Rechargeable silver-modified mercuric oxide-zinc cell for cardiac pacemakers

Tests were conducted on rechargeable mercury-zinc pacemaker batteries under simulated and actual biologic conditions, using a variety of discharge rates and charging schedules. In tests on 96 cells at a 6.4 milliampere (ma) discharge, recharging once every 15 months of simulated pacing at a 25 microampere (mua) drain, the earliest cell failure occurred after an equivalent of 50 years of pacing. The mean pacing equivalent for all 96 cells was more than 140 years. In 6.4 ma discharge tests on 24 cells, recharging once every 8 days of simulated pacing, only 1 cell in 24 failed after an equivalent of more than 500 years of pacing (actual time 2 years). In tests on 13 cells pacing at a 200 mua drain without recharging, the simulated mean duration of pacing before total discharge was 4.8 years. Seven other cells at a 200 mua drain with periodic recharging continue to function normally after more than 7 years of actual time, simulating 56 years of pacing at a 25 mua drain. Cardiac pacemakers using the rechargeable mercury-zinc cell have been implanted in animals for more than 2 1/2 years and in patients for more than 1 year with all units continuing to function satisfactorily. It has been demonstrated unequivocally that a rechargeable mercury-zinc pacemaker will function continuously for more than 4 years without recharging and that periodic recharging will extend pacing life far beyond that predicted for lithium and nuclear primary power sources.     

3' non-coding region sequences in eukaryotic messenger RNA

The sequence A-A-U-A-A-A is present in six different purified messenger RNA molecules (specifically the alpha-and beta-globulin mRNAs of rabbit and human, the immunoglobulin light chain mRNA of mouse (MOPC 21) and the ovalbumin mRNA of chicken) about 20 residues away from the 3'-terminal poly (A) sequence. In addition, a large selection of the 3' non-coding regions of rabbit and human globulin mRNAs (both the alpha and beta globin mRNAs) are 85% homologous, demonstrating that this region is significantly conserved in evolution.     

Mass spectrometric and toxicological assays of Athabasca oil sands naphthenic acids

This work concerns the analysis of model naphthenic acids and authentic naphthenic acids from the tailings ponds of the Athabasca tar sands. A first objective was to compare atmospheric pressure chemical ionization mass spectrometry (APCI-MS) with the previously studied electrospray mass spectrometry (ESI-MS) in this analysis. APCI-MS had a wider range of quantitation than ESI-MS, but its detection limit was poorer and model compounds showed greater variation in calibration sensitivity. A second objective was fractionation of naphthenic acids from tailings pond water and analysis by the Microtox toxicity assay. Fractionation on the basis of solubility gave fractions that did not differ significantly either in their congener distribution by ESI-MS or in their response to the Microtox assay. When partial separation was achieved by anion exchange chromatography, fractions with a higher proportion of multi-ring structures exhibited lower toxic potency. This finding is consistent with field observations that indicate that the toxic potency of tailings ponds water declines as the samples age-multi-ring structures are more highly branched and therefore more resistant to microbial degradation.     

Establishment and molecular characterization of five cell lines derived from renal and extrarenal malignant rhabdoid tumors

Malignant rhabdoid tumor (MRT) is a rare, enigmatic childhood cancer characterized by extreme aggressiveness and resistance to chemotherapy. To understand better the origin of the tumor and the mechanisms by which it develops and resists treatment, five cell lines were established from patients presenting with MRT (two renal and three extrarenal tumors). All of the cell lines display the light microscopic and ultrastructural features, as well as the variable immunohistochemical profile, characteristic of MRT. All are capable of forming tumors in nude mice. Three of the cell lines have detectable abnormalities of chromosome 22: one a t(22, 22) unbalanced translocation and two others a loss of heterozygosity of polymerase chain reaction-based microsatellite markers. Northern blot analysis showed that overexpression of the c-myc message was a consistent characteristic of the five MRTs evaluated. Although mutations of the p53 gene were not detectable by sequence analysis, all of the cell lines showed nuclear accumulation of the p53 protein by an immunocytochemical analysis in a minority of the cells. This result suggests that dysfunction in a p53-dependent apoptotic pathway might play a role in the multiple drug resistance phenotype of these tumors.