Habitual coffee consumption and blood pressure: A study of self-defense officials in Japan

The degree of fat hydrogenation and the trans fatty acid content of the diet affect the fatty acid composition of membranes, and the amount and the activity of some membrane enzymes. We describe the effects of four isocaloric diets containing either sunflower oil (SO, 0% trans), fish oil (FO, 0.5% trans), partially hydrogenated fish oil (PHFO, 30% trans), or highly hydrogenated fish oil (HHFO, 3.6% trans) as fat sources on the lipid composition and the trans fatty acid content of rat hepatic microsomes. We also describe the effect of these diets on the cytochrome P-450 content and on the aminopyrine N-demethylase, aniline hydroxylase, and UDP-glucuronyl transferase microsomal activities. Cytochrome P-450 content was dependent on the degree of unsaturation of the diet, being higher for the FO-containing diet and lower for the HHFO diet. Aminopyrine N-demethylase activity also correlated with the degree of unsaturation of the diet as did the cytochrome P-450 content did (FO > SO > PHFO > HHFO). Aniline hydroxylase activity appeared to be independent of the degree of unsaturation of the dietary fat, but correlated with the trans fatty acid content of the diet, which was also reflected in the trans content of the microsomal membranes. UDP-glucuronyl transferase activity was higher for the FO-containing diet than for the SO diet, showing intermediate values after the PHFO and HHFO diets.     

Modification of physicochemical properties of actin filaments suppresses cell fragmentation in the execution phase of staurosporine-induced apoptotic processes

Effects of jasplakinolide (JSP), a stabilizer of F-actin, and latrunculin A (LTA), a destabilizer of F-actin, on a series of events occurring in the execution phase of staurosporine (STS)-induced apoptotic processes were studied using human osteosarcoma 143B cells. Time-dependent apparent increases of the population of cells with collapsed membrane potential of mitochondria (Delta Psi(m)) caused by STS treatment were not due to actual decreases in the Delta Psi(m) per cell, but due to the fragmentation of cells resulting in decreases in the number of active mitochondria per cell. Decreases in the Delta Psi(m) in fragmented cells occurred late in the execution phase. Both JSP and LAT failed to prevent STS-induced release of cytochrome c from mitochondria followed by the activation of caspases 3 and 9, the cleavage of poly (ADP-ribose) polymerase (PARP) and apoptotic nuclear fragmentation. However, both drugs prevented STS-induced apoptotic cell fragmentation and decreases in the Delta Psi(m). These results indicate that physicochemical states of actin filaments play a certain role in the execution phase of STS-induced apoptotic processes.     

Characterization of polymer-adhesive interfaces on a nanometre scale by elemental mapping and image EELS using EFTEM

Energy-filtering transmission electron microscopy (EFTEM) was applied for investigating interfaces between a polymer and an adhesive. The sample employed in this work is polybutylene terephtharate (PBT) sheets laminated with an epoxy adhesive. It was found that heat aging of the PBT at 180 degrees C in air for > 9 h prior to adhesion decreases the adhesion strength drastically. To investigate this unfavourable aging effect on the adhesion strength, we performed elemental mapping and image EELS using EFTEM. A weak boundary layer with a thickness of < 50 nm was visualized at the PBT-adhesive interface by elemental mapping in the sample subjected to the heat aging and image EELS revealed the origin of this layer. Thus, we clearly correlated the nanoscale interfacial structure with the adhesion strength by EFTEM.     

Formation of the myosin.ADP.gallium fluoride complex and its solution structure by small-angle synchrotron X-ray scattering

The products of the SOS-regulated umuDC operon are required for most UV and chemical mutagenesis in Escherichia coli, a process that results from a translesion synthesis mechanism. The UmuD protein is activated for its role in mutagenesis by a RecA-facilitated autodigestion that removes the N-terminal 24 amino acids. A previous genetic screen for nonmutable umuD mutants had resulted in the isolation of a set of missense mutants that produced UmuD proteins that were deficient in RecA-mediated cleavage (J. R. Battista, T. Ohta, T. Nohmi, W. Sun, and G. C. Walker, Proc. Natl. Acad. Sci. USA 87:7190-7194, 1990). To identify elements of the UmuD' protein necessary for its role in translesion synthesis, we began with umuD', a modified form of the umuD gene that directly encodes the UmuD' protein, and obtained missense umuD' mutants deficient in UV and methyl methanesulfonate mutagenesis. The D39G, L40R, and T51I mutations affect residues located at the UmuD'2 homodimer interface and interfere with homodimer formation in vivo. The D75A mutation affects a highly conserved residue located at one end of the central strand in a three-stranded beta-sheet and appears to interfere with UmuD'2 homodimer formation indirectly by affecting the structure of the UmuD' monomer. When expressed from a multicopy plasmid, the L40R umuD' mutant gene exhibited a dominant negative effect on a chromosomal umuD+ gene with respect to UV mutagenesis, suggesting that the mutation has an effect on UmuD' function that goes beyond its impairment of homodimer formation. The G129D mutation affects a highly conserved residue that lies at the end of the long C-terminal beta-strand and results in a mutant UmuD' protein that exhibits a strongly dominant negative effect on UV mutagenesis in a umuD+ strain. The A30V and E35K mutations alter residues in the N-terminal arms of the UmuD'2 homodimer, which are mobile in solution.