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Biomedical subjects

P Kimball

Publications and source records attributed to P Kimball.

24 records · Page 2Linked to original sources
PubMed1989

A worksite smoking cessation intervention involving the media and incentives.

This study evaluated an attempt at 38 workplaces to help employees stop or reduce their levels of smoking. In past research, worksite support groups, in combination with a media smoking cessation program and self-help manuals, were found to be effective in helping employees quit smoking. Unfortunately, recidivism was found at the follow-up evaluations. The present study replicated the results of the previous worksite smoking cessation program with support groups, a television intervention, and self-help manuals. At this postpoint, 42% of employees provided groups plus incentives were abstinent compared to only 15% who were only provided self-help materials. An important difference in this study was that there were also monthly follow-up support groups and incentives. Work settings can be a source of stress and conflict, which can precipitate relapse. At a 12-month follow-up, 26% of those participants who were provided support and incentives were abstinent compared to 16% who were only provided the self-help materials.

Adult↗
PubMed1980

The threshold for binaural interaction.

The absolute sensitivity of the binaural auditory system was studied by asking subjects to discriminate tones that were truly monaural from dichotic tones that sounded monaural because of an extremely large interaural difference of intensity. Thresholds for this discrimination across the range of frequencies from 250 to 4000 Hz were achieved when the tones in the weaker channel were in the region from -45 to -50 dB relative to tones in the stronger channel. Since the monaural reference tones, as well as the stronger signals in the dichotic conditions, were chosen to be 61 dB sensation level (SL), the weakest levels for which binaural interaction could be measured appear to have been on the order of 10 to 15 dB SL.

Adult↗
PubMed1976

Sialylatin of glycoproteins of murine mammary tumor virus, murine leukemia virus, and Mason-Pfizer monkey virus.

Neuraminidase treatment of mouse mammary tumor virus, Rauscher murine leukemia virus, and Mason-Pfizer monkey virus resulted in loss of their capacity to inhibit hemagglutination of influenza virus. Hemagglutination-inhibition activity of these RNA tumor viruses could be restored by in vitro resialylation catalyzed by sialyl transferase. The major glycoprotein in the intact envelope of desialylated and, to some extent, native virions could be specificallly labeled in vitro with CMP-(14C) sialic acid. These studies further characterize the individual glycoproteins of mouse mammary tumor virus, Rauscher murine leukemia virus, and Mason-Pfizer monkey virus.

Animals↗
PubMed1975

Molecular mechanism of in vitro transformation of mammalian cells by chemical carcinogens.

BHK21 clone 13 cells transformed by dimethylnitrosamine (DMN) or nitrosomethylurea (NMU) ("alkylating" chemical carcinogens) appear to be restricted by temperature in the expression of their transformed phenotype. When grown at 38.5 degrees C, they exhibit a transformed phenotype (clonal morphology and ability to plate in agar), when grown at 32 degrees C, their phenotype is normal. Conversion from the normal to the transformed phenotype and the reverse is possible by temperature shifts. Conversely of the BHK21 clone 13 cells, of the rat fibroblasts (R111) transformed by 4-nitroquinoline-N-oxide (NQN), some exhibit a transformed phenotype restricted by temperature while others are not restricted by temperature in the expression of transformation. A working hypothesis is proposed suggesting that the phenotype of cells transformed by chemical carcinogens may be determined by the nature of the chemical reaction with the cell DNA. "Alkylating" carcinogens cause prevalently point mutation in bacteria (of the base substitution kind); in the case of transformation of mammalian cells temperature-sensitive phenotypes will be obtained. "Frameshift" carcinogens cause frameshift mutation in bacteria and cells transformed by this class of carcinogens will exhibit a transformed phenotype unrestricted by temperature.

Animals↗