Titanium nitride cardiac pacemaker electrodes

The sensing and pacing performance of pacemaker electrodes is characterized by the electrochemical properties of the electrodes/tissue layer; the usually smooth metallic electrode surface results in a high pass filter characteristic. Consequently, the detected intracardiac signals, which control the implantable systems, are not optimally matched to the spectral contents of the depolarisation signal. To avoid interference caused by noise (EMI, muscle potentials, etc.) a shift of the frequency of the band pass towards the lower frequency spectrum is required. As previously reported, the electrochemical properties of sintered and surface-treated electrodes prove the predicted improvement of sensing performance if titanium-nitride coated electrodes are used. Our results demonstrate their superiority above all the other electrodes presently known. The advantages can be referred to the micro-crystalline surface structure achieved by sputter-deposited electrode coatings and the kinetics of the ionic exchange. Furthermore, the acute thresholds achieved with the TiN-systems were significantly better than those of the smooth metallic surface. These results were also confirmed for chronic implants and are attributable to the known biocompatibility of titanium and its alloys.     

Aphidicolin does not inhibit DNA repair synthesis in ultraviolet-irradiated HeLa cells. A radioautographic study.

A radioautographic examination of nuclear DNA synthesis in unirradiated and u.v.-irradiated HeLa cells, in the presence and in the absence of aphidicolin, showed that aphidicolin inhibits nuclear DNA replication and has no detectable effect on DNA repair synthesis. Although the results establish that in u.v.-irradiated HeLa cells most of the DNA repair synthesis is not due to DNA polymerase alpha, they do not preclude a significant role for this enzyme in DNA repair processes.     

Plasmid- and strain-specific factors drive variation in ESBL-plasmid spread in vitro and in vivo

Horizontal gene transfer, mediated by conjugative plasmids, is a major driver of the global rise of antibiotic resistance. However, the relative contributions of factors that underlie the spread of plasmids and their roles in conjugation in vivo are unclear. To address this, we investigated the spread of clinical Extended Spectrum Beta-Lactamase (ESBL)-producing plasmids in the absence of antibiotics in vitro and in the mouse intestine. We hypothesised that plasmid properties would be the primary determinants of plasmid spread and that bacterial strain identity would also contribute. We found clinical Escherichia coli strains natively associated with ESBL-plasmids conjugated to three distinct E. coli strains and one Salmonella enterica serovar Typhimurium strain. Final transconjugant frequencies varied across plasmid, donor, and recipient combinations, with qualitative consistency when comparing transfer in vitro and in vivo in mice. In both environments, transconjugant frequencies for these natural strains and plasmids covaried with the presence/absence of transfer genes on ESBL-plasmids and were affected by plasmid incompatibility. By moving ESBL-plasmids out of their native hosts, we showed that donor and recipient strains also modulated transconjugant frequencies. This suggests that plasmid spread in the complex gut environment of animals and humans can be predicted based on in vitro testing and genetic data.Subject terms: Antibiotics, Microbial ecology, Phylogenomics