Biomedical subjects
Publications and source records attributed to C F Simpson.
The construction and evaluation of a gamma-ray detector for capillary zone electrophoresis is described. The detector was shown to have a linear response from the limit of detection 10 to 500 Bqcm-3 corresponding to 5.1 x 10(-17) to 2.55 x 10(-15) gcm-3 43Tc99m. The application of the detector for the analysis of some radiopharmaceuticals is presented.
A sample of amosite asbestos was modified by effectively adding C8 and C18 hydrocarbon chains to the fibre surfaces. The altered fibres interacted less readily with cells in vitro and were less cytotoxic. In whole animals the number of mesotheliomas produced by the C8 material was the same as that with the parent material but the tumours occurred earlier. The C18 derivatized fibre was markedly less active in the production of tumours. This is the first report demonstrating that similar size fibres with differing surfaces have different pathogenic properties.
We have been examining a number of chemically modified mineral fibers, derived from amosite asbestos, by in vitro methods to clarify the role of the fiber surface in determining biological activity. The various fibers have identical size distributions but differ in their affinities for components of the cell membrane. They were treated with boiling toluene or chemically modified by treatment with alkyldimethylchlorosilanes (R = C8, C18) that react with free-surface hydroxyl groups to form the corresponding siloxanes. Fibers in MEM supplemented with 15% fetal calf serum were added to a suspension of V79-4 cells labeled with tritiated thymidine and the mixture was incubated. Aliquots of this mixture were spun down on a density gradient to determine the degree of cell-fiber interaction. At 37 degrees C native amosite (UICC standard) stuck to cells within 15 min of incubation, and the amount of sticking was maximum within 70 min. Decreasing the temperature decreased the amount of sticking, and at 20 degrees C no sticking was observable. The chemically modified amosite and the amosite treated with boiling toluene did not stick to the cells even after 70 min. Soaking the toluene-treated amosite with aqueous solutions at room temperature for 48 hr produced a material that had the same sticking properties as the original untreated fiber. These results indicate that the silanol content, and possibly the degree of hydration of the fiber surface, is important for a fiber to stick to a cell surface.
The conformational changes of the protein alpha-chymotrypsinogen which may take place on reversed-phase chromatographic material of differing hydrocarbon chain lengths e.g. C4, C6, C8, C10 and phenyl, have been studied by circular dichroism as a function of 1-propanol concentration and pH of the solvent before and after binding to the reversed-phase material.
Six dogs with spontaneous heartworm disease were injected with a single dose of ivermectin. After 48 h of treatment, microfilariae counts were reduced by 92%-98% of pretreatment counts. In pretreatment biopsies examined by light and electron microscopy, microfilariae were unaltered in the sinusoids of the liver and also in the glomerular capillaries and interstitial blood vessels of the kidney. However, there was irregular thickening and dense deposits in the basement membranes of glomerular capillaries, along with a modest increase in mesangial cells and matrix. In post-treatment liver biopsies examined by light microscopy, there were numerous granulomas in the sinusoids which contained degenerated microfilariae. In post-treatment kidney biopsies there was moderate thickening of glomerular basement membranes along with pronounced proliferation of mesangial cells and matrix. Glomerular capillaries were partially or completely occluded by degenerated microfilariae. In addition, there were interstitial granulomas in the kidney. It was observed with the aid of electron microscopy that highly vacuolated and degenerated microfilariae were incorporated into granulomas in the liver sinusoids of post-treatment biopsies. In post-treatment kidney biopsies glomerular capillaries were usually occluded by degenerated microfilariae. Basement membranes were thickened and contained dense deposits. Mesangial cells and matrix were extensively increased. Interstitial granulomas in the kidney contained dead microfilariae.
The erythrocytes of 2 cats experimentally infected with Cytauxzoon felis were examined by light and electron microscopy. In stained blood smears, parasitized erythrocytes usually contained a single, roundish organism, but occasionally up to 4 were present in a cell. Chains of these roundish organisms also were seen. Elongated parasites, sometimes with ear-like projections, were present in a few erythrocytes. By electron microscopy, the parasite contained a poorly defined nucleus, rough endoplasmic reticulum, ribosomes, nonplicated mitochondria, food vacuoles, and a cytostome on its limiting membrane. Usually, the parasite was oval, but budding forms also were evident. Crystalloid inclusions were present in parasitized and nonparasitized erythrocytes.
Schizonts in the liver of 2 cats with cytauxzoonosis were studied by both light and electron microscopies. By light microscopy, the cytoplasm of macrophages in the sinusoids and small vascular channels contained schizonts with cytomeres or both cytomeres and mature merozoites. By electron microscopy, it was determined that schizogony occurred in 4 stages. The earliest stage was the presence of a multilobed structure containing finely granular protoplasm in the cytoplasm of the macrophage. The 2nd stage was an increase in height and number of the lobulations on the surface of the schizont. The 3rd stage involved the development of cytomeres and the appearance of a polar ring and rhoptries in everted sacculations on the cytomere membrane. Nuclei and mitochondria were incorporated into the sacculations before the release of mature merozoites into the host cell cytoplasm. In the last stage of schizogony, following massive merozoite formation and reduction in size of the schizont, residual nuclei divided by multiple fission. Each nuclear division became incorporated into a developing merozoite having preformed rhoptries, mitochondria, and a polar ring.
Broad-Breasted White male turkeys were fed a control diet until 4 weeks of age, at which time they were randomized into a control group and two treatment groups which received 0.06% (38.7 mg/kg) and 0.09% (58.2 mg/kg) phenytoin, respectively, until termination of the experiment at 12 weeks of age. Plasma concentrations of phenytoin on the two dosages were 8.0 +/- 0.8 and 15.7 +/- 1.7 micrograms/ml. Systemic arterial blood pressure in the control turkeys was 214 +/- 5/171 +/- mm Hg and was reduced in a dose-related fashion to 185 +/- 8/143 +/- 11 and 156 +/- 5/125 +/- 4 mm Hg in the two treatment groups; likewise, the rate of systolic ejection (dp/dt maximum) was less in the phenytoin-treated turkeys. Heart rate also dropped significantly with drug administration but the difference between the two treatment groups was not significant. Evidence of neurotoxicity developed in 25% of the turkeys on the lower drug schedule; these birds had mean plasma phenytoin levels of 12.8 micrograms/ml as contrasted to the concentration of 8.0 micrograms/ml for the entire group. On 0.09% phenytoin 50% of the birds had abnormal signs and a mean phenytoin concentration of 20.5 micrograms/ml, whereas the mean drug level for the entire group on this drug level was 15.7 micrograms/ml. Early signs of neurotoxicity developed within 2 to 3 days of initiation of phenytoin and consisted of extensor rigidity of the neck and hyperactivity; at the higher drug concentrations, back pedaling and somersaulting appeared. General health and weight gain were not affected. No qualitative or quantitative changes were found in the Purkinje cells in the cerebellum of the affected turkeys.
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Nineteen weanling ponies and 1 adult pony were given a single oral dose of aflatoxin B1 (AFB1). Dosages were: 0, 0.5, 1, 2, 4, 5, 6, and 7.4 mg of AFB1/kg of body weight. Vital signs were monitored, and whole blood and serum collected for analysis of serum enzymes, prothrombin time, blood cell counts, and serum urea nitrogen. Ponies that died were examined for gross lesions, and tissues were collected for histopathologic examination and analysis of AFB1 and AFM1 residues. Two of the 4 ponies given the 2 mg/kg dose and all ponies given the larger dosages died within 76 hours. Clinical signs included increased rectal temperature, faster heart and respiratory rates, abdominal straining, bloody feces, and tetanic convulsions. At necropsy, ponies that died of acute aflatoxicosis showed visceral petechiae and hepatic focal lesions. Histopathologic changes included severe hepatic necrosis, vacuolation, and bile duct hyperplasia. Aflatoxins B1 and M1 were recovered from liver, kidney, skeletal muscle, and gastrointestinal contents. One other pony given the 2 mg/kg dose died 32 days after dosing, and 1 control pony died after 70 days. Continuous elevations in prothrombin time and serum aspartate aminotransferase, alanine aminotransferase, and gamma-glutamyl transpeptidase levels were observed in ponies dosed at 4 mg/kg or more. Significant (P less than 0.05) elevations in these values, which peaked 2 to 3 days after dosing, were seen in ponies given the 2 mg/kg dose. This group also had significant increases over controls in PCV and hemoglobin concentration 5 days after dosing.
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Four splenectomized Welsh ponies were infected with Babesia equi. Two ponies were treated with imidocarb dipropionate, and two were not treated. By light microscopic examination, 1% to 2% of the parasitized erythrocytes of treated ponies contained crystalline inclusions. The crystals were rectangular, diamond, or burr shaped. They occupied most of the erythrocytic cytoplasm, and, as a result, the remainder of the pale staining cytoplasm was inconspicuous in Wright-Giemsa-stained blood smears. The size and shape of intraerythrocytic inclusions varied when examined by electron microscopy, but in most instances they were either adhered to or were located close to the parasite. The sides of crystals were either smooth or serrated, and corners were either sharp or notched. Fractures or faults were common in large crystals. Parasitized erythrocytes of nontreated ponies and nonparasitized erythrocytes of treated ponies did not contain crystals. Four hemoglobulin types were identified in five noninfected, nontreated Welsh ponies from the same herd.
The light and electron microscopic appearance of venom glands from two Siamese cobra snakes with a history of production of poor-quality venom was determined. Light microscopy revealed degeneration and necrosis of patches of columnar epithelial cells of glands and infiltration of the subepithelium by inflammatory cells. The lumina contained debris, venom, and necrotic cells. Electron microscopy revealed a deficiency of microvilli on the luminal surfaces of both degenerated and necrotic epithelial cells. The lumina contained fragmented microvilli, coated vesicles containing venom, and degenerated and necrotic cells. Naked and enveloped herpesvirus-like particles were seen in necrotic and ruptured cells. Occasionally, naked herpesvirus-like particles were seen in the nuclei of attached epithelial cells. It was concluded that herpesvirus-like infection of the venom gland was the probable cause of the production of poor-quality venom.
Canine ehrlichiosis was diagnosed in wolves, dogs, and wolf-dog crosses at a small zoo in northcentral Florida. Five of 9 adult canids and all 8 pups confined to a common kennel died as a result of the infection. The epizootic was associated with a massive Rhipicephalus sanguineus infestation. Hematologic and pathologic findings in an adult wolf-dog cross that died were characteristic of canine ehrlichiosis. That animal and four other canids were seropositive for Ehrlichia canis. No deaths occurred following the oral treatment of remaining canids with tetracycline hydrochloride and the treatment of canids and premises with acaricides.
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Hypercalcemia and ectopic calcification were induced in 5 lambs by supplementing the diet with the dried leaves of the plant Cestrum diurnum, for 8 to 9 weeks. Lambs developed mineralization of blood vessels, heart, kidneys, and lungs. These tissues were examined by light and electron microscopy. In the vascular tissue there was calcification of elastic fibers in the hyperplastic intima and the media, along with mineralization of mitochondria of aortic smooth muscle cells. Myocardial cells and their mitochondria were mineralized. In the kidney, there was calcification of the epithelium of the distal convoluted tubules and collecting tubules, Bowman's capsule, and the mesangial cells of the glomeruli. In the lung, there was mineralization of the alveolar septal walls and the bronchi and bronchioles. Feeding of the calcinogenic plant to lambs caused extensive soft tissue calcification. Results of the study indicated that degeneration was the early soft tissue lesion in this plant toxicity.
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