Auricular vulnerability: what information can be obtained from the study of auricular vulnerability? How to perform this study?

The factors involved in atrial vulnerability are the presence of intra-atrial conduction disorders and abnormalities of refractory periods which are short, dispersed and poorly adapted to heart rate. All these factors are arrthythmogenic. The main value of the study of atrial vulnerability consists of investigation of unexplained ischaemic cerebrovascular accidents in young subjects. In practice, atrial vulnerability can be measured in the context of a classical endocavitary electrophysiological investigation. The stimulation and recording parameters must be standardized. Latent atrial vulnerability can be considered to be present when at least one of the following elements are found: significant inducibility, very short and poorly adapted effective refractory periods, decreased latent atrial vulnerability index.     

An evaluation of the bactericidal effect of the Nd:YAP laser

The aim of this in vitro study was to compare the efficacy of a classical irrigant with that of a laser in disinfecting a contaminated root canal. Thirty canals of extracted single-root teeth were prepared with files to size #20. The teeth were sterilized with Germispad (Spad, France) for 30 min and then inoculated with Streptococcus mitis ATCC 33399. By randomization, the teeth were divided into six groups of five teeth each. In the first group, teeth were neither inoculated nor prepared. This was the sterility control group (1). In the second group (2) teeth were inoculated without any preparation: as positive controls. The third group was inoculated and then hand-instrumented with files to size #30 with 5.25% NaOCl as irrigant. This was the hand instrumentation group. The other groups were prepared with hand instrumentation with files to size #30, using sterile water as an irrigant, and the canal was then lased with different frequencies as follows: group 4, frequency of 5 Hz and power of 260 mJ; group 5, frequency of 10 Hz and power of 310 mJ; and group 6, frequency of 30 Hz and power of 300 mJ. After experimentation, the residual colonies were counted. The results indicated that (i) the treatment with NaOCl and manual instrumentation effectively inhibited the growth of Streptococcus mitis ATCC 33399; and (ii) the antibacterial effect of the Nd:YAP laser depended on the frequency. Only a frequency of 30 Hz of the Nd:YAP laser inhibited the growth of Streptococcus mitis ATCC 333999.     

Normal processing of AP sites in Apn1-deficient Saccharomyces cerevisiae is restored by Escherichia coli genes expressing either exonuclease III or endonuclease III

Escherichia coli exonuclease III and endonuclease III are two distinct DNA-repair enzymes that can cleave apurinic/apyrimidinic (AP) sites by different mechanisms. While the AP endonuclease activity of exonuclease III generates a 3'-hydroxyl group at AP sites, the AP lyase activity of endonuclease III produces a 3'-alpha,beta unsaturated aldehyde that prevents DNA-repair synthesis. Saccharomyces cerevisiae Apn1 is the major AP endonuclease/3'-diesterase that also produces a 3'-hydroxyl group at the AP site, but it is unrelated to either exonuclease III or endonuclease III. apn1 deletion mutants are unable to repair AP sites generated by the alkylating agent methyl methane sulphonate and display a spontaneous mutator phenotype. This work shows that either exonuclease III or endonuclease III can functionally replace yeast Apn1 in the repair of AP sites. Two conclusions can be derived from these findings. The first of these conclusions is that yeast cells can complete the repair of AP sites even though they are cleaved by AP lyase. This implies that AP lyase can contribute significantly to the repair of AP sites and that yeast cells have the ability to process the alpha,beta unsaturated aldehyde produced by endonuclease III. The second of these conclusions is that unrepaired AP sites are strictly the cause of the high spontaneous mutation rate in the apn1 deletion mutant.     

The complete amino acid sequence of a Kunitz family trypsin inhibitor from seeds of Acacia confusa

The complete amino acid sequence of a Kunitz-type two-chain trypsin inhibitor was determined for the first time. The sequence of the inhibitor from Acacia confusa (ACTI) was determined by analysis of peptides obtained from the reduced and S-carboxymethylated protein by digestion with endopeptidase Lys-C, endopeptidase Arg-C, and V8 endopeptidase. ACTI is comprised of two chains, namely A and B chains linked by the disulfide bridge between Cys(133) and Cys(141), and the inhibitor consists of 175 amino acid residues, 136 residues in the A-chain and 39 residues in the B-chain. The N-terminal amino acid sequence of ACTI shows extensive homology to the trypsin inhibitors from Acacia elata and Albizzia julibrissin, while the whole amino acid sequence of ACTI has a high degree of homology to the other Kunitz-type trypsin inhibitors from soybeans, winged bean seeds [Psophocarpus tetragonolobus (L) DC.], and seeds of Erythrina species.     

Inhibitors of phospholipase promote apoptosis of human endothelial cells

In order to understand the signal transduction system that regulates apoptosis of human umbilical vein endothelial cells (HUVEC), we investigated the effects of inhibitors of the activity of phospholipases. All three tested inhibitors of phospholipase A2 (PLA2), namely, manoalide, 3-(4-octadecyl)benzoylacrylic acid (OBAA), and oleyoxyethylphosphorylcholine (OOPC), induced apoptotic cell death of HUVEC. After 16 h of treatment, almost all of the cells had disintegrated into apoptotic bodies, and DNA ladders characteristic of apoptotic cell death were clearly observed upon analysis of DNA on agarose gels. The release of arachidonic acid from the cells that had been treated with manoalide, OBAA or OOPC (at the same concentrations as those at which these compounds induced apoptosis) was inhibited. We also studied the effects of two inhibitors of phosphatidylinositol-specific phospholipase C (PLC), U73122, and compound 48/80. Both compounds promoted the apoptosis of HUVEC. After 16 h of treatment, few cells remained intact, and DNA fragmentation was clearly detectable after only 12 h. Quantitation of inositol released from cells treated with U73122 and compound 48/80 showed that the release of inositol was blocked. By contrast, U73343, a similar aminosteroid that does not inactivate PLC, had no such effects. Our results suggest that PLA2 and phosphatidylinositol-specific PLC might be involved in the signaling pathway of apoptosis in HUVEC, and that the metabolism of arachidonic acid and of inositol might play important roles in the present apoptotic signal-transduction system.