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Biomedical subjects

S Lock

Publications and source records attributed to S Lock.

At least 37 records · Page 2Linked to original sources
PubMed1988

Structured abstracts.

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Abstracting and Indexing↗
PubMed1988

Fraud in medicine.

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Biomedical Research↗
PubMed1987

Role of exposure parameters in toxicity of aerosolized diesel fuel in the rat.

Sprague-Dawley rats were exposed to aerosolized diesel fuel (ADF) to determine the potential health effects in military troops during exposure to this visual obscurrant. Acute range finding studies were performed to estimate exposure conditions at which minimal (less than 1%) mortality would occur. This information was used in the design of a repeated exposure study to test the relative significance of the frequency of exposures, the duration of exposure, and aerosol concentration in any toxicity which might occur. Animals were exposed once or three times per week for a total of nine times to concentrations ranging from 1.3 mg ADFl-1 to 6 mg ADFl-1 and exposure durations of 2 or 6 h. Body weight and food consumption were recorded at weekly intervals during the exposure period and in animals that were retained for 2 weeks after the last exposure. Animals were used for a variety of endpoints, including neurotoxicological tests, pulmonary function tests, hematology, clinical chemistry, organ weights, and histopathology, either within 2 days of the last exposure or after the 2-week recovery period. Animals exposed to ADF showed an initial depression in body weight followed by a slower rate of growth than the sham exposed controls. No exposure related changes were observed in any of the neurotoxicology assays. The lung was the primary site of toxicity. Focal accumulations of pulmonary free cells were observed histologically, with thickening and hypercellularity of nearby alveolar walls. The number of lavaged pulmonary free cells increased similarly. Both pulmonary wet and dry weights increased. Lung volumes were altered by exposure, including increased FRC and decreased TLC. Carbon monoxide diffusing capacity was decreased. Histologic abnormalities were not observed in any other organs. Of the exposure parameters tested, the frequency of exposure appeared to be the most significant in relation to degree of toxicity.

Aerosols↗
PubMed1986

Use of multiparameter analysis to quantitate hematological damage from exposure to a chemical (ethylene oxide).

This study was designed to test the value of a multiparameter approach in evaluating perturbations in bone marrow and peripheral blood elements of mice exposed to ethylene oxide (EtO). Mice exposed to 255 ppm EtO for 5 h/d were removed for analysis after 1, 2, 8, and 14 d (sequential exposure) and 4, 6, 8, and 10 wk (5 d/wk). Prior to sacrifice, blood was removed from the orbital sinus for blood cell counts, hemoglobin determination, and hematocrit. A blood film was made for differential leukocyte counts. Bone marrow was flushed from femurs and tibias and counted, and aliquot were used for stem-cell assay (CFU-S) or flow cytometry (FCM) analysis. One aliquot of marrow was stained with propidium iodide for cell-cycle analysis and another was reacted with fluorescein-conjugated monoclonal antibody for B-cell analysis. The preparations were analyzed for forward and 90 degrees scatter and fluorescence on an Ortho 50H cytofluorograph. Perturbations of peripheral leukocytes occurred after one exposure. After multiple exposures, hematocrit, red-cell number, and hemoglobin were generally depressed, with transient compensatory bursts, and bone marrow cellularity and CFU-S were below normal. However, white-cell numbers fluctuated dramatically during the exposure period. There was a shift in differential toward granulocytes, at times resulting in severely depressed numbers of lymphocytes in the peripheral blood. The FCM analysis showed an early depletion of granulocytes in the bone marrow followed by replacement and a relative lymphocyte deficit, especially pronounced at 10 wk. The B-cell changes reflected general lymphocyte perturbations. Shifts in numbers of cells in S and G/M were observed, consistent with a moderate bone marrow response to cell loss.

Animals↗
PubMed1985

Pulmonary toxicity of cyclophosphamide: a 1-year study.

The development of cyclophosphamide-induced pulmonary lesions over a 1-year period was studied in mice. Male BALB/c mice received a single intraperitoneal injection of 100 mg/kg of cyclophosphamide. Within 3 weeks there were scattered foci of intraalveolar foamy macrophages. With time, these foci increased in size and, 1 year later, occupied large areas in all lung lobes. There was also diffuse interstitial fibrosis. Chemical determination done 3, 12, 24, and 52 weeks after cyclophosphamide showed that lungs of animals treated with cyclophosphamide had significantly more hydroxyproline per lung than controls. One year after cyclophosphamide pressure-volume curves measured in vivo were shifted down and to the right and total lung volumes were decreased. A single injection of cyclophosphamide produced an irreversible and progressive pulmonary lesion.

Animals↗
PubMed1985

The effect and mode of action of zinc pyrithione on cell growth. I. In vitro studies.

The effects of zinc pyrithione (ZnPTO) were studied in a series of in vitro tests to determine whether its mode of action is primarily cytostatic or cytotoxic. Sodium pyrithione (NaPTO) was also studied, to check that pyrithione was the active moiety, and the known cytostatic chemical hydroxyurea was included for comparison. ZnPTO had a reversible inhibitory effect on the growth of BHK 21 cells at 0.1 microgram/ml, but had a rapid, irreversible inhibitory effect at 1 microgram/ml associated with cell rounding and detachment. NaPTO produced a similar effect but hydroxyurea produced an essentially reversible inhibition even at a dose well above that producing complete inhibition. ZnPTO and NaPTO both caused contraction, rounding and blebbing of BHK 21 cells in perfusion-chamber tests, at higher levels (1 and 10 micrograms/ml) than required for growth inhibition, but only 10 micrograms ZnPTO/ml caused lactate dehydrogenase (LDH) release. Hydroxyurea had no effects in these tests. ZnPTO and NaPTO also reduced the survival of Chinese hamster V79 cells sharply over a narrow dose range (0.01-0.03 microgram/ml), but the effect of hydroxyurea was not as sharp and occurred at much higher doses. All three showed elements of cytostasis and cytotoxicity as demonstrated by analysis of the relationship between survival and colony area. Of the three, only ZnPTO (at greater than or equal to 5 micrograms/ml) caused significant LDH release from the cells, though both ZnPTO and NaPTO (at 0.1-1 microgram/ml) inhibited cell growth as indicated by total LDH values. In studies with rat peritoneal mast cells, ZnPTO and NaPTO (at 10 ng/ml) both suppressed histamine release induced by 48/80 or Ca ionophore A23187, though neither caused histamine release directly. The combined results of these tests show that ZnPTO is primarily cytotoxic, rather than cytostatic.

Animals↗