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Biomedical subjects

I Mills

Publications and source records attributed to I Mills.

At least 37 records · Page 2Linked to original sources
PubMed1994

Induced mood, phobic responding and the return of fear.

The link between depression and phobic responding is poorly understood. Forty-eight spider phobics were exposed to videotaped spider sequences whilst in relatively depressed or relatively elated moods, then presented the same stimuli whilst in a neutral mood. Results indicated that depressed mood increased initial responding, and was associated with greater return of fear during the second (non-mood) sequence. The return of fear was not attributable solely to differential habituation rates during the first sequence, suggesting that the differences observed may have been due to cognitive effects.

Adolescent↗
PubMed1994

Adaptive responses of coronary circulation and myocardium to chronic reduction in perfusion pressure and flow.

We tested the hypothesis that chronic reduction in perfusion pressure and flow in the coronary circulation induces a state of myocardial "hibernation" characterized not only by a steady-state reduction in myocardial O2 consumption (MVO2) but also by evidence of persistent dilator reserve of the distal vasculature. Biochemical and morphological changes in the coronary vasculature were also assessed. Experiments were conducted in swine with an extraluminal coronary stenosis placed 4-32 wk before study. Stenosis reduced lumen diameter by approximately 80% at the time of final experimentation. Baseline, regional myocardial blood flow distal to the stenosis in both endocardial and epicardial layers was reduced vs. that of the normal zone. Vasodilator reserve persisted in both endocardial and epicardial layers of the stenosis zone. Flow increased in each layer in response to adenosine plus phenylephrine and failed to decline despite a marked reduction in perfusion pressure in response to adenosine alone. Regional MVO2 at baseline was reduced vs. historical controls without coronary stenosis. Protein synthesis rate in coronary vessels of the stenosis zone was reduced vs. that of the normal zone. Morphological responses of stenosis zone vessel walls were heterogeneous. Smaller microvessels exhibited mild hypertrophy of their walls, whereas walls of larger microvessels tended to atrophy. Thus chronic reduction in perfusion pressure and flow induces a state of myocardial hibernation characterized by a steady-state reduction in MVO2 in association with persistent dilator capacity. Biochemical and morphological changes occur in microvessel walls and may contribute to observed physiological responses.

Acclimatization↗
PubMed1993

Phospholipase C: a putative mechanotransducer for endothelial cell response to acute hemodynamic changes.

Endothelial cells (EC) in vivo are exposed to a multitude of physical forces with each pulse of the cardiac cycle. Ongoing studies support the concept that EC respond to these forces through specific signal transduction pathways. Previous investigations in our laboratory have shown that EC respond to the initiation of cyclic strain or to an acute increase in cyclic strain frequency with the production of inositol 1,4,5-trisphosphate (IP3). This study demonstrates that EC also respond to an acute decrease in cyclic stretch frequency with a transient increase in IP3 production. Thus, EC detect both increases and decreases in cyclic stretch frequency with phospholipase C (PLC) activation leading to IP3 generation.

Animals↗
PubMed1993

Vancouver General Hospital Palliative Care Unit utilization review.

This paper describes the utilization pattern in the Palliative Care Unit at Vancouver General Hospital for a six-month period (1 April-30 September 1991) and relates the information provided to the mandate of the palliative care program. It is a retrospective study of 139 patients discharged during this period. Data were collected from the Hospital Medical Records Institute (HMRI), the Medical Records Department of Vancouver General Hospital, patients' charts, the palliative care unit admission/discharge book, and palliative care consultation statistics.

Adult↗
PubMed1992

Intracellular cyclic AMP levels in endothelial cells subjected to cyclic strain in vitro.

Human saphenous vein endothelial cells (EC) were grown to confluence in fibronectin-coated culture plates with flexible membrane bottoms and maintained in M-199 supplemented with substrates. One hour prior to experimentation 5 mM IBMX, a phosphodiesterase inhibitor, was added. Vacuum was used to deform the membrane bottoms to 24% strain at 60 cycles/min (0.5 sec elongation alternating with 0.5 sec relaxation). After 10-60 min of cyclic strain, or upon exposure of EC to 100 microM forskolin or 0.1 microM galanin, intracellular cyclic AMP (cAMP) was measured by radioimmunoassay. In parallel experiments, tissue plasminogen activator (tPA) secretion was determined after 24 hr of cyclic strain in the absence or presence of forskolin or galanin. The results demonstrate that exposure of EC to cyclic strain led to no change in cAMP levels and confirmed our previous observation that tPA secretion was enhanced with cyclic strain. Addition of forskolin, which led to an almost 10-fold increase in cAMP levels, or galanin, which led to a 34% decrease in cAMP levels, did not significantly alter the rise in tPA induced by cyclic strain.

Cells, Cultured↗
PubMed1990

Mechanosensitive adenylate cyclase activity in coronary vascular smooth muscle cells.

The purpose of the present study was to test the hypothesis that adenylate cyclase activity of porcine coronary artery smooth muscle cells is sensitive to mechanical stretch. Cultured vascular smooth muscle cells were stretched at 24% maximal strain at 60 cycles/min for 30 minutes. Both basal and maximal catalytic activity of adenylate cyclase (as assessed by stimulation by 100 microM forskolin with 5 mM manganese chloride) were reduced by 30% (P less than 0.05) in membranes obtained from stretch versus unstretched cells. The magnitude of the stretch-induced reduction in Gpp(NH)p was identical over the entire time course studied (5-30 minutes). Furthermore, basal adenylate cyclase activity was inversely related to the magnitude of stretch. Thus, cyclic stretch can influence adenylate cyclase activity in coronary vascular smooth muscle cells. These data provide important information concerning potential biochemical mechanisms involved in the myogenic response of vascular smooth muscle and also suggest a potential mechanism by which the coronary circulation may adapt to chronically reduced perfusion pressure.

Adenylyl Cyclases↗
PubMed1990

Cultured vascular smooth muscle cells from porcine coronary artery possess A1 and A2 adenosine receptor activity.

This study tested the hypothesis that an A1 adenosine receptor capable of inhibiting adenylate cyclase activity is present in porcine coronary vascular smooth muscle cells. In the absence of blockade of the A2 adenosine receptor, the A1 adenosine receptor agonists phenylisopropyladenosine (PIA) and cyclopentyladenosine (CPA) (10(-9) M) failed to inhibit Gpp(NH)p stimulated adenylate cyclase activity. However, after blockade of the A2 adenosine receptor with 30 nM CGS 15943A, cyclopentyladenosine (10(-9) M) inhibited Gpp(NH)p stimulated adenylate cyclase activity by 27 +/- 3% (4.3 +/- 0.7, Mean +/- SEM; pmoles/min/mg vs 5.9 +/- 0.8, P less than .05). The data demonstrate that both A1 and A2 adenosine receptors are present in coronary vascular smooth muscle. The results indicate that adenosine may mediate both vasodilation and vasoconstriction in the coronary circulation via A2 and A1 adenosine receptors, respectively.

Adenosine↗
PubMed1990

Contracting data.

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Contract Services↗
PubMed1990

The role of symmetrical and asymmetrical social conflict in cognitive change.

We asked whether dyads consisting of nonconservers of liquid would be more likely than solo controls to change to a conservation answer when each child gave symmetrically conflicting answers from different perspectives ("more" versus "less" from different viewpoints). We also asked whether nonconservers are more likely than conservers to abandon their answers in conserver + nonconserver dyads. In order to stimulate the perspectival conflicts in the nonconserver + nonconserver dyads, the partners experienced artificial displays in which the two possible answers were afforded by different views of the apparatus. We found no evidence that social conflict of the kind engineered in the nonconserver + nonconserver dyads stimulates cognitive change. Our evidence that nonconservers tend to adopt the conservation answer of their partners was less strong than that collected in previous studies, but this may have been due to the fact that, contrary to previous studies, the children's social dominance relations were affecting the outcome. We concluded that the ineffectiveness of symmetrical social conflict is consistent with Piaget's conception of nonconservers as children insensitive to the perspective-relative nature of their judgments.

Child↗
PubMed1989

Effect of thyroid status on catecholamine stimulation of thyroxine 5'-deiodinase in brown adipocytes.

We examined type II 5'-iodothyronine deiodinase activation by adrenergic agonists in dispersed brown adipocytes from euthyroid and hypothyroid rats. In euthyroid cells, basal deiodinase activity was 30-100 fmol I-.h-1.10(6) cells-1 and increased four- to fivefold during exposure to norepinephrine, an effect that was enhanced by alprenolol. In cells from hypothyroid rats, norepinephrine caused a three- to fourfold greater deiodinase stimulation than occurred in euthyroid cells but alprenolol inhibited the response. In euthyroid cells, phenylephrine caused greater stimulation than did norepinephrine, but this was inhibited by alprenolol. Isoproterenol and 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP) inhibited the phenylephrine response but were modestly stimulatory alone. Although both alpha 1- and beta-adrenergic agonists increased deiodinase activity modestly in hypothyroid cells, in combination they caused a marked synergistic stimulation. This synergism was induced by 8-BrcAMP and forskolin, as well as by isoproterenol. The stimulation of deiodinase in both cell types was due to an increase in Vmax without an alteration in the Km and required mRNA synthesis. The markedly greater deiodinase response of the hypothyroid brown adipocyte to catecholamines may serve to enhance the impaired thermogenic response of this tissue to cold exposure.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1988

Phorbol esters, protein kinase C, and thyroxine 5'-deiodinase in brown adipocytes.

Protein kinase C activity has been identified in the rat brown adipocyte. About 60% of this activity is found in the cytosolic fraction under basal conditions, and 12-O-tetradecanoylphorbol 13-acetate (TPA) causes a rapid shift from the cytosol to the particulate fraction. Norepinephrine and phenylephrine cause a similar redistribution that can be blocked by prazosin but not by alprenolol. alpha 1-Adrenergic agonists cause three- to fivefold stimulation of type 2 iodothyronine 5'-deiodinase activity in brown adipocytes. TPA has no effect on basal deiodinase activity and reduces the response of the enzyme to alpha 1-adrenergic agonists. These results suggest that the translocation of protein kinase C from cytosol to particulate fraction is not sufficient to increase deiodinase activity but can modulate the alpha 1-adrenergic agonist-mediated responses in these cells.

Adipose Tissue, Brown↗
PubMed1987

Insulin stimulation of iodothyronine 5'-deiodinase in rat brown adipocytes.

Insulin (100-3333 microU/ml) stimulates iodothyronine 5'-deiodinase 3 to 4 fold in dispersed rat brown adipocytes. Deiodinase activity increased steadily from 1 to 4 hours. Insulin increased enzyme activity via an increase in the Vmax while the Km remained unchanged. Omission of glucose from the medium did not affect the insulin response. Studies with alpha-amanitin suggested that the increase in deiodinase activity was not due to an increase in the rate of transcription. The insulin effect was not additive to that of alpha 1-catecholamines, suggesting the two stimulators might have one or more common elements.

Adipose Tissue, Brown↗
PubMed1987

Catecholamine stimulation of iodothyronine 5'-deiodinase activity in rat dispersed brown adipocytes.

We describe an in vitro system for evaluating the direct effects of catecholamines on the activity of the type II iodothyronine 5'-deiodinase in dispersed rat brown adipocytes. Incubation with norepinephrine or phenylephrine for 3-4 h causes up to a 5-fold increase in deiodinase activity in these cells. As found in vivo studies, the norepinephrine stimulation is blocked by coincubation with the alpha 1-adrenergic antagonist prazosin. The beta-adrenergic antagonist alprenolol either has no effect or increases stimulation by norepinephrine. These results suggest that beta-adrenergic agonists inhibit the activation or synthesis of the deiodinase in these cells.

Adipose Tissue, Brown↗
PubMed1986

Pertussis toxin effects on adenylate cyclase activity, cyclic AMP accumulation and lipolysis in adipocytes from hypothyroid, euthyroid and hyperthyroid rats.

Adipocytes from hypothyroid rats have a decreased responsiveness to agents that activate adenylate cyclase, whereas cells from hyperthyroid rats have an increased responsiveness as compared to the controls. This is reflected in cyclic AMP accumulation as well as lipolysis. Administration of pertussis toxin to rats or its in vitro addition to adipocytes increased basal lipolysis and cyclic AMP accumulation as well as the response to norepinephrine or forskolin. The effects of thyroid status was not abolished by toxin treatment. Pertussis toxin-catalyzed ADP ribosylation of Ni was increased in adipocyte membranes from hypothyroid rats as compared to those from euthyroid rats. However, no change in sensitivity to N6-(phenylisopropyl)adenosine was observed. The data suggest that the amount of Ni might not be rate-limiting for the inhibitory action of adenosine. A consistent decrease in maximal lipolysis was observed in freshly isolated adipocytes from hypothyroid animals as compared to those from the controls. Such defective maximal lipolysis was not corrected by adenosine deaminase or in vivo administration of pertussis toxin. The relationship between cyclic AMP levels and lipolysis suggests that in fat cells from hypothyroid rats either the cyclic AMP-dependent protein kinase or the lipase activity itself may limit maximal lipolysis. There appears to be multiple effects of thyroid status on lipolysis involving factors other than those affecting adenylate cyclase activation.

Adenosine Deaminase↗