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Biomedical subjects

D S Turner

Publications and source records attributed to D S Turner.

36 records · Page 2Linked to original sources
PubMed1984

Preventing death and injury in childhood: a synthesis of child safety seat efforts.

Virtually all children are at risk for injury and death as passengers in moving vehicles. Between 70% to 90% of the injury and death could be reduced or prevented if children were restrained in safety seats. However, studies show that only a minority of children are properly protected. Numerous efforts have been made to increase the number of children riding in car safety seats. This article reviews and synthesizes the various attempts to motivate safety seat usage by examining the literature on (1) informational and educational programs; (2) safety seat loaner programs; (3) state laws requiring seat usage; (4) behavioral improvement emphasis programs; (5) reward-based programs; and (6) passive prevention approaches through airbags. No one approach appears to be the solution to the complex problem of motivating the preventive behavior of acquiring and consistently using safety seats. Recommendations are forwarded for: (1) developing and determining the best techniques for which settings through comparative research; (2) utilizing a developmental perspective in identifying when and what interventions are needed; and (3) implementing creative and comprehensive programs in communities.

Accidents, Traffic↗
PubMed1980

Variations in cell form and cytoskeleton in human breast carcinoma cells in vitro.

Cell form and cytoskeletal organization were investigated in 13 human breast carcinoma cell lines in vitro. Using tubulin antibodies and indirect immunofluorescence to detect the arrangement of cytoplasmic microtubules, three distinct cell phenotypes were recognized: (a) cells with extensive arrays of microtubules (type 1); (b) cells which were diffusely stained with microtubules apparent only near the cell margins (type II intermediate); and (c) cells in which individual microtubules could not be detected and only diffuse fluorescence was apparent (type II diffuse). Type I cells were flattened epithelial-like cells, much like normal mammary epithelial cells, which when stained with actin antibody displayed many brightly fluorescent parallel cables or "stress fibers." Many microtubules and microfilament bundles were observed in type I cells when examined by transmission electron microscopy. Type II cells were more rounded, often grew in multilayered colonies, and displayed fewer microtubules and microfilament bundles when examined by either immunofluorescence or electron microscopy. Type II cells ranged from very small rounded cells with diffuse tubulin and actin immunofluorescence (type II diffuse) to more flattened cells in which microtubules and actin cables were observed near the flattened cell margins (type II intermediate). Since all of the cells were derived initially from malignant metastatic lesions and some were tumorigenic when injected into athymic nude mice, we assume that they remained malignant in vitro. Thus, in human breast carcinoma cells in vitro, it is not possible to associate any specific cell morphology or cytoskeletal phenotype with cancer or metastasis in vivo. Whether or not these same conclusions hold for breast tumor cells in situ remains to be determined.

Actins↗
PubMedDate not supplied

Symptomatic vitamin A and D deficiencies in an eight-year-old with autism.

An 8-year-old boy with autism developed a limp and periorbital swelling. He was found to have hypocalcemia and radiographic evidence of rickets. Ophthalmologic examination revealed xerophthalmia and corneal erosions. Serum vitamin A was undetectable and serum 25-hydroxyvitamin D was decreased. Dietary history revealed a markedly altered intake consisting of only french fried potatoes and water for several years. All biochemical and physical abnormalities reversed with appropriate supplementation. The nutritional content of french fries is reviewed. Feeding dysfunction is an integral part of autism and closer attention should be paid to potential nutritional deficiencies.

Autistic Disorder↗
PubMedDate not supplied

Selenium distribution in mammary epithelial cells reveals its possible mechanism of inhibition of cell growth.

The subcellular and macromolecular distribution of 75Se-selenite was determined in murine mammary epithelial cell lines which demonstrated marked differences in their growth response to 5 microM selenite. MOD cells responded sooner to the inhibitory effects of selenite than COMMA-D cells. The MOD cells also incorporated a slightly higher percentage of 75Se-selenite into proteins and attained a higher ratio of selenoprotein to selenonucleic acids than did COMMA-D cells. Most selenium and selenoproteins were located in the cytoplasm as revealed by autoradiography and subcellular fractionations. These data suggest that a cytoplasmic selenoprotein may be an intermediate for selenite's nontoxic growth inhibitory effects.

Animals↗
PubMedDate not supplied

Mitochondrial inclusions and mitochondrial respiratory function in selenite-treated mammary epithelial cell lines.

The effect of selenite on mitochondrial morphology, selenoprotein synthesis, membrane potential, phosphorylating respiration, P/O ratio and respiratory control index were evaluated relative to selenite inhibition of DNA synthesis in murine mammary epithelial cell lines. No inhibition of mitochondrial function was noted. Mitochondrial inclusions and most mitochondrial specific selenoproteins were not observed until after DNA synthesis was inhibited. Pyruvate, methionine, hydroxybutyrate, dexamethasone or carnitine had no effect on the inclusions. The results provide evidence for the hypothesis emphasizing the importance of cytosolic selenoproteins modulating the growth inhibitory effects of selenite.

Animals↗