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Biomedical subjects

D L Mitchell

Publications and source records attributed to D L Mitchell.

At least 109 records · Page 6Linked to original sources
PubMed1989

Nutrition education and social learning interventions for type II diabetes.

Two diabetes education programs were compared to a control condition. Seventy-eighty type II (non-insulin-dependent) diabetic outpatients were randomly assigned to nutrition education, nutrition education plus social learning intervention, or wait-list control conditions. Both interventions involved five weekly meetings that focused on reducing calorie intake, increasing dietary fiber, and decreasing fat consumption. The social learning condition also included individualized goal setting and feedback and training in problem-solving and relapse prevention. Within-group analyses and between-group comparisons generally revealed greater improvement in targeted goals (e.g., calorie intake, fat reduction) among intervention conditions than the control condition. There were few differences in more distal measures of outcome such as weight or glycosylated hemoglobin. The social learning component did not improve outcome more than the nutrition education program. Possible reasons for the observed findings and the advantages and limitations of focused time-limited diabetes education efforts are discussed.

Diabetes Mellitus, Type 1↗
PubMed1988

Repair of (6-4)photoproducts correlates with split-dose recovery in UV-irradiated normal and hypersensitive rodent cells.

Chinese hamster ovary cells and two UV-hypersensitive derivatives were used to determine the importance of DNA excision repair for split-dose recovery. In the wild-type cells 75% of the maximum theoretical recovery was observed when the fractions were delivered at 2-h intervals. Very little recovery was evident in the two hypersensitive cell lines. Using radioimmunoassays specific for (6-4)photoproducts and cyclobutane dimers, the ability of UV-irradiated repair-deficient cells representing 5 complementation groups to repair these 2 photoproducts was determined. Removal of antibody-binding sites specific for (6-4)photoproducts was 80% complete in 6 h and was defective in the UV-sensitive cells. In contrast, only 20-60% of antibody-binding sites specific for cyclobutane dimers were removed 18 h post-irradiation, and the extent of removal was the same in normal and defective cell lines. We conclude that repair of (6-4)photoproducts accounts for split-dose recovery. In addition, we conclude that a consequence of DNA repair in CHO cells is modification rather than removal of cyclobutane dimers.

Animals↗
PubMed1988

The induction and repair of lesions produced by the photolysis of (6-4) photoproducts in normal and UV-hypersensitive human cells.

A radioimmunoassay was used to study the induction and repair of damage produced by the photolysis of (6-4) photoproducts in normal and UV-sensitive human cells. Photochemical conditions were established to optimize the production of photolyzed (6-4) photoproducts in human cell DNA with minimal induction of other photoproducts. The repair of this photoproduct, presumed to be a Dewar pyrimidinone, was similar to that determined for the (6-4) photoproduct, with most of the antibody-binding sites removed within 4 h post-photolysis. Whereas xeroderma pigmentosum group A cells were deficient in the repair of this lesion, an XP variant and two cell lines selectively hypersensitive to UVB-irradiation were shown to have normal repair. The radioimmunoassay was further used to demonstrate the alkali-lability of the (6-4) photolysis product.

DNA Repair↗
PubMed1988

Ear syringing.

Explore the source record for details and available documents.

Ear Canal↗
PubMed1987

Xeroderma pigmentosum variant cells are not defective in the repair of (6-4) photoproducts.

Using radioimmunoassays specific for (6-4) photoproducts and cyclobutane dimers, Xeroderma pigmentosum variant cells appear to have a normal capacity for the repair of each of these lesions. However, these assays measure an early stage in the repair pathway and we do not exclude the possibility that repair is not successfully completed following UV irradiation and excision of DNA photoproducts.

Cell Line↗
PubMed1987

Unique DNA repair properties of a xeroderma pigmentosum revertant.

A group A xeroderma pigmentosum revertant with normal sensitivity was created by chemical mutagenesis. It repaired (6-4) photoproducts normally but not pyrimidine dimers and had near normal levels of repair replication, sister chromatid exchange, and mutagenesis from UV light. The rate of UV-induced mutation in a shuttle vector, however, was as high as the rate in the parental xeroderma pigmentosum cell line.

4-Nitroquinoline-1-oxide↗
PubMed1986

A photoelastic study of rests on solitary abutments for distal-extension removable partial dentures.

With a distal-extension removable partial denture, maximum use of existing oral structures can aid in the total support of the prosthesis and reduce the force on the solitary abutment. Four rests with relieved and unrelieved guide plates were evaluated for optimum stress distribution around the root of a solitary premolar abutment. These rests were the mesial, the distal, the mesial and distal, and the continuous rest. The findings demonstrated that The continuous rest had the most favorable stress concentration. All other rest designs demonstrated more lateral stress than the continuous rest. Relieved guide plates demonstrated 58% less maximum shear stress in the apical portion than unrelieved guide plates.

Dental Abutments↗
PubMed1986

The DNA of UV-irradiated normal and excision-deficient mammalian cells undergoes relaxation in an initial stage of DNA repair.

Using a radioimmunoassay specific for Pyr(6-4)Pyo photoproducts, we have demonstrated the removal of these lesions from denaturated DNA isolated from UV-irradiated Chinese hamster ovary cells at various times post irradiation. When assayed undenatured, these same DNA samples, which are initially 10-20 times less capable of binding antibody, show a substantial increase in binding capacity during the first few hours of repair. At 3 h post irradiation the difference between native and heat-denatured DNA samples is negligible, indicating that all of the residual lesions are contained in a single-stranded (relaxed) configuration. This relaxation also occurs in UV-hypersensitive cell lines, that are deficient in the ability to remove Pyr(6-4)Pyo photoproducts. Novobiocin, an inhibitor of topoisomerase II, prevents both the initial increase in binding and the subsequent excision of the antibody-binding sites.

Animals↗