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D A Clare

Publications and source records attributed to D A Clare.

25 records · Page 2Linked to original sources
PubMed1984

Tissue distribution of mammalian sulfhydryl oxidase.

Sulfhydryl oxidase activity is present in cow, goat, sow, human, and rat milks, and can also be measured in several rat tissues following homogenization in 1% polyoxyethylene-9-lauryl ether. These include lactating mammary tissue, kidney, and pancreas. Bovine kidney homogenates also exhibit sulfhydryl oxidase activity; however, no activity could be detected in rat thymus, brain, heart, liver, spleen, lung, or small intestinal tissue homogenates. Indirect immunofluorescent staining of tissue sections using rabbit antibodies directed against highly purified bovine milk sulfhydryl oxidase preparations revealed that the enzyme is closely associated with the plasma membrane of lactating cow and rat mammary tissues and the basal-lateral membrane of rat kidney cortex. In addition, the oxidase appears to be associated with endothelial cells lining the capillaries of rat kidney, heart, and small intestine, and centroacinar cells in pancreatic tissue slices also stain for sulfhydryl oxidase. In contrast, liver, brain, and thymus tissues do not exhibit fluorescent staining and appear to be devoid of sulfhydryl oxidase activity.

Animals↗
PubMed1983

Positive correlation between superoxide dismutase and resistance to paraquat toxicity in the green alga Chlorella sorokiniana.

Paraquat (10-30 microM) exerted a dose-dependent and light-dependent toxicity on Chlorella sorokiniana. Paraquat was also seen to increase the superoxide dismutase content of these cells and to cause the appearance of a new electrophoretically distinct isozyme. Cells grown in the absence of paraquat contained one manganese-superoxide dismutase and two iron-superoxide dismutases, while the paraquat-grown cells contained an additional manganese-superoxide dismutase. Cells which were grown in the presence of 25 microM Paraquat, and which therefore possessed elevated levels of superoxide dismutase, were resistant to 30 microM Paraquat, whereas control cells were bleached and killed by this level of Paraquat. Electron micrography and chemical analysis revealed that Paraquat decreased the starch content of the cells and caused a failure of dividing cells to separate. It appears that Paraquat increases the photoproduction of O2- in C. sorokiniana and that an increase in the cell content of superoxide dismutase is an adaptive response which provides protection against this herbicide.

Cell Division↗
PubMed1983

Effect of dietary regimen on rotavirus-Escherichia coli weanling diarrhea of piglets.

Previously, we induced weanling diarrhea in piglets by infecting them with rotavirus followed by hemolytic enteropathogenic Escherichia coli. We postulated that rotavirus, by damaging the epithelium of the small intestines, produced an enteroenvironment which favored the selection and growth of enteropathogenic E. coli. Furthermore, diet might affect the enteroenvironment and influence the course of the disease. To test this, newly weaned 3-week-old piglets were assigned to one of four dietary regimens and infected with rotavirus followed 24 h later with enteropathogenic E. coli. The course of the disease was followed by monitoring the severity of diarrhea and the fecal shedding of rotavirus and enteropathogenic E. coli in these dually infected piglets. The dietary regimen designed to tax the digestive and absorptive capacities of the piglets (high nutrient intake fed three times a day) produced the most prolonged diarrhea, colonization of the gut by hemolytic enteropathogenic E. coli, and persistent shedding of rotavirus (P less than 0.01). The same nutrient intake divided into 24 equal increments and fed hourly produced a less severe response (P less than 0.01). The least severe response was seen in piglets fed one-third the nutrient intake either hourly or three times a day (P less than 0.01). We conclude that dietary regimen plays an important role in rotavirus-E. coli-induced weanling diarrhea.

Animals↗
PubMed1982

Rotavirus and hemolytic enteropathogenic Escherichia coli in weanling diarrhea of pigs.

Since the turn of the century, Escherichia coli has been implicated in the etiology of weanling diarrhea (colibacillosis). However, rotavirus--a virus that destroys enterocytes--has been shown recently to be causally associated with weanling diarrhea of pigs. The role of both rotavirus and hemolytic enteropathogenic E. coli in weanling diarrhea was assessed in this study. Pigs from a closed herd were farrowed and weaned by two markedly different systems: an "intensive care sanitary" system and a "conventional unsanitary" system. Pigs weaned at 3 weeks of age in the sanitary system usually experienced a rotaviral diarrhea about 16 days postweaning. No hemolytic E. coli were detected in feces from these pigs. Peers weaned at the same time by the unsanitary system commenced diarrhea 3 days postweaning. Rotavirus and nonhemolytic E. coli were detected in the feces at the onset of diarrhea and for a few days thereafter. Then, the aerobic fecal flora shifted to nearly pure hemolytic enteropathogenic E. coli. About 10 days later, the diarrhea waned, and the fecal flora shifted back to nonhemolytic E. coli. This hemolytic E. coli shedding pattern could not be duplicated in artificially inoculated sanitary pigs unless they were inoculated with the hemolytic E. coli during a rotaviral-associated diarrhea. Otherwise, the shedding of hemolytic E. coli was fleeting, and the diarrhea, if present, was mild. Pigs developed humoral antibodies to the rotavirus but not to the hemolytic E. coli. We conclude that rotavirus damages the epithelium of the small intestines, which changes the luminal environment to one that favors colonization by enteropathogenic E. coli.

Animals↗