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Biomedical subjects

W J Thompson

Publications and source records attributed to W J Thompson.

At least 127 records · Page 7Linked to original sources
PubMed1981

Begg and straight wire: a combination approach to treatment.

Orthodontic appliances should be designed to satisfy goals for denture, patient, and doctor. An appliance that is able to achieve these goals more closely approaches the ideal treatment system. Analysis of appliances of the Begg and straight wire types indicates that each treatment system has significant advantages and that the advantages of one system frequently are the disadvantages of the other. A technique that uses both the tipping principles of Begg and the bodily movement principles of the straight wire type of appliance has been designed and clinically evaluated. The unique capability of the combined treatment approach is in the mechanical design of the new combination four-stage bracket. A description of the appliance and the technique, as well as a clinical case presentation, is included in this article.

Humans↗
PubMed1981

Histamine regulation of adenylyl cyclase of enriched rat gastric parietal cells.

Rat gastric parietal cells were isolated to 90% or greater purity by discontinuous gradient ultracentrifugation in sucrose-Ficoll. Adenylyl cyclase activity was initiated by histamine in the presence of 5'-guanylyl imidodiphosphate, but not by pentagastrin or acetylcholine. The concentration of histamine needed for half-maximal activation of adenylyl cyclase was 38 microM. The histamine H2-receptor antagonist, metiamide, inhibited histamine (100 microM) activation with a Ki of 0.9 microM. The effects of other histamine agonists and antagonists suggest that presence of H2-type histaminic receptors on parietal cells. Adenylyl cyclase activity was also stimulated by isoproterenol, norepinephrine, and epinephrine, but not by methoxamine. Half-maximal activation by isoproterenol occurred at 0.5 microM. Propranolol, but not phentolamine, prevented activation by these agents, indicating the presence of beta-adrenergic receptors on parietal cells. Prostaglandins E2 stimulated adenylyl cyclase of partially purified (30%), but not the enriched (90%), parietal cell populations.

Adenylyl Cyclases↗
PubMed1981

Isolated parietal cells: histamine response and pharmacology.

Isolated, partially purified or enriched rat gastric mucosal parietal cells were shown to respond to histamine and other histaminic H2-receptor agonists as measured by an increased accumulation of [14C]aminopyrine. The response was temperature-dependent, related to parietal cell purity and inhibited selectively and reversibly by H2-receptor antagonists. H1-receptor antagonists noncompetitively inhibited histamine, carbamylcholine and dibutyryl cyclic AMP-stimulated aminopyrine accumulation. The affinity constants calculated for the H2-receptor agonists and antagonists were similar to those previously determined in the studies of activation and inhibition of adenylyl cyclase in enriched parietal cell preparations. The results strongly suggest that a correlation exists between the ability of histamine and its analogs to stimulate isolated rat parietal cell function and their ability to stimulate adenylyl cyclase activity. Potentiation of aminopyrine accumulation in the presence of histamine and carbamylcholine is due to specific receptor effects of each secretagogue.

Aminopyrine↗
PubMed1980

Effects of insulin on glycogen metabolism of serum-deprived BHK-21 fibroblasts.

We have studied the effects of insulin on glycogen metabolism of cultured BHK-21 fibroblasts. Addition of insulin to cells cultured in 0.5% serum stimulated incorporation of 5mM 14C-glucose into glycogen and increased cellular glycogen content, without inducing proliferation. With serum-deprived cells incubated for 2 hr, maximal stimulation of incorporation of glucose into glycogen was 3.5-fold and the half-maximal dose of insulin was 5nM. After culture for 24 hr with 100nM insulin, incorporation was increased 13-fold and glycogen content was increased by 44%. Incorporation of glucose into glycogen was reduced by agents which elevate cellular adenosine 3',5-cyclic monophosphate (cyclic AMP): 10 microM prostaglandin E1 (PGE1), 0.25 mM 1-methyl-3-isobutylxanthine (MIX), 10 microM L-epinephrine (L-EPI), and 10 microM L-isoproterenol (L-ISO). Culture with 100nM insulin for 2 hr stimulated incorporation three-fold in the presence of any of these compounds, but insulin did not affect cellular cyclic AMP. At all times from 1 hr to 24 hr after addition of insulin to serum-deprived cultures, the 1-min uptake of 10 microM 3H-2-deoxyglucose (3H-2DG) was increased. There were small (30 to 40%) increases in glycogen synthase I activity at 15 and 30 min but not 4 hr after addition of insulin. After 24 hr with insulin, total glycogen synthase and phosphorylase activities were increased approximately two-fold, without changes in their activation states. We conclude that insulin promotes glycogenesis in serum-deprived BHK-21 cells. This response is mediated principally by increased entry of glucose into cells, and is not mediated by a change in cellular cyclic AMP concentration.

Cell Line↗
PubMed1980

Isolated parietal cells: [3H]QNB binding to putative cholinergic receptors.

The tritiated muscarinic cholinergic antagonist quinuclidinyl benzilate, [3H]QNB, was used as a direct probe for the detection and characterization of muscarinic cholinergic receptors associated with the particulate fraction of isolated and purified rat gastric muscosal parietal cells. Specific binding is saturable (Bmax = 55 fmol/mg protein, KD = 0.78 nM), shows a single population of binding sites, and has appropriate pharmacological specificity. Nanomolar concentrations of muscarinic cholinergic antagonists, such as atropine and scopolamine, inhibit [3H]QNB binding by 50%, whereas micromolar concentrations are needed for agonists, such as acetylcholine, oxotremorine, and carbamylcholine. Binding is also stereoselective as shown by the more than 1,000-fold difference in inhibitory potencies of the stereoisomers of benzetimide. Noncholinergic agents, including pentagastrin, histamine, and the H2-receptor antagonists cimetidine and metiamide, have little or no effect on [3H]QNB binding at concentrations of 100 microM. These data support the existence of specific parietal cell muscarinic cholinergic receptors with which the secretagogue acetylcholine may directly interact to initiate gastric acid secretion.

Animals↗
PubMed1980

Activation of human lymphocyte high affinity cyclic AMP phosphodiesterase by culture with 1-methyl-3-isobutylxanthine.

When 1-methyl-3-isobutylxanthine (MIX), a potent inhibitor of human lymphocyte cyclic AMP phosphodiesterase in vitro, was added to intact lymphocyte cultures, MIX caused an activation of this enzyme. Activation by MIX which showed an EC50 = 0.2 mM, required 24 hr in culture, reached a maximum near 48 hr, and remained at maximum through 144 hr. The effect of MIX was to increase the maximum velocity of the 3.5-4S form but not the 5.5-6S form of the lymphocyte high affinity enzyme system. Activation required serum, occurred in calcium depleted media, and was unaffected by sodium azide, adenosine, cycliheximide, or actinomycin D. Further, the effect of MIX was not mimicked by cyclic AMP, cyclic GMP, or by a variety of cyclic nucleotide derivatives with the exception of N6-monobutyryl- and N6-2'0 dibutyryl cyclic AMP in the culture medium. No correlation was observed between the in vitro IC.50 value and the amount of intact cell activation with other phosphodiesterase inhibitors. Although MIX prevented the mitogenic response of lymphocytes to phytohemaglutinin (PHA), a synergistic effect to activate cyclic nucleotide phosphodiesterase was obtained when both agents were included in the culture medium. These data are discussed as an example of a novel modulation of a specific high affinity form of cyclic AMP phosphodiesterase by an apparent non-genetic regulatory mechanism.

1-Methyl-3-isobutylxanthine↗
PubMed1980

Cyclic nucleotide alterations in mixed leukocyte reaction: a preliminary report.

Endogenous cyclic adenosine and guanosine monophosphate (cAMP, cGMP) levels were studied in human peripheral blood lymphocytes during mixed leukocyte reactions (MLR). cAMP level was consistently elevated in one-way MLR, with good correlation to 3H-thymidine uptake in these reactions. In contrast, cGMP level was practically unchanged. Irradiation of reacting cell populations resulted in inhibition of cyclic nucleotide phosphodiesterase (PDE) activity. These results suggest that metabolic alterations in cAMP may be associated with immune reactions of cellular recognition.

Cyclic AMP↗
PubMed1979

Immunotherapy with levamisole: early decrease of cAMP levels in lymphocytes from treated cancer patients.

Lymphocyte cyclic nucleotide content was studied before and after Levamisole administration to cancer patients. Twelve patients with disseminated cancer received 100 mg/m2 on two consecutive days; nine comparable patients with disseminated cancer served as controls. Endogenous cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) were measured in lymphocytes before, 24, and 48 hours after ingestion of the first dose of Levamisole. A statistically significant decline in lymphocyte cAMP level was observed after drug administration and no significant changes were noted in cGMP levels. Further studies will be necessary to correlate this biochemical change in cyclic nucleotides with modulation of the functional level of cellular immune mechanisms.

Breast Neoplasms↗
PubMed1979

Regulation of cyclic nucleotide phosphodiesterase forms by serum and insulin in cultured fibroblasts.

A rapid reduction of cyclic nucleotide phosphodiesterase activity occurs after the replating of confluent cultures of BHK 21 c/13 fibroblasts into fresh medium. This reduction in activity depends on the density to which the cultures are reseeded and the concentration of serum in the medium. Enzyme activity in BHK cells is restored after 24 to 48 hours if cells are diluted into medium containing 10% fetal calf serum or 0.5% fetal calf serum supplemented with insulin (10(-6)M), but not into 0.5% serum alone. The restoration in enzyme activity is blocked by cycloheximide or Actinomycin D. When BHK cells become quiescent by maintanance in 0.5% serum conditions for 48 hours, a rapid (15--60 minutes) increase in cyclic AMP phosphodiesterase activity occurs when 10% serum is added to the cultures. Enzyme activity is increased even further after 24 to 48 hours in the 10% serum. Cycloheximide or Actinomycin D do not affect the rapid increase in enzyme activity in response to serum, but completely inhibit the long term increase. In contrast to serum, insulin (10(-8) to 10(-6)M) has no short term effect, but does increase enzyme activity after 24 to 48 hours to levels comparable to those seen with addition of 10% serum. As is the case with serum, this long term effect of insulin on enzyme activity is prevented by inhibitors of protein and RNA synthesis. Kinetic analyses of cyclic AMP phosphodiesterase activity in homogenates of quiescent BHK cells indicate the presence of only high Km (congruent to 20 muM) enzyme activity. Addition of serum or insulin to quiescent cells results in the appearance of apparent low Km enzyme activity in homogenates. Sucrose gradient analysis of BHK cells displays two forms of cyclic AMP phosphodiesterase enzyme activity: a 3--4 S form and 5--6 S form. In quiescent cells, the 5--6 S form greatly predominates relative to the 3--4 S form. Addition of serum to quiescent cells results in a rapid appearance of increased 3--4 S form enzyme activity. Insulin also increases the activity of this higher affinity 3--4 S enzyme form after 24 to 48 hours in culture. The functional significance of short and long term regulation of cyclic nucleotide phosphodiesterase(s) in cells is discussed.

3',5'-Cyclic-AMP Phosphodiesterases↗