Biomedical subjects
Publications and source records attributed to S Sparrow.
The use of Phaneuf's Nursing Audit in an action research project that is investigating quality assessment and peer review is discussed. A brief description of the project is given followed by an analysis of the audit tool. This analysis suggests that the tool has more disadvantages than advantages. The paper concludes with a discussion about why the tool may be of use despite the disadvantages identified.
The nursing staff on an acute medical hospital ward elected to wear their own clothes to work for a period of 2 months. The trial was evaluated using a variety of research methods and it raised a number of issues about the role of uniform, about patients' perceptions of nurses and nurses' perceptions of their role. The study has led to questions being raised about the assumptions that are made if uniform is worn and the appropriateness of a uniform dress.
Sodium chromate (20 mg/kg, s.c.), which in male rats inflicted necrotic damage mainly in the P1 region (proximal part of the proximal convoluted tubules), protected against proximal tubular necrosis induced by 0.5 or 3.0 mg Hg2+/kg in the P2 (distal part of the proximal convoluted tubules) and P3 (pars recta part of the proximal tubules) regions. Histochemical staining for mercury indicated that chromate increased mercury deposition in those cells of the P1 region which were unaffected by chromate (had intact brush border) but did not decrease mercury deposition in the most severely affected P3 region. Chromate pretreatment actually increased mercury deposition in the kidneys of animals killed 24 h after the injection of 0.5 mg Hg2+. The protective effect was mutual. Cellular proliferation and fibrosis observed 4-5 days after chromate were prevented by injecting 0.5 mg Hg2+/kg 3 days after chromate treatment.
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The protective effect of selenite, seleno-dl-methionine and biological selenium against the renotoxicity of mercury was tested in rats. As the source of biological selenium, the liver soluble fraction of rats given 60 mumoles/kg selenite 3 days before sacrifice was used. The aim of the experiments was to test whether protective efficiency follows the reported order of ability to form HgSe. Mercury was given subcutaneously in doses of 2.5, 5.0 and 7.5 mumoles/kg HgCl2 and selenium was given in equimolar doses at the same time as Hg2+. Liver soluble fraction, biological selenium or liver soluble fraction supplemented with selenite or seleno-dl-methionine were given orally, while in experiments without liver soluble fraction the two selenium compounds were given subcutaneously. Biological selenium was tested only at the two lower dose levels. Both biological selenium and seleno-dl-methionine decreased the urinary excretion of mercury in the first 48 h, but less so than selenite and only selenite decreased the renal content of mercury at the end of this period. Urinary alkaline phosphatase activity and plasma urea nitrogen at the 2.5 and 5.0 mumoles/kg dose levels decreased in the order of no selenium greater than biological selenium greater than seleno-dl-methionine greater than selenite. As the reported HgSe formation increases in the same order, the experiments support the role of HgSe formation in the protective effect. The degree of necrotic damage in the P2 and P3 regions of the proximal tubular cells increased in the same order as the biochemical indicators at the 5.0 and 7.5 mumoles/kg dose levels.(ABSTRACT TRUNCATED AT 250 WORDS)
The static exposure of rats to 0.25 mg/l methyl isocyanate for 1 h resulted in damage to the epithelium of the proximal bronchioles and upper airways. Bronchiolar cells exhibited both nuclear and cytoplasmic damage; many epithelial cells, particularly in the bronchi and trachea, were killed and/or dislodged from the basement membrane. A "raft" of cell debris and fibrin lined most of the airways during the 1st week after exposure but repair to the underlying epithelium was well advanced within 2-3 days. The majority of airways were lined by a normal epithelium within 3 weeks of exposure, but isolated foci of hyperplasia and occluded airways probably accounted for continued respiratory impairment.
The fact that the only chemicals known to be potent carcinogens for the esophagus in animals are certain nitrosamines suggests that these environmental carcinogens could be a cause of human esophageal cancer. Epidemiological investigations support this concept. The level of exposure alone is not considered sufficient to account for the very high incidence of the disease in certain regions, but potentiating factors have been shown to have a dramatic effect on nitrosamine-induced esophageal cancer in animal experiments. A likely enhancing factor is consumption of food contaminated by molds, especially by Fusaria spp, a group known to produce trichothecene mycotoxins. The effect of simultaneous treatment with diacetoxyscirpenol (DS) on methyl-benzyl-nitrosamine (NMBzA)-induced esophageal cancer was studied. Feeding a diet containing DS at 10 ppm for 10 weeks caused thickening of the basal cell layer of the esophageal epithelium, but feeding DS (10 ppm) simultaneously with NMBzA (4, 8, 16 ppm) for 10 weeks, or feeding a lower dose of DS with NMBzA for a longer period, or administration of DS per os at intervals during NMBzA treatment, did not potentiate but possibly reduced esophageal tumors. Toxicity, revealed by reduced growth rate of DS-fed animals, may have inhibited carcinogenesis. In contrast to the rapid potentiating effect of zinc deficiency, DS does not appear to cause an early enhancement of esophageal cancer.
During the routine serial passage of over 30 human tumour xenografts in athymic (nu. nu.) mice over a period of 6 years the induction of murine fibrosarcomas at the site of transplantation has been observed on three occasions. In two cases it has been possible to follow the development of these tumours over successive transplant generations. These sarcomas had growth rates, tumour karyotypes and isoenzyme patterns which clearly distinguished them from the original human xenografts.
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The extensive renal tubular necrosis that results in male rats after the intravenous injection of a single, low dose of equine kidney cadmium (Cd), zinc(Zn)-metallothionein (MT) (0.2 mg MT-bound-Cd/kg body wt.) is followed within 72 h by active regeneration. With repeated administration of the same dose at 3- or 4-day intervals, lesion resolves although, at least initially, the kidney content of Cd increases progressively. At any time during treatment, about 40% of the accumulated Cd is bound as the endogenous (Cd, Cu)MT. The rate of increase in the renal Cd content is dependent on the ratio of Cd:Zn in the injected metalloprotein, and is appreciably less when the constant dose of protein-bound Cd is given as a (2.4 Cd:1 Zn)MT, than as a (3.0 Cd:1 Zn)MT. On repeated administration of the latter preparation, however, the concentration of Cd in the kidney does not attain a critical concentration, above which persistent tubular damage occurs, but reaches a maximum of about 150-160 micrograms Cd/g wet wt. (after 16 doses) and then declines. After 19 doses of the (2.4 Cd:1 Zn)MT under the same conditions, the renal Cd concentration is submaximal and is less (92 micrograms Cd/g wet wt.) than that after either 16 or 27 doses of the (3.0 Cd:1 Zn)MT. In animals that are dosed with either of the heterologous MT preparations, the first dose, although not innocuous, seems to protect the kidneys against further damage by subsequent doses. Repeated doses, however, lead to vascular changes, e.g. lymphoid infiltration, periarteriole oedema and dilation of the arcuate veins, and to dilation of the glomerular spaces.
Neurotoxicity and renotoxicity were compared in rats given by gastric gavage five daily doses of 8.0 mg Hg/kg methyl- or ethylmercuric chloride or 9.6 mg Hg/kg ethylmercuric chloride. Three or 10 days after the last treatment day rats treated with either 8.0 or 9.6 mg Hg/kg ethylmercury had higher total or organic mercury concentrations in blood and lower concentrations in kidneys and brain than methylmercury-treated rats. In each of these tissues the inorganic mercury concentration was higher after ethyl- than after methylmercury. Weight loss relative to the expected body weight and renal damage was higher in ethylmercury-treated rats than in rats given equimolar doses of methylmercury. These effects became more severe when the dose of ethylmercury was increased by 20%. Thus in renotoxicity the renal concentration of inorganic mercury seems to be more important than the concentration of organic or total mercury. In methylmercury-treated rats damage and inorganic mercury deposits were restricted to the P2 region of the proximal tubules, while in ethylmercury-treated rats the distribution of mercury and damage was more widespread. There was little difference in the neurotoxicities of methylmercury and ethylmercury when effects on the dorsal root ganglia or coordination disorders were compared. Based on both criteria, an equimolar dose of ethylmercury was less neurotoxic than methylmercury, but a 20% increase in the dose of ethylmercury was enough to raise the sum of coordination disorder scores slightly and ganglion damage significantly above those in methylmercury-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Male Wistar (Porton) rats were dosed by gavage with trimethyltin chloride in arachis oil at doses of 3, 6 and 10 mg/kg. Water consumption and urine production were monitored for 3 days after dosing and at the end of this period the rats were killed and the kidneys were examined histologically. Within 6 h of dosing there was an increase in urine production and in the pH of the urine in all treated groups. Within 24 h of dosing there was an increase in water consumption. Histopathological examination of the kidney at 3 days post-treatment showed nephrotoxic changes ranging from slight vacuolisation of the proximal tubular cells with loss of the brush borders in the 3 mg/kg group to extensive vacuolar degeneration with tubular dilation and evidence of cellular regeneration in the 10 mg/kg group. The results suggest that trimethyltin causes a rapid kidney dysfunction in rats by cytotoxic action on the cells of the proximal tubular epithelium and that this action is dose-related.
Static exposure of rats to methyl isocyanate, for one hour, led to respiratory impairment during and after exposure. The resultant changes in breathing pattern suggest that this compound is both a sensory and a pulmonary irritant. Low concentrations resulted in extensive necrosis and loss of epithelial cells in the proximal airways but widespread alveolar damage was found only after exposure to high, lethal concentrations. At high concentrations methyl isocyanate probably caused peracute death through reflex inhibition of breathing. Animals surviving the exposure exhibited signs of airway narrowing and development of (haemorrhagic) pulmonary oedema. The epithelial lesions were repaired rapidly, but residual peribronchial fibrosis and signs of renewed injury/inflammation were apparent.
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