'Neurological' complications of extradural bupivacaine.
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Biomedical subjects
Publications and source records attributed to M Logan.
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Three bovine cell lines and four ovine cell lines infected with Theileria parva or Theileria annulata were examined for the production of interferon (IFN). Biologically active IFN was detected in the tissue culture supernatants of four of the cell lines. Only one, a bovine cell line infected with T. parva, produced IFN-gamma as measured by specific neutralization with a monoclonal antibody to bovine IFN-gamma. This observation was confirmed by analysing RNA from the cell lines on Northern blots using an IFN-gamma cDNA probe. The other three cell lines which produced IFN were infected with T. annulata. The IFN produced by those lines was not IFN-gamma.
The pharmacokinetics of tazobactam (500 mg) administered intravenously alone were compared with the pharmacokinetics of tazobactam coadministered with piperacillin (4 g), and the penetration into an inflammatory exudate in six healthy males was studied. Piperacillin influenced the pharmacokinetics of tazobactam. The mean levels of tazobactam in plasma at 4 h were 0.6 microgram/ml when it was given alone and 1.2 micrograms/ml when it was given with piperacillin (P = 0.0003). The mean total clearances of tazobactam were 203.5 and 134.2 ml/min (P = 0.035) when it was given alone and with piperacillin, respectively There were no significant differences in the elimination half lives, areas under the concentration-time curve from 0 h to infinity, or volumes of distribution. Inflammatory exudate penetration was rapid, and the mean maximum levels of tazobactam attained were 6.4 and 11.3 micrograms/ml when it was given alone or with piperacillin, respectively (P less than 0.06). The mean percent penetration of tazobactam and the area under the concentration-time curve from 0 h to infinity in inflammatory exudate were greater when tazobactam was given with piperacillin. The mean 24-h urinary recoveries of tazobactam were 63.7% +/- 7.9% when it was given alone and 56.8% +/- 2.7% when it was given with piperacillin. The explanation for the differences in the pharmacokinetics of tazobactam when it was administered alone compared with those when it was given with piperacillin was unclear.
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The experience of selecting and implementing a nursing model appropriate to the nursing course in the first year of the generic baccalaureate programme of the University of Ottawa School of Nursing is described. Many challenges surfaced for the professors in year one as this curriculum change was implemented. Four challenges: (1) adapting the course to be congruent with the Roy model, (2) developing teaching tools suitable for student learning, (3) sequencing of content for student learning, and (4) obtaining competent role models, and how they were met, are discussed.
In this article, current knowledge of nursing diagnosis is compared to the assumptions of the Roy Adaptation Model for Nursing. More specifically the relationship between the aetiology component of diagnostic statements and stimuli is explored. Examples of nursing diagnoses from the literature are also presented to analyse the relationship between aetiologies and independent nurse functions.
The pharmacokinetics and penetration into a cantharidine-induced inflammatory exudate of meropenem was studied in six volunteers following a single 1-g intravenous dose. Concentrations in plasma, urine, and the inflammatory exudate were determined by a microbiological assay. The mean elimination half-life of meropenem in plasma was 1.1 h, with the concentration in plasma declining from a mean of 23.6 micrograms/ml at 1 h to 0.7 micrograms/ml at 6 h. The inflammatory fluid penetration was rapid (time to maximum concentration of drug in serum, 0.75 h), and the penetration was 111%. The recovery of meropenem in urine at 24 h was 65.4% of the administered dose.
Suspensions of Nitrosomonas europaea catalyzed the ammonia-stimulated aerobic transformation of the halogenated aliphatic compounds dichloromethane, dibromomethane, trichloromethane (chloroform), bromoethane, 1,2-dibromoethane (ethylene dibromide), 1,1,2-trichloroethane, 1,1,1-trichloroethane, monochloroethylene (vinyl chloride), gem-dichloroethylene, cis- and trans-dichloroethylene, cis-dibromoethylene, trichloroethylene, and 1,2,3-trichloropropane, Tetrachloromethane (carbon tetrachloride), tetrachloroethylene (perchloroethylene), and trans-dibromoethylene were not degraded.
Four patients on continuous ambulatory peritoneal dialysis (CAPD) developed large, symptomatic pleural effusions after commencing peritoneal dialysis. Pleuroperitoneal fistula in each case was diagnosed by the presence of a high glucose content in pleural fluid, with a normal corresponding blood sugar, and was confirmed by isotope or contrast peritoneography. Two patients had their effusions drained percutaneously, and then underwent pleural sclerosis with intracavitary tetracycline. Two patients had a thoracotomy performed, of which no fistula was identified in one case, and the other patient underwent pleurectomy. All four patients successfully recommenced CAPD several weeks after therapy, without recurrence of effusions. We conclude that pleuroperitoneal connections associated with CAPD do not mandate cessation of peritoneal dialysis and conversion to maintenance haemodialysis. Definitive diagnosis requires aspiration of pleural effusions for glucose estimation. Contrast or isotopic peritoneography is helpful in localising the fistula, but in our experience did not alter management. Simple sclerotherapy is effective and avoids the need for a formal thoracotomy.
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Suspensions of Nitrosomonas europaea are shown to cause the complete disappearance of 10 microM trichloroethylene at rates of 1 microM mg protein-1. The reaction continues at nearly this rate for many hours. Fresh cells catalyze the reaction in the absence of added ammonium (presumably utilizing endogenous ammonia or stored reductant). In older cells, trichloroethylene degradation depends on the addition of ammonia. Acetylene, 2-chloro 6-trichloromethylpyridine and alpha alpha'dipyridyl, which inhibit the oxidation of ammonia by cells, inhibit the degradation of trichloroethylene. Thus degradation of trichloroethylene is dependent on- and possibly catalyzed by the ammonia oxidizing enzyme.
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