17515). The conventional PKC group includes PKCalpha, PKCbetaI, PKCbetaII, and PKCgamma. With the exception of PKCgamma, each of these isoenzymes was detected in human monocytes. In these studies, we investigated the requirement for select PKC isoenzymes in the process of monocyte-mediated LDL lipid oxidation. Our data indicate that PKC activity was rapidly induced upon monocyte activation with the majority of the activity residing in the membrane/particulate fraction. This enhanced PKC activity was sustained for up to 24 h after activation. PKCalpha, PKCbetaI, and PKCbetaII protein levels were induced upon monocyte activation, and PKCalpha and PKCbetaII substantially shifted their location from the cytosol to the particulate/membrane fraction. To distinguish between these isoenzymes for regulating monocyte O-2 production and LDL oxidation, PKCalpha or PKCbeta isoenzyme-specific antisense oligonucleotides were used to selectively suppress isoenzyme expression. We found that suppression of PKCalpha expression inhibited both monocyte-mediated O-2 production and LDL lipid oxidation by activated human monocytes. In contrast, inhibition of PKCbeta expression (including both PKCbetaI and PKCbetaII) did not affect O-2 production or LDL lipid oxidation. Further studies demonstrated that the respiratory burst oxidase responsible for O-2 production remained functionally intact in monocytes with depressed levels of PKCalpha because O-2 production could be restored by treating the monocytes with arachidonic acid. Taken together, our data reveal that PKCalpha, and not PKCbetaI or PKCbetaII, is the predominant isoenzyme required for O-2 production and maximal oxidation of LDL by activated human monocytes.     

RNA-Mediated interference of a cdc25 homolog in Caenorhabditis elegans results in defects in the embryonic cortical membrane, meiosis, and mitosis

Infrared spectra of a carbon dioxide sample enriched with oxygen-17 have been recorded with a resolution of about 0.0025 cm-1 in the region of the laser bands near 10 and 9 μm, using the long path difference Fourier Transform Spectrometer of the LPMA in Paris. The two laser bands of the 16O12C17O and 17O12C18O species have been analyzed for the first time. Line intensities for several isotopic species have been measured in this region and the rotationless transition dipole moments and Herman-Wallis coefficients of the corresponding bands have been reported. In particular intensities, alternation in the spectra of 17O12C17O has been analyzed. Copyright 1999 Academic Press.     

Optimal reliability of systems subject to imperfect fault-coverage

This paper maximizes the reliability of systems subjected to imperfect fault-coverage. The results include the effect of common-cause failures and `maximum allowable spare limit'. The generalized results are presented and then the policies for some specific systems are given. The systems considered include parallel, parallel-series, series parallel, k-out-of-n, and NMR (k-out-of-(2k-1)) systems. The results are generalized for the non s-identical component case