Biomedical subjects

M C Moore

Publications and source records attributed to M C Moore.

At least 37 records · Page 2Linked to original sources

PubMed1999

The catastrophic misinterpretation of physiological distress.

Cognitive theories of panic disorder suggest that the catastrophic misinterpretation of bodily sensations is the trigger for a panic attack. A challenge to cognitive theories is the suggestion that dyspnea (shortness of breath) is central to the development of panic and that negative cognitions are by-products of panic. To examine these seemingly contradictory theoretical perspectives, the present study investigated panic symptomatology in a sample of patients with chronic shortness of breath (i.e. pulmonary patients). Past studies have shown an increased prevalence of panic in pulmonary patients, a finding that may be useful in elucidating panic etiology. The current sample of pulmonary patients (N = 28) confirmed previous reports of high prevalence rates of panic in this population. Based on self-report of panic symptomatology, a total of nine patients (32%) met DSM-IV criteria that were consistent with panic disorder. Multivariate comparison of participants with and without panic symptomatology revealed that panickers had significantly higher levels of anxiety, depression and agoraphobic cognitions. However, these groups showed no significant differences on physiological measures of pulmonary functioning. The authors conclude that dyspnea alone is inadequate in predicting panic development. High levels of panic symptomatology in pulmonary samples may reflect increased opportunities for these patients to misinterpret bodily sensations and, in particular, their pulmonary symptoms.

Aged↗

PubMed1999

Another look at the psychometric properties of the Anxiety Control Questionnaire.

This study examined the psychometric properties of the Anxiety Control Questionnaire (AxCQ), a recently developed 30-item instrument intended to assess an individual's perceived level of control over anxiety related events. The sample consisted of 303 college students (189 females, 110 males, 4 no response). Although the scale is reported to have a two factor solution, results of an exploratory factor analysis in this sample indicated a three factor solution was more appropriate. Significant correlations were found between the three factor scales (r's ranged from 0.28 to 0.62). Internal consistency appeared good for the total AxCQ and for the factor scales derived from both the two and three factor models. There were no significant gender differences. We conclude that the psychometric properties of the scale look promising, but recommend that the factor structure of the AxCQ continue to be explored.

Adult↗

PubMed1999

Insulin- and glucagon-independent effects of calcitonin gene-related peptide in the conscious dog.

Calcitonin gene-related peptide (CGRP) causes vasodilation in many vascular beds, resulting in hypotension and tachycardia. The current studies were conducted in overnight-fasted conscious dogs to determine the effect of different CGRP dosages on carbohydrate metabolism and catecholamine release resulting from hemodynamic changes. During a pancreatic clamp, dogs received intraportal infusions of CGRP at 13, 26, and 52 (n = 3) or 52, 105, and 210 pmol x kg(-1) x min(-1) (n = 4; 60 minutes at each rate). Blood pressure decreased (P < .05) and the heart rate and hepatic blood flow (HBF) increased a maximum of 100% and 30%, respectively (P < .05). For the five CGRP infusion rates, arterial plasma epinephrine increased approximately 1.3-, 2.4-, 7.4-, 12-fold, and eightfold basal, respectively; norepinephrine increased about 2.3-, 3.3-, 4.1-, 4.6-, and 4.8-fold basal, respectively; and cortisol increased about twofold, 3.4-fold, fivefold, sixfold, and 6.2-fold basal, respectively. At CGRP infusion rates of 52 pmol x kg(-1) x min(-1) or higher, increases (P < .05) occurred for plasma glucose, endogenous glucose production (EndoRa), and net hepatic uptake of gluconeogenic substrates (maximum change, 24 mg/dL, 1.3 mg x kg(-1) x min(-1), and 9.9 micromol x kg(-1) x min(-1), respectively). Arterial blood glycerol concentrations increased only a maximum of 30%. At the two highest CGRP infusion rates, glycerol returned to basal concentrations and arterial plasma nonesterified fatty acids (NEFAs) decreased. The increased net hepatic uptake of gluconeogenic substrates during CGRP infusion was sufficient to account for 49% to 58% of the increase in EndoRa. CGRP has no apparent direct effects on hepatic carbohydrate metabolism, but the catecholamines, at levels similar to those observed during CGRP infusion, stimulate hepatic glycogenolysis. Therefore, some factor(s) other than CGRP, probably an increase in circulating catecholamine concentrations, would appear to be responsible for at least 42% to 51% of the increase in EndoRa.

Alanine↗

PubMed1999

Net hepatic gluconeogenic amino acid uptake in response to peripheral versus portal amino acid infusion in conscious dogs.

These studies were conducted to determine the effect of route of gluconeogenic amino acid delivery on the hepatic uptake of the amino acids. After a sampling period with no experimental intervention (basal period), conscious dogs deprived of food for 42 h received somatostatin, intraportal infusions of insulin (3-fold basal) and glucagon (basal), and a peripheral infusion of glucose to increase the hepatic glucose load 1.5-fold basal for 240 min. A mixture of alanine, glutamate, glutamine, glycine, serine and threonine was infused intraportally at 7.6 micromol. kg(-1). min(-1) (PorAA group, n = 6) or peripherally at 8.1 micromol. kg(-1). min(-1) (PerAA, n = 6), to match the hepatic load of gluconeogenic amino acids in PorAA. During the infusion period, there were no differences in PerAA and PorAA, respectively, with regard to arterial plasma insulin (144 +/- 18 and 162 +/- 18 pmol/L), glucagon (51 +/- 8 and 47 +/- 11 ng/L), hepatic glucose load (199.8 +/- 22.2 and 210.9 +/- 16.6 micromol. kg(-1). min(-1)), net hepatic glucose uptake (2.8 +/- 2.2 and 2.2 +/- 1.7 micromol. kg(-1). min(-1)), hepatic load of amino acids (68 +/- 14 and 62 +/- 7 micromol. kg(-1). min(-1)), or net hepatic glycogen synthesis (11.1 +/- 2.2 and 8.9 +/- 2.2 micromol. kg(-1). min(-1)). The net hepatic uptake of glutamine (2.1 +/- 0.4 vs. 0.8 +/- 0.3 micromol. kg(-1). min(-1)) and the net hepatic fractional extractions of glutamine (0.11 +/- 0.02 vs. 0.05 +/- 0.02) and serine (0.41 +/- 0.03 vs. 0.34 +/- 0.02) were greater in PorAA than in PerAA (P < 0.05). We speculate that one or more of the amino acids in the mixture causes enhancement of the net hepatic uptake and fractional extraction of glutamine, and perhaps other gluconeogenic amino acids, during intraportal amino acid delivery.

Amino Acids↗

PubMed1999

Differential effect of amino acid infusion route on net hepatic glucose uptake in the dog.

Concomitant portal infusion of gluconeogenic amino acids (GNGAA) and glucose significantly reduces net hepatic glucose uptake (NHGU), in comparison with NHGU during portal infusion of glucose alone. To determine whether this effect on NHGU is specific to the portal route of GNGAA delivery, somatostatin, intraportal insulin (3-fold basal) and glucagon (basal), and intraportal glucose (to increase the hepatic glucose load by approximately 50%) were infused for 240 min. GNGAA were infused peripherally into a group of dogs (PeAA), at a rate to match the hepatic GNGAA load in a group of dogs that were given the same GNGAA mixture intraportally (PoAA) at 7.6 micromol. kg-1. min-1 (9). The arterial blood glucose concentrations and hepatic glucose loads were the same in the two groups, but NHGU (-0. 9 +/- 0.2 PoAA and -2.1 +/- 0.5 mg. kg-1. min-1 in PeAA, P < 0.05) and net hepatic fractional extraction of glucose (2.6 +/- 0.7% in PoAA vs. 5.9 +/- 1.4% in PeAA, P < 0.05) differed. Neither the hepatic loads nor the net hepatic uptakes of GNGAA were significantly different in the two groups. Net hepatic glycogen synthesis was approximately 2.5-fold greater in PeAA than PoAA (P < 0.05). Intraportal, but not peripheral, amino acid infusion suppresses NHGU and net hepatic glycogen synthesis in response to intraportal glucose infusion.

Amino Acids↗

PubMed1999

Rapid reversal of the effects of the portal signal under hyperinsulinemic conditions in the conscious dog.

Experiments were performed on two groups of 42-h-fasted conscious dogs (n = 6/group). Somatostatin was given peripherally with insulin (4-fold basal) and glucagon (basal) intraportally. In the first experimental period, glucose was infused peripherally to double the hepatic glucose load (HGL) in both groups. In the second experimental period, glucose (21.8 micromol. kg-1. min-1) was infused intraportally and the peripheral glucose infusion rate (PeGIR) was reduced to maintain the precreating HGL in the portal signal (PO) group, whereas saline was given intraportally in the control (CON) group and PeGIR was not changed. In the third period, the portal glucose infusion was stopped in the PO group and PeGIR was increased to sustain HGL. PeGIR was continued in the CON group. The glucose loads to the liver did not differ in the CON and PO groups. Net hepatic glucose uptake was 9.6 +/- 2.5, 11.6 +/- 2.6, and 15.5 +/- 3.2 vs. 10.8 +/- 1.8, 23.7 +/- 3.0, and 15.5 +/- 1.1 micromol. kg-1. min-1, and nonhepatic glucose uptake (non-HGU) was 29.8 +/- 1.1, 40.1 +/- 4.5, and 49.5 +/- 4.0 vs. 26.6 +/- 4.3, 23.2 +/- 4.0, and 40.4 +/- 3.1 micromol. kg-1. min-1 in the CON and PO groups during the three periods, respectively. Cessation of the portal signal shifted NHGU and non-HGU to rates similar to those evident in the CON group within 10 min. These results indicate that even under hyperinsulinemic conditions the effects of the portal signal on hepatic and peripheral glucose uptake are rapidly reversible.

Animals↗

PubMed1999

The head arterial glucose level is not the reference site for generation of the portal signal in conscious dogs.

Experiments were performed on twelve 42-h-fasted, conscious dogs to determine whether the head arterial glucose level is used as a reference standard for comparison with the portal glucose level in bringing about the stimulatory effect of portal glucose delivery on net hepatic glucose uptake (NHGU). Each experiment consisted of an 80-min equilibration, a 40-min control, and two 90-min test periods. After the control period, somatostatin was given along with insulin (7.2 pmol. kg(-1). min(-1); 3.5-fold increase) and glucagon (0.6 ng. kg(-1). min(-1); basal) intraportally. Glucose was infused intraportally (22.2 micromol. kg(-1). min(-1)) and peripherally as needed to double the hepatic glucose load. In one test period, glucose was infused into both vertebral and carotid arteries (HEAD(G); 22.2 +/- 0.8 micromol. kg(-1). min(-1)); in the other test period, saline was infused into the head arteries (HEAD(S)). One-half of the dogs received HEAD(G) first. When all dogs are considered, the blood arterial-portal glucose gradients (-0.52 +/- 0.07 vs. -0.49 +/- 0.03 mM) and the hepatic glucose loads (339 +/- 14 vs. 334 +/- 20 micromol. kg(-1). min(-1)) were similar in HEAD(G) and HEAD(S). NHGU was 24.1 +/- 3.8 and 25.1 +/- 4.6 micromol. kg(-1). min(-1), and nonhepatic glucose uptake was 46.1 +/- 4.2 and 48.8 +/- 7.0 micromol. kg(-1). min(-1) in HEAD(G) and HEAD(S), respectively. The head arterial glucose level is not the reference standard used for comparison with the portal glucose level in the generation of the portal signal.

Animals↗

PubMed1999

Adenosine upregulates VEGF expression in cultured myocardial vascular smooth muscle cells.

We tested whether adenosine has differential effects on vascular endothelial growth factor (VEGF) expression under normoxic and hypoxic conditions, and whether A(1) or A(2) receptors (A(1)R; A(2)R) mediate these effects. Myocardial vascular smooth muscle cells (MVSMCs) from dog coronary artery were exposed to hypoxia (1% O(2)) or normoxia (20% O(2)) in the absence and presence of adenosine agonists or antagonists for 18 h. VEGF protein levels were measured in media with ELISA. VEGF mRNA expression was determined with Northern blot analysis. Under normoxic conditions, the adenosine A(1)R agonists, N(6)-cyclopentyladenosine and R(-)-N(6)-(2-phenylisopropyl)adenosine did not increase VEGF protein levels at A(1)R stimulatory concentrations. However, adenosine (5 microM) and the adenosine A(2)R agonist N(6)-[2-(3, 5-dimethoxyphenyl)-2-(2-methylphenyl)]ethyl adenosine (DPMA; 100 nM) increased VEGF protein levels by 51 and 132% and increased VEGF mRNA expression by 44 and 90%, respectively, in cultured MVSMCs under normoxic conditions. Hypoxia caused an approximately fourfold increase in VEGF protein and mRNA expression, which could not be augmented with exogenous adenosine, A(2)R agonist (DPMA), or A(1)R agonist [1,3-diethyl-8-phenylxanthine (DPX)]. The A(2)R antagonist 8-(3-chlorostyryl)-caffeine completely blocked adenosine-induced VEGF protein and mRNA expression and decreased baseline VEGF protein levels by up to approximately 60% under normoxic conditions but only by approximately 25% under hypoxic conditions. The A(1)R antagonist DPX had no effect. These results are consistent with the hypothesis that 1) adenosine increases VEGF protein and mRNA expression by way of A(2)R. 2) Adenosine plays a major role as an autocrine factor regulating VEGF expression during normoxic conditions but has a relatively minor role during hypoxic conditions. 3) Endogenous adenosine can account for the majority of basal VEGF secretion by MVSMCs under normoxic conditions and could therefore be a maintenance factor for the vasculature.

Adenosine↗

PubMed1998

Hepatic glucose disposition during concomitant portal glucose and amino acid infusions in the dog.

The effect of concomitant intraportal infusion of glucose and gluconeogenic amino acids (AA) on net hepatic glucose uptake (NHGU) and glycogen synthesis was examined in 42-h-fasted dogs. After a basal period, there was a 240-min experimental period during which somatostatin was infused continuously into a peripheral vein and insulin and glucagon (at 3-fold basal and basal rates, respectively) and glucose (18.3 mumol.kg-1.min-1) were infused intraportally. One group (PoAA, n = 7) received an AA mixture intraportally at 7.6 mumol.kg-1.min-1, whereas the other group (NoAA, n = 6) did not receive AA. Arterial blood glucose concentrations and hepatic glucose loads were the same in the two groups. NHGU averaged 4.8 +/- 2.0 (PoAA) and 9.4 +/- 2.0 (NoAA) mumol.kg-1.min-1 (P < 0.05), and tracer-determined hepatic glucose uptake was 4.6 +/- 1.6 (PoAA) and 10.0 +/- 1.7 (NoAA) mumol.kg-1.min-1 (P < 0.05). AA data for PoAA and NoAA, respectively, were as follows: arterial blood concentrations, 1,578 +/- 133 vs. 1,147 +/- 86 microM (P < 0.01); hepatic loads, 56 +/- 3 vs. 32 +/- 4 mumol.kg-1.min-1 (P < 0.01); and net hepatic uptakes, 14.1 +/- 1.4 vs. 5.6 +/- 0.4 mumol.kg-1.min-1 (P < 0.01). The rate of net hepatic glycogen synthesis was 7.5 +/- 1.9 (PoAA) vs. 10.7 +/- 2.3 (NoAA) mumol.kg-1.min-1 (P = 0.1). In a net sense, intraportal gluconeogenic amino acid delivery directed glucose carbon away from the liver. Despite this, net hepatic carbon uptake was equivalent in the presence and absence of amino acid infusion.

Amino Acids↗

PubMed1998

Hepatic glucose uptake rapidly decreases after removal of the portal signal in conscious dogs.

The aim of this study was to assess the decay of the effect of the portal signal on net hepatic glucose uptake (NHGU). Experiments were performed on five 42-h-fasted conscious dogs. After the 40-min basal period, somatostatin was given peripherally along with insulin (1.8 pmol. kg-1. min-1) and glucagon (0.65 ng. kg-1. min-1) intraportally. In the first experimental period (Pe-GLU-1; 90 min), glucose was infused into a peripheral vein to double the glucose load to the liver (HGL). In the second experimental period (Po-GLU; 90 min), glucose (20.1 micromol. kg-1. min-1) was infused intraportally and the peripheral glucose infusion was reduced to maintain the same HGL. In the third period (Pe-GLU-2; 120 min), the portal glucose infusion was stopped and the peripheral glucose infusion was increased to again sustain HGL. Arterial insulin levels (42 +/- 3, 47 +/- 3, 43 +/- 3 pmol/l) were basal and similar in the Pe-GLU-1, Po-GLU, and Pe-GLU-2 periods, respectively. Arterial glucagon levels were also basal and similar (51 +/- 3, 49 +/- 2, 46 +/- 2 ng/l) in the three experimental periods. The glucose loads to the liver were 251 +/- 11, 274 +/- 14, and 276 +/- 12 micromol. kg-1. min-1, respectively. NHGU was 6.3 +/- 2.4, 19.1 +/- 2.8, and 9.2 +/- 1.2 micromol. kg-1. min-1, and nonhepatic glucose uptake (non-HGU) was 23.6 +/- 3.0, 5.3 +/- 1.8, and 25.5 +/- 3.7 micromol. kg-1. min-1 in the three periods, respectively. Cessation of the portal signal for only 10 min shifted NHGU and non-HGU to 9.4 +/- 2.2 and 25.0 +/- 2.8 micromol. kg-1. min-1, respectively; thus the effect of the portal signal was rapidly reversed both at the liver and peripheral tissues.

Animals↗

PubMed1998

Sodium induces hypertrophy of cultured myocardial myoblasts and vascular smooth muscle cells.

The mechanisms of sodium-induced myocardial hypertrophy and vascular hypertrophy are poorly understood. We tested the hypothesis that a high sodium concentration can directly induce cellular hypertrophy. Neonatal rat myocardial myoblasts (MMbs) and vascular smooth muscle cells (VSMCs) were cultured in a 50:50 mixture of DMEM and M199 supplemented with 10% fetal bovine serum. When the monolayers reached approximately 80% confluence, normal sodium medium (146 mmol/L) was replaced with high sodium media (152 mmol/L, 160 mmol/L, and 182 mmol/L) for up to 5 days. Increasing sodium from a baseline concentration of 146 mmol/L to the higher concentrations for 5 days caused dose-related increases in cell mean diameter, cell volume, and cellular protein content in both MMbs and VSMCs. Increasing the sodium concentration by only 4% (from 146 mmol/L to 152 mmol/L) caused the following respective changes in MMbs and VSMCs: 8.5% and 8.7% increase in cell mean diameter, 27.6% and 27.0% increase in cell volume, and 55.7% and 46.7% increase in cellular protein content. The rate of protein synthesis, expressed as [3H]leucine incorporation, increased by 87% and 99% in MMbs after exposure to 152 mmol/L and 160 mmol/L sodium, respectively, compared with the 146-mmol/L sodium control group. Exposure of MMbs to medium with a sodium concentration of 10% above normal, ie, 160 mmol/L, caused a significant decrease (range, 26% to 44%) in the rate of protein degradation at multiple time points over a 48-hour period compared with normal sodium control cells. The increase in cellular protein content caused by 160 mmol/L sodium returned to normal within 3 days after MMbs were returned to a normal sodium medium. These findings support the hypothesis that sodium has a direct effect to induce cellular hypertrophy and may therefore be an important determinant in causing myocardial and/or vascular hypertrophy in subjects with increased sodium concentration in the extracellular fluid.

Animals↗

PubMed1998

Autoregulation of hepatic glucose production.

In vitro evidence indicates that the liver responds directly to changes in circulating glucose concentrations with reciprocal changes in glucose production and that this autoregulation plays a role in maintenance of normoglycemia. Under in vivo conditions it is difficult to separate the effects of glucose on neural regulation mediated by the central nervous system from its direct effect on the liver. Nevertheless, it is clear that nonhormonal mechanisms can cause significant changes in net hepatic glucose balance. In response to hyperglycemia, net hepatic glucose output can be decreased by as much as 60-90% by nonhormonal mechanisms. Under conditions in which hepatic glycogen stores are high (i.e. the overnight-fasted state), a decrease in the glycogenolytic rate and an increase in the rate of glucose cycling within the liver appear to be the explanation for the decrease in hepatic glucose output seen in response to hyperglycemia. During more prolonged fasting, when glycogen levels are reduced, a decrease in gluconeogenesis may occur as a part of the nonhormonal response to hyperglycemia. A substantial role for hepatic autoregulation in the response to insulin-induced hypoglycemia is most clearly evident in severe hypoglycemia (< or = 2.8 mmol/l). The nonhormonal response to hypoglycemia apparently involves enhancement of both gluconeogenesis and glycogenolysis and is capable of supplying enough glucose to meet at least half of the requirement of the brain. The nonhormonal response can include neural signaling, as well as autoregulation. However, even in the absence of the ability to secrete counterregulatory hormones (glucocorticoids, catecholamines, and glucagon), dogs with denervated livers (to interrupt neural pathways between the liver and brain) were able to respond to hypoglycemia with increases in net hepatic glucose output. Thus, even though the endocrine system provides the primary response to changes in glycemia, autoregulation plays an important adjunctive role.

Animals↗

PubMed1998

Review of counselling in a transfusion service: the London (UK) experience.

Donor (and recipient) counselling within the Transfusion Service in the UK has grown in volume and complexity over the last 10 years. The addition of new tests for donated blood and the growth of bone marrow transplantation have increased the demands on counselling staff. New initiatives, such as the HCV look-back programme, have required an extension of the skills and knowledge of staff involved in counselling.

Blood Donors↗

PubMed1997

Reproductive endocrinology of the explosively breeding desert spadefoot toad, Scaphiopus couchii.

The spadefoot toad, Scaphiopus couchii, is an explosively breeding, desert dwelling amphibian that shows two characteristics hypothesized to select for a dissociated breeding pattern: it lives in a harsh environment and it has a very short, but predictable breeding period. We tested the hypothesis that these factors select for a dissociated breeding cycle by measuring plasma steroid hormones and the gametogenic cycles in a free-living population of S. couchii. Blood and tissue samples were obtained from prebreeding, calling (males only), amplexed, and postbreeding toads. In males, plasma testosterone (T), dihydrotestosterone (DHT), and corticosterone (B) differed significantly among reproductive groups, with calling and amplexing toads having the highest levels of each of these steroids. In females, plasma T, DHT, B, progesterone (P), and estradiol (E2) were measured; all steroids except B changed significantly among mating groups. Plasma T and E2 were greatest in prebreeding and amplexed females, while P and DHT were highest only in amplexed females. Primary spermatogonia (SPG I), secondary spermatogonia (SPG II), spermatocytes, spermatids (SPT), and spermatozoa embedded in Sertoli cells (SPS) all changed significantly among male breeding groups. Although all stages were present in all breeding groups, early stages of spermatozoa (SPG I and SPG II) were greatest in postbreeding males, while late stages (SPT and SPS) were highest in prebreeding, calling, and amplexing males. In females, oocyte stages I, II, III, V, and VI and atretic follicles also differed significantly among mating groups. Prebreeding female ovaries were dominated by late-stage (V and VI) oocytes which were subsequently ovulated during amplexus. In postbreeding females, oogenesis was well under way as indicated by the rising numbers of stage II and III oocytes. These results indicate that aspects of gametogenesis occur during and after breeding in both sexes. Although the results demonstrate that gonadal activity was high during the period of sexual activity, suggesting that S. couchii most closely fits an associated pattern of reproduction as defined by Crews (1984, Horm. Behav. 18, 22-28), we also found that gonadal activity continued past the breeding season. For this reason, S. couchii does not completely conform to an associated pattern.

Animals↗

PubMed1997

Male morphs in tree lizards have different testosterone responses to elevated levels of corticosterone.

Changes in circulating glucocorticoid and androgen levels mediate agonistic behaviors in many vertebrates. Individual variation in the magnitude of the glucocorticoid response to stressful stimuli, the negative effects of elevated glucocorticoid levels on androgen levels, or both could mediate individual differences in subsequent agonistic behavior. In a series of previous studies, we found that both alternative male reproductive morphs in the tree lizard, Urosaurus ornatus, can exhibit elevated levels of plasma corticosterone following male-male encounters, but that the territorial morph appears less likely to exhibit coincident decreases in plasma testosterone. Two studies tested the hypothesis that the two morphs differ in the degree to which testosterone levels are influenced by elevated corticosterone levels. In the first study, physically restraining males elicited endogenous elevations of circulating corticosterone levels. Testosterone levels were significantly negatively correlated with corticosterone levels in the nonterritorial morph, but there was no correlation between levels of the two steroids in territorial males. In the second study, corticosterone levels were artificially elevated in free-living male tree lizards using a noninvasive dermal patch. This exogenous elevation of corticosterone significantly depressed testosterone levels in both morphs, but it produced a significantly greater depression in the nonterritorial morph. Nonterritorial males appear to be more sensitive than territorial males to the testosterone-suppressing effects of elevated circulating levels of corticosterone. This difference between the morphs in the effects of a stress hormone on the reproductive axis may be a fundamental part of the mechanism (1) underlying behavioral tactic switching within the nonterritorial morph or (2) contributing to behavioral differences between the morphs.

Administration, Cutaneous↗

PubMed1997

Sympathetic mediation of stress and aggressive competition: plasma catecholamines in free-living male tree lizards.

The sympathetic nervous system and adrenal catecholaminergic tissue act to prepare an animal for "fight or flight" by release of catecholamines into synapses and plasma. However, few studies have measured plasma catecholamines in nonmammalian vertebrates and none have measured them in free-living animals. We report plasma levels of norepinephrine (NE), epinephrine (EPI) and dopamine (DA) in free-living tree lizards (Urosaurus ornatus) bled in the field: 1) immediately after capture, 2) after 10 minutes of restraint, 3) immediately after a staged territorial encounter and 4) four minutes after the end of a staged territorial encounter. Time to capture and time to bleed after capture were also recorded for each sample. Time to capture had little effect on plasma catecholamines suggesting that plasma catecholamines do not rise during the brief pursuit by the investigator necessary to capture the lizards in the field. In contrast, plasma NE and EPI increased during blood collection. However, this response was very consistent allowing comparisons to be made using analysis of covariance to control for time to bleed. Results indicate that restraint stress caused a large increase in plasma levels of NE, E and DA. Plasma levels of NE and E, but not plasma DA, were also significantly elevated both immediately and 4 minutes after aggressive encounters, although less so than following restraint stress. These studies show that stress and aggression activate the sympatho-adrenal system. This activation could be involved in behavioral changes during aggression, meeting metabolic demands of the encounter, or both.

Adrenal Glands↗

PubMed1997

Does anti-HBc reactivity reflect 'lifestyle' risk in north London blood donors?

BACKGROUND AND OBJECTIVES: To determine whether antibody to hepatitis B core (anti-HBc) reactivity, as a marker of hepatitis B virus infection, reflects a 'lifestyle' risk in donors in North London, we have obtained detailed histories from donors with various manifestations of HBV infection. MATERIALS AND METHODS: Interviews based on a standardised questionnaire were conducted with 70 donors confirmed to be anti-HBc reactive. RESULTS: Comparison with controls (known to be anti-HBc-negative) and donors reactive for anti-hepatitis-C virus showed that current donor strategies are effective; in our area, reactivity for anti-HBc is not associated with a lifestyle risk for those donors who are unreactive in current mandatory screening tests. CONCLUSIONS: Blood from donors positive for both anti-HBc and anti-HBs should be considered suitable for transfusion purposes. This is consistent with the practice of accepting blood from naturally immune donors for preparation of hepatitis B immunoglobulin.

Antibodies, Viral↗

PubMed1997

Physiological changes in circulating glucagon alter hepatic glucose disposition during portal glucose delivery.

This study examined whether physiological changes in glucagon alter net hepatic glucose uptake (NHGU) or glycogen synthesis under conditions of hyperglycemia, hyperinsulinemia, and portal vein glucose concentrations exceeding those in the arterial circulation. Somatostatin was infused into 42-h-fasted dogs, insulin and glucagon were replaced intraportally at basal rates, and peripheral infusion of glucose maintained the hepatic glucose load twofold basal for 90 min (period 1). In period 2 (240 min) the insulin infusion was increased fourfold, glucose was infused intraportally, the hepatic glucose load was twofold basal, and glucagon was infused to create levels 150% basal (HiGGN, n = 6) or 40% basal (LoGGN, n = 6). NHGU rates (mg.kg-1.min-1) were low during period 1 (-0.9 +/- 0.7 in LoGGN and -0.2 +/- 0.4 in HiGGN, not significant) but increased during period 2 (-4.1 +/- 0.6 in LoGGN and -1.9 +/- 0.2 in HiGGN, P < 0.05). Endogenous glucose production (Endo Ra) declined during period 2 in LoGGN (P < 0.01 vs. basal) but did not change in HiGGN. Tracer-determined hepatic glucose uptake did not differ between groups. The poststudy increment in liver glycogen synthase I (12.5 +/- 3 vs. 6.5 +/- 2% of total) was greater in LoGGN (P < 0.05), as was net glycogen synthesis (27 +/- 8 vs. 13 +/- 3 mg/g liver, P = 0.06). An elevation in glucagon reduced NHGU (because of failure to suppress Endo Ra) and glycogen synthase activation and tended to reduce glycogen deposition.

Animals↗