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Biomedical subjects

D L Gill

Publications and source records attributed to D L Gill.

16 recordsLinked to original sources
PubMed1992

Strengthening physical self-perceptions through exercise.

Two studies examined the effects of physical activity/exercise on physical self-perceptions, self-efficacy, body satisfaction, fitness and relationships among these variables. In study 1, 34 female undergraduates participated in a 10-week exercise/activity program. Participants were selected from existing classes forming a weight training, aerobic exercise and activity control group. Results revealed changes in physical self-perceptions, strength, and body composition over the 10-weeks. Improvements in physical self-perceptions and fitness occurred independent of exercise/activity group. Groups differed in the perceived importance attached to physical self-perceptions. Correlations among the measures revealed relationships among physical self-perceptions, body satisfaction, global self-esteem, and fitness. In study 2, we hypothesized that weight training would have a greater effect on physical self-perceptions and body image perceptions than physical education activity classes. Thirty-seven males and 28 females were selected from existing classes forming a weight training and activity group. Results revealed no significant changes in physical self-perceptions, body image, or global self-esteem over the 10-week program, while strength and physical self-efficacy improved. Correlations among measures from both studies offer preliminary support for Sonstroem and Morgan's model for the examination of self-esteem in exercise settings.

Adolescent↗
PubMed1991

Persistent intracellular calcium pool depletion by thapsigargin and its influence on cell growth.

The intracellular Ca2+ pump inhibitor, thapsigargin, added to DDT1MF-2 smooth muscle cells in culture, irreversibly inhibited accumulation of Ca2+ within cells, permanently emptied the inositol 1,4,5-trisphosphate (InsP3)-sensitive Ca2+ pool, and simultaneously induced profound alteration of cell growth. After only a brief (30-min) treatment of cultured cells with 3 microM thapsigargin followed by extensive washing, the total releasable InsP3-sensitive Ca2+ pool remained entirely empty, even after 7 days of culture without thapsigargin. After thapsigargin treatment, cells retained viability, usual morphology, and normal mitochondrial function. Despite the otherwise normal appearance and function of thapsigargin-treated cells, cell division was completely blocked by thapsigargin. DNA synthesis was completely inhibited when thapsigargin was added immediately after passaging, but was suppressed only slowly (4-6 h) when added to rapidly synthesizing cells (24 h after passaging). Protein synthesis was reduced by approximately 70% in thapsigargin-treated cells. The sensitivity of thapsigargin-mediated inhibition of cell division, DNA synthesis, protein synthesis, and Ca(2+)-pumping activity were all similar with the EC50 values for thapsigargin in each case being close to 10 nM. Upon application to DDT1MF-2 cells, thapsigargin transiently increased resting cytosolic Ca2+ (0.15 microM) to a peak of 0.3 microM within 50 s; thereafter, free Ca2+ declined to 0.2 microM by 150 s and continued to slowly decline toward resting levels. Cells treated with thapsigargin for 1-72 h in culture displayed normal resting cytosolic Ca2+ levels. However, application of thapsigargin or epinephrine to such cells resulted in no change in the intracellular Ca2+, indicating that the internal Ca2+ pool remained completely empty. These results suggest that emptying of Ca2+ from intracellular thapsigargin-sensitive Ca(2+)-pumping pools induces profound alteration of cell proliferation.

Animals↗
PubMed1991

Identification of intracellular calcium pools. Selective modification by thapsigargin.

Recent studies have identified inositol 1,4,5-tris-phosphate(InsP3)-sensitive and -insensitive Ca2+ pools and a GTP-dependent mechanism that transfers Ca2+ between them. Here, the Ca2+ pump-inhibitory sesquiterpene lactone, thapsigargin, is shown to distinguish these two Ca2+ pools and identify a third Ca2+ pumping pool unresponsive to InsP3 or GTP. Using saponin-permeabilized DDT1MF-2 smooth muscle cells, approximately 75% of total intracellular ATP-dependent Ca2+ accumulation is blocked by thapsigargin with an IC50 of 30 nM. In contrast, 1 mM vanadate or 5 microM A23187 block 100% of Ca2+ accumulation. The thapsigargin-responsive Ca2+ pool corresponds exactly to that released by 10 microM InsP3 in the presence of 10 microM GTP. Indeed, addition of InsP3 with GTP has no effect on Ca2+ accumulated in the presence of 3 microM thapsigargin whereas A23187 releases all the remaining Ca2+. Added after maximal Ca2+ uptake, thapsigargin induces only slow Ca2+ release consistent with blockade of pumping activity. Unlike InsP3, the action of thapsigargin is entirely heparin insensitive. The large increment in Ca2+ uptake caused by 12 mM oxalate is completely reversed by thapsigargin, indicating that thapsigargin functions on an oxalate-permeable pool. Moreover, the still larger uptake induced by GTP in the presence of oxalate is also completely reversed by either thapsigargin or InsP3. The results indicate that thasigargin blocks Ca2+ uptake into two discrete pools: the InsP3-sensitive, oxalate-permeable Ca2+ pool and the InsP3-insensitive, oxalate-impermeable Ca2+ pool that can be "recruited" into the InsP3-sensitive pool by GTP-dependent Ca2+ translocation (Ghosh, T. K., Mullaney, J.M., Tarazi, F.I., and Gill, D.L. (1989) Nature 340, 236-239). Additionally, a third Ca2+ pool is defined, unreleasable by InsP3 or GTP, and containing a thapsigargin-insensitive Ca2+ pump.

Animals↗
PubMed1990

Intracellular calcium release mediated by sphingosine derivatives generated in cells.

Soluble and hydrophobic lipid breakdown products have a variety of important signaling roles in cells. Here sphingoid bases derived in cells from sphingolipid breakdown are shown to have a potent and direct effect in mediating calcium release from intracellular stores. Sphingosine must be enzymically converted within the cell to a product believed to be sphingosine-1-phosphate, which thereafter effects calcium release from a pool including the inositol 1,4,5-trisphosphate-sensitive calcium pool. The sensitivity, molecular specificity, and reversibility of the effect on calcium movements closely parallel sphingoid base-mediated inhibition of protein kinase C. Generation of sphingoid bases in cells may activate a dual signaling pathway involving regulation of calcium and protein kinase C, comparable perhaps to the phosphatidylinositol and calcium signaling pathway.

Adenosine Diphosphate↗
PubMed1978

Characterization of thyrotropin binding to specific receptors in human fat tissue.

Specific receptors for thyrotropin were found to exist in membranes from whole human subcutaneous fat tissue. The characteristics of the interaction of 125I-labelled thyrotropin with such receptors were determined and compared with the stable, high-affinity thyrotropin receptor shown previously to exist in guinea pig fat membranes. Specific binding was readily detectable using low concentrations of membranes (up to 80 microgram/ml), though specific binding was reduced at higher membrane concentrations. Increasing concentrations of unlabelled thyrotropin reduced fractional binding, revealing saturation of a population of mixed affinity sites (highest Ka of the order of 0.3 X 10(9) M-1). Little cross-reactivity was observed with other lipolytic or structurally related hormones, though some cross-reactivity was observed in the presence of human chorionic gonadotropin. Association was temperature-dependent and rapid at 37 degrees C, though prolonged incubation revealed some instability of binding at this temperature. Binding was reversible with a high dissociation rate constant, and was particularly sensitive to the presence of low concentrations of sodium or calcium ions. Using membranes prepared from isolated human fat cells, binding of thyrotropin was equally sensitive to the addition of cations.

Adipose Tissue↗
PubMed1976

Competitive trait anxiety, success-failure and sex as determinants of motor performance.

Two experiments determined the effects of competitive trait anxiety, success-failure, and sex on the performance of 10- to 12 yr.-old children competing on a complex motor maze. Competitive trait anxiety was assessed by the Sport Competition Anxiety Test and success-failure was induced by giving bogus win-loss feedback. High and low competitive trait-anxiety children were randomly assigned to one of three conditions: winning 80%, 50% or 20% of 20 contests. The average completion time and the variability of times within each of two blocks of 10 contests were the two performance measures. State-anxiety was assessed with Spielberger's State Anxiety Inventory for Children as an indicant of arousal prior to and during competition. The findings of Exp. 1 yielded no significant performance differences. In Exp. 2 a significant interaction of competitive trait anxiety X success-failure X sex for performance time and variability was obtained. This interaction was largely attributed to sex differences.

Achievement↗
PubMedDate not supplied

Ca2+ release from endoplasmic reticulum is mediated by a guanine nucleotide regulatory mechanism.

Ca2+ accumulation and release from intracellular organelles is important for Ca2+-signalling events within cells. In a variety of cell types, the active Ca2+-pumping properties of endoplasmic reticulum (ER) have been directly studied using chemically permeabilized cells. The same preparations have been extensively used to study Ca2+ release from ER, in particular, release mediated by the intracellular messenger inositol 1,4,5-trisphosphate (InsP3). So far, these studies and others using microsomal membrane fractions have revealed few mechanistic details of Ca2+ release from ER, although a recent report indicated that InsP3-mediated Ca2+ release from liver microsomes may be dependent on GTP. In contrast to the latter report, we describe here the direct activation of a specific and sensitive guanine nucleotide regulatory mechanism mediating a substantial release of Ca2+ from the ER of cells of the neuronal cell line N1E-115. These data indicate the operation of a major new Ca2+ gating mechanism in ER which is specifically activated by GTP, deactivated by GDP, and which appears to involve a GTP hydrolytic cycle.

Animals↗