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Biomedical subjects

M Marnell

Publications and source records attributed to M Marnell.

4 recordsLinked to original sources
PubMed1995

Does interpersonal therapy help patients with binge eating disorder who fail to respond to cognitive-behavioral therapy?

The aim of this quasi-experimental study was to examine the effectiveness of group interpersonal therapy (IPT) in treating overweight patients with binge eating disorder who did not stop binge eating after 12 weeks of group cognitive-behavioral therapy (CBT). Participants in this study were randomly allocated to either group CBT or to an assessment-only control group. After 12 weeks of treatment with CBT, 55% of participants met criteria for improvement and began 12 weeks of weight loss therapy, whereas the nonresponders began 12 weeks of group IPT. Over the 24-week period, participants who received treatment reduced binge eating and weight significantly more than the waiting-list control group. However, IPT led to no further improvement for those who did not improve with CBT. Predictors of poor outcome were early onset of, and more severe, binge eating.

Adult↗
PubMed1987

Thermolabile proton translocating ATPase and pump activities in a clathrin-coated vesicle fraction from an acidification defective Chinese hamster cell line.

We have recently described a mutant of Chinese hamster ovary cells, termed G.7.1, that contains a temperature-sensitive, conditionally lethal mutation resulting in defective vacuolar acidification (Marnell, M. H., Mathis, L. S., Stookey, M., Shia, S.-P., Stone, D.K., and Draper, R. K. (1984) J. Cell Biol. 99, 1907-1916). To further characterize the lesion, clathrin-coated vesicles were partially purified from wild type and G.7.1 cells, and the thermolabilities of vanadate and oligomycin-insensitive, N-ethylmaleimide-sensitive, H+-ATPase activity, 32Pi-ATPase exchange activity, and proton pumping were compared. All three parameters of H+ pump activity were markedly diminished by preincubation at 44 degrees C for vesicles harvested from the G.7.1 cells, but not for those from wild type cells. Phosphatidylserine did not protect against heat inactivation in vesicle fractions prepared from G.7.1 cells. The results suggest that the mutation responsible for defective acidification in G.7.1 cells is expressed at the level of the proton pump of organelles present in our clathrin-coated vesicle-enriched preparation.

Adenosine Triphosphate↗