Fluoride programs in the school setting: preventive dental health.
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Biomedical subjects
Publications and source records attributed to J Weintraub.
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Open-ended telephone interviews were conducted with 294 families who refused participation in a school-based program of professionally applied topical fluoride. While the program was conducted in a flouride-deficient community, the level of topical fluoride contact in the homes of the nonparticipants was high. The traditional antifluoridationist reasons for nonparticipation were not expressed with frequency. Instead, the most frequent reason for returning a negative consent form was that the child was already receiving topical flouride applications from the family dentist. The second most frequent reason was that the child did not wish to participate. Many of the reasons given for nonparticipation were not cogent, suggesting that if the parents had been more informed about the nature of the project and about fluoride in general their responses might have been positive.
The kinetics of various specific and nonspecific immunologic responses were examined in BALB/c mice infected with 17X nonlethal Plasmodium berghei yoelii (a self-limiting infection). The sequence of events after infection was characterized by rapid sensitization of splenic T cells to malaria antigen and polyclonal B cell activation, followed by a period of depressed splenic proliferative responses in vitro to mitogens (PHA and LPS) and malaria (specific) antigen. At the same time, suppressed primary in vitro splenic PFC responses to trinitrophenyl-aminoethylcarbamylmethyl-Ficoll (TNP-F) were seen. This suppression was an active process requiring adherent cells. During this period, levels of antimalarial antibody also increased exponentially. As the infection was cleared, splenic malaria antigen-specific proliferative responses were again observed and splenic PFC and in vitro mitogen responses returned to preinfection levels after variable periods of time. Both splenic proliferative responses to malaria antigen and antimalarial antibody responses remained persistently elevated. In addition, some responses were examined in mice infected with 17X lethal P.b. yoelii (a fatal infection); in comparison to the early responses of mice infected with the nonlethal substrain, there was a decrease and delay in the development of a splenic T cell response to malaria antigen and a blunted antimalarial antibody response.
Patients with severe nodulo-cystic acne are known to have elevated serum antibody levels and increased immediate hypersensitivity reactions to Propionibacterium acnes. This organism is the predominant bacterium in normal pilosebaceous follicles of human skin, and can be consistently isolated from pustular lesions in acne. Previously it had been observed that delayed cutaneous hypersensitivity reactions to P. acnes were negative in patients with acne. The present study investigated the proliferative response of lymphocytes from patients with nodulo-cystic acne to phytohaemagglutinin (PHA) and P. acnes antigen stimulation. The response to PHA stimulation was within normal limits. The response to P. acnes antigen showed a significant increase over control values obtained by testing lymphocytes from acne-free subjects. Thus cell mediated immunity to P. acnes may be present in subjects with severe inflammatory acne. These findings raise the possibility that reactions to P. acnes may contribute to intensifying the inflammatory response in acne lesions.
The effect of administration of live Bacillus Calmette-Guerin (BCG), a nonspecific immunostimulant, on the course of experimental cutaneous leishmaniasis in mice was investigated. BALB/c mice were injected in the footpad with Leishmania tropica, NIH S-strain; in mice that were not pretreated with BCG this produced a reproducible fatal infection characterized by local inflammation, regional lymphadenopathy, and dissemination of parasites with hepatosplenomegaly. In mice that were pretreated with BCG and similarly infected with L. tropica there was a reduction in the severity of cutaneous disease and a significant (p less than 0.005) decrease in mortality without evidence of visceralization.
The records of 47 patients with Ménière's syndrome were analyzed in a retrospective computerized study to determine the effect of different medical regimens on the long term course of hearing loss. Four treatment groups, including histamine (subcutaneous), other vasodilators (oral), vitamins, and untreated controls were examined. Results suggest that there was no statistically significant difference among the four groups in the rates or absolute level of hearing loss or SRT despite different therapeutic regimens. The ability of these agents to conserve hearing in patients with Ménière's syndrome remains unproven on the basis of clinical and laboratory evidence.
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Explore the source record for details and available documents.
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