The effect of home visitation on patient motivation to receive dental prophylaxis.
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Biomedical subjects
Publications and source records attributed to R L Anderson.
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Studies of microbial contamination were carried out on a carpet strip (acrilan) installed in a laboratory corridor and on two carpet strips (acrilan and wool) installed in two rooms in a pediatric hospital. A sampling procedure of randomly removing 8-mm plugs from the carpets was used for subsequent enumeration and identification of contaminating microorganisms. Microbial counts increased with time, reached a "plateau" at about 4 weeks, and appeared to be related to the amount of activity present in the carpeted area. Vacuuming of carpets showed only a slight reduction in the number of recoverable microorganisms. Qualitative studies on a strip of acrilan carpet installed in a hospital room indicated that Staphylococcus epidermidis and gram-positive nonsporeforming rods were the predominating microorganisms. Coagulase-positive S. aureus organisms were isolated during every sampling period, and gram-negative rods were also regularly isolated. Most nitrate-reducing gram-negative rods belonged to the Enterobacter and Escherichia groups. Survival studies conducted on carpet strips after hospital installation showed relatively constant levels of contamination for about 6 weeks, followed by a gradual reduction in numbers; coagulase-positive S. aureus were found for 35 days, whereas the proportions of most organisms remained relatively constant with time.
Growth of Aerobacter aerogenes PRL-R3 on the unnatural hexose l-mannose as a sole carbon source is dependent upon the selection of a mutant. Growth of the mutant on l-mannose did not require the synthesis of novel enzymes for the degradation of l-mannose, since enzymes of the l-rhamnose degradative pathway could serve this function. However, unlike most other apparent gain mutations that have been described, the mutant was not constitutive for the degradative enzymes; isomerase, kinase, and aldolase activities functional in the degradation of both l-mannose and l-rhamnose were induced by either of these hexoses in the wild type as well as in the mutant. The fact that the wild type could metabolize l-mannose also ruled out the possibility that the cells were not permeable to l-mannose. Growth of the wild type on nutrient broth was severely inhibited by l-mannose coincident with the onset of l-mannose metabolism. A similar inhibition of growth of the mutant was overcome in about 2 hr. Both strains utilized l-rhamnose and l-mannose sequentially in a mineral medium containing both of these hexoses; at the onset of l-mannose metabolism, growth of the wild type, but not of the mutant, was inhibited. Thus, wild-type A. aerogenes cannot grow on l-mannose because of the toxicity of l-mannose or its metabolites. A mutation which overcomes the toxicity enables the organism to utilize l-mannose as a sole source of carbon and energy for growth.
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The relative significance of the pathways for the conversion of d-fructose to d-fructose 1,6-diphosphate via d-fructose 1-phosphate or d-fructose 6-phosphate in Aerobacter aerogenes PRL-R3 was assessed by observing growth patterns of mutants lacking either d-fructose 6-phosphate kinase or d-fructose 1,6-diphosphatase. The mutant lacking d-fructose 6-phosphate kinase grew well on d-fructose or glycerol but not on d-glucose, whereas the mutant lacking d-fructose 1,6-diphosphatase grew on d-glucose but not on d-fructose or glycerol. The data indicate that the pathway of d-fructose metabolism is primarily through d-fructose 1-phosphate rather than d-fructose 6-phosphate.
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