Endothelial dysfunction in cardiovascular and endocrine-metabolic diseases: an update

The endothelium plays a vital role in maintaining circulatory homeostasis by the release of relaxing and contracting factors. Any change in this balance may result in a process known as endothelial dysfunction that leads to impaired control of vascular tone and contributes to the pathogenesis of some cardiovascular and endocrine/metabolic diseases. Reduced endothelium-derived nitric oxide (NO) bioavailability and increased production of thromboxane A2, prostaglandin H2 and superoxide anion in conductance and resistance arteries are commonly associated with endothelial dysfunction in hypertensive, diabetic and obese animals, resulting in reduced endothelium-dependent vasodilatation and in increased vasoconstrictor responses. In addition, recent studies have demonstrated the role of enhanced overactivation ofβ-adrenergic receptors inducing vascular cytokine production and endothelial NO synthase (eNOS) uncoupling that seem to be the mechanisms underlying endothelial dysfunction in hypertension, heart failure and in endocrine-metabolic disorders. However, some adaptive mechanisms can occur in the initial stages of hypertension, such as increased NO production by eNOS. The present review focuses on the role of NO bioavailability, eNOS uncoupling, cyclooxygenase-derived products and pro-inflammatory factors on the endothelial dysfunction that occurs in hypertension, sympathetic hyperactivity, diabetes mellitus, and obesity. These are cardiovascular and endocrine-metabolic diseases of high incidence and mortality around the world, especially in developing countries and endothelial dysfunction contributes to triggering, maintenance and worsening of these pathological situations.

Hypertensive effects of the iv administration of picomoles of ouabain

Ouabain, an endogenous digitalis compound, has been detected in nanomolar concentrations in the plasma of several mammals and is associated with the development of hypertension. In addition, plasma ouabain is increased in several hypertension models, and the acute or chronic administration of ouabain increases blood pressure in rodents. These results suggest a possible association between ouabain and the genesis or development and maintenance of arterial hypertension. One explanation for this association is that ouabain binds to the α-subunit of the Na+ pump, inhibiting its activity. Inhibition of this pump increases intracellular Na+, which reduces the activity of the sarcolemmal Na+/Ca2+ exchanger and thereby reduces Ca2+ extrusion. Consequently, intracellular Ca2+ increases and is taken up by the sarcoplasmic reticulum, which, upon activation, releases more calcium and increases the vascular smooth muscle tone. In fact, acute treatment with ouabain enhances the vascular reactivity to vasopressor agents, increases the release of norepinephrine from the perivascular adrenergic nerve endings and promotes increases in the activity of endothelial angiotensin-converting enzyme and the local synthesis of angiotensin II in the tail vascular bed. Additionally, the hypertension induced by ouabain has been associated with central mechanisms that increase sympathetic tone, subsequent to the activation of the cerebral renin-angiotensin system. Thus, the association with peripheral mechanisms and central mechanisms, mainly involving the renin-angiotensin system, may contribute to the acute effects of ouabain-induced elevation of arterial blood pressure.

Cardiac autonomic modulation during progressive upper limb exercise by patients with coronary artery disease

The purpose of this study was to investigate the behavior of heart rate (HR) and HR variability (HRV) during different loads of resistance exercise (incline bench press) in patients with coronary artery disease (CAD) and healthy sedentary controls. Ten healthy men (65 ± 1.2 years, control group, CG) and 10 men with clinically stable CAD (66 ± 2.4 years, CADG) were recruited. A discontinuous progressive protocol was applied with an initial load of 10% of the maximum load achieved in the 1RM (1 repetition maximum) with increases of 10% until 30% 1RM was reached, which was followed by subsequent increases of 5% 1RM until exhaustion. HRV was analyzed by linear and non-linear methods. There was a significant reduction in rMSSD (CG: 20 ± 2 to 11 ± 3 ms; CADG: 19 ± 3 to 9 ± 1 ms) and SD1 indexes (CG: 14 ± 2 to 8 ± 1 ms; CADG: 14 ± 2 to 7 ± 1 ms). An increase in HR (CG: 69 ± 5 to 90 ± 5 bpm; CADG: 62 ± 4 to 75 ± 4 bpm) and in systolic blood pressure (CG: 124 ± 3 to 138 ± 3 mmHg; CADG: 122 ± 6 to 126 ± 9 bpm) were observed (P < 0.05) when comparing pre-effort rest and 40% 1RM in both groups. Furthermore, an increase in RMSM index was also observed (CG: 28 ± 3 to 45 ± 9 ms; CADG: 22 ± 2 to 79 ± 33 ms), with higher values in CADG. We conclude that loads up to 30% 1RM during incline bench press result in depressed vagal modulation in both groups, although only stable CAD patients presented sympathetic overactivity at 20% 1RM upper limb exercise.

Estrous cycle and stress: influence of progesterone on the female brain

The female brain operates in a constantly changing chemical milieu caused by cyclical changes in gonadal hormones during the estrous cycle (menstrual cycle in women). Such hormones are highly lipophilic and pass readily from the plasma to the brain where they can influence neuronal function. It is becoming clear that the rapid reduction in peripheral circulating progesterone, which occurs during the late diestrous phase of the cycle, can trigger a withdrawal-like response, in which changes in GABA A receptor expression render hyper-responsive certain brain areas involved in processing responses to stressful stimuli. The periaqueductal gray matter (PAG) is recognised as an important region for integrating anxiety/defence responses. Withdrawal from progesterone, via actions of its neuroactive metabolite allopregnanolone, triggers up-regulation of extrasynaptic GABA A receptors on GABAergic neurons in the PAG. As a consequence, ongoing GABAergic tone on the output cells decreases, leading to an increase in functional excitability of the circuitry and enhanced responsiveness to stressful stimuli during the late diestrous phase. These changes during late diestrus could be prevented by short-term neurosteroid administration, timed to produce a more gradual fall in the peripheral concentration of allopregnanolone than the rapid decrease that occurs naturally, thus removing the trigger for the central withdrawal response.

Time course of the hemodynamic responses to aortic depressor nerve stimulation in conscious spontaneously hypertensive rats

The time to reach the maximum response of arterial pressure, heart rate and vascular resistance (hindquarter and mesenteric) was measured in conscious male spontaneously hypertensive (SHR) and normotensive control rats (NCR; Wistar; 18-22 weeks) subjected to electrical stimulation of the aortic depressor nerve (ADN) under thiopental anesthesia. The parameters of stimulation were 1 mA intensity and 2 ms pulse length applied for 5 s, using frequencies of 10, 30, and 90 Hz. The time to reach the hemodynamic responses at different frequencies of ADN stimulation was similar for SHR (N = 15) and NCR (N = 14); hypotension = NCR (4194 ± 336 to 3695 ± 463 ms) vs SHR (3475 ± 354 to 4494 ± 300 ms); bradycardia = NCR (1618 ± 152 to 1358 ± 185 ms) vs SHR (1911 ± 323 to 1852 ± 431 ms), and the fall in hindquarter vascular resistance = NCR (6054 ± 486 to 6550 ± 847 ms) vs SHR (4849 ± 918 to 4926 ± 646 ms); mesenteric = NCR (5574 ± 790 to 5752 ± 539 ms) vs SHR (5638 ± 648 to 6777 ± 624 ms). In addition, ADN stimulation produced baroreflex responses characterized by a faster cardiac effect followed by a vascular effect, which together contributed to the decrease in arterial pressure. Therefore, the results indicate that there is no alteration in the conduction of the electrical impulse after the site of baroreceptor mechanical transduction in the baroreflex pathway (central and/or efferent) in conscious SHR compared to NCR.

Linear and nonlinear analysis of heart rate variability in healthy subjects and after acute myocardial infarction in patients

The objectives of this study were to evaluate and compare the use of linear and nonlinear methods for analysis of heart rate variability (HRV) in healthy subjects and in patients after acute myocardial infarction (AMI). Heart rate (HR) was recorded for 15 min in the supine position in 10 patients with AMI taking β-blockers (aged 57 ± 9 years) and in 11 healthy subjects (aged 53 ± 4 years). HRV was analyzed in the time domain (RMSSD and RMSM), the frequency domain using low- and high-frequency bands in normalized units (nu; LFnu and HFnu) and the LF/HF ratio and approximate entropy (ApEn) were determined. There was a correlation (P < 0.05) of RMSSD, RMSM, LFnu, HFnu, and the LF/HF ratio index with the ApEn of the AMI group on the 2nd (r = 0.87, 0.65, 0.72, 0.72, and 0.64) and 7th day (r = 0.88, 0.70, 0.69, 0.69, and 0.87) and of the healthy group (r = 0.63, 0.71, 0.63, 0.63, and 0.74), respectively. The median HRV indexes of the AMI group on the 2nd and 7th day differed from the healthy group (P < 0.05): RMSSD = 10.37, 19.95, 24.81; RMSM = 23.47, 31.96, 43.79; LFnu = 0.79, 0.79, 0.62; HFnu = 0.20, 0.20, 0.37; LF/HF ratio = 3.87, 3.94, 1.65; ApEn = 1.01, 1.24, 1.31, respectively. There was agreement between the methods, suggesting that these have the same power to evaluate autonomic modulation of HR in both AMI patients and healthy subjects. AMI contributed to a reduction in cardiac signal irregularity, higher sympathetic modulation and lower vagal modulation.

Memory mood congruency phenomenon in bipolar I disorder and major depression disorder patients

The objective of the present study was to evaluate memory performance in tasks with and without affective content (to confirm the mood congruency phenomenon) in acutely admitted patients with bipolar I disorder (BD) and major depression disorder (MDD) and in healthy participants. Seventy-eight participants (24 BD, 29 MDD, and 25 healthy controls) were evaluated. Three word lists were used as the memory task with affective content (positive, negative and indifferent). Psychiatric symptoms were also evaluated with rating scales (Young Mania Rating Scale for mania and Hamilton Depression Rating Scale for depression). Patients were selected during the first week of hospitalization. BD patients showed higher scores in the word span with positive tone than MDD patients and healthy controls (P = 0.002). No other difference was observed for tests with affective tone. MDD patients presented significantly lower scores in the Mini-Mental State Exam, logical memory test, visual recognition span, and digit span, while BD patients presented lower scores in the visual recognition test and digit span. Mood congruency effect was found for word span with positive tone among BD patients but no similar effect was observed among MDD patients for negative items. MDD patients presented more memory impairment than BD patients, but BD patients also showed memory impairment

Pleiotropic effects of simvastatin in physically trained ovariectomized rats

This study tested the hypothesis that simvastatin treatment can improve cardiovascular and autonomic functions and membrane lipoperoxidation, with an increased effect when applied to physically trained ovariectomized rats. Ovariectomized rats were divided into sedentary, sedentary+simvastatin and trained+simvastatin groups (n = 8 each). Exercise training was performed on a treadmill for 8 weeks and simvastatin (5 mg/kg) was administered in the last 2 weeks. Blood pressure (BP) was recorded in conscious animals. Baroreflex sensitivity was evaluated by the tachycardic and bradycardic responses to BP changes. Cardiac vagal and sympathetic effects were determined using methylatropine and propranolol. Oxidative stress was evaluated based on heart and liver lipoperoxidation using the chemiluminescence method. The simvastatin-treated groups presented reduced body weight and mean BP (trained+simvastatin = 99 ± 2 and sedentary+simvastatin = 107 ± 2 mmHg) compared to the sedentary group (122 ± 1 mmHg). Furthermore, the trained group showed lower BP and heart rate compared to the other groups. Tachycardic and bradycardic responses were enhanced in both simvastatin-treated groups. The vagal effect was increased in the trained+simvastatin group and the sympathetic effect was decreased in the sedentary+simvastatin group. Hepatic lipoperoxidation was reduced in sedentary+simvastatin (≈21%) and trained+simvastatin groups (≈57%) compared to the sedentary group. Correlation analysis involving all animals demonstrated that cardiac lipoperoxidation was negatively related to the vagal effect (r = -0.7) and positively correlated to the sympathetic effect (r = 0.7). In conclusion, improvement in cardiovascular and autonomic functions associated with a reduction of lipoperoxidation with simvastatin treatment was increased in trained ovariectomized rats.

Acute but not chronic metabolic acidosis potentiates the acetylcholine-induced reduction in blood pressure: an endothelium-dependent effect

Metabolic acidosis has profound effects on vascular tone. This study investigated the in vivo effects of acute metabolic acidosis (AMA) and chronic metabolic acidosis (CMA) on hemodynamic parameters and endothelial function. CMA was induced by ad libitum intake of 1% NH4Cl for 7 days, and AMA was induced by a 3-h infusion of 6 M NH4Cl (1 mL/kg, diluted 1:10). Phenylephrine (Phe) and acetylcholine (Ach) dose-response curves were performed by venous infusion with simultaneous venous and arterial blood pressure monitoring. Plasma nitrite/nitrate (NOx) was measured by chemiluminescence. The CMA group had a blood pH of 7.15±0.03, which was associated with reduced bicarbonate (13.8±0.98 mmol/L) and no change in the partial pressure of arterial carbon dioxide (PaCO2). The AMA group had a pH of 7.20±0.01, which was associated with decreases in bicarbonate (10.8±0.54 mmol/L) and PaCO2 (47.8±2.54 to 23.2±0.74 mmHg) and accompanied by hyperventilation. Phe or ACh infusion did not affect arterial or venous blood pressure in the CMA group. However, the ACh infusion decreased the arterial blood pressure (ΔBP: -28.0±2.35 mm Hg [AMA] to -4.5±2.89 mmHg [control]) in the AMA group. Plasma NOx was normal after CMA but increased after AMA (25.3±0.88 to 31.3±0.54 μM). These results indicate that AMA, but not CMA, potentiated the Ach-induced decrease in blood pressure and led to an increase in plasma NOx, reinforcing the effect of pH imbalance on vascular tone and blood pressure control.

Natural born weight gainers: The mechanisms of obesity in transgenic mice overexpressing neuropeptide Y

Neuropeptide Y (NPY) is a neurotransmitter promoting energy storage by activating Y-receptors and thus affecting food intake, thermogenesis and adipose tissue metabolism. NPY is expressed both in the central and sympathetic nervous system. Hypothalamic NPY is known to stimulate feeding, but the effects of noradrenergic neuron NPY are more ambiguous. Chronic stress stimulates fat accumulation via NPY release from noradrenergic neurons. Furthermore, polymorphism in the human Npy gene has been associated with metabolic disturbances and increased NPY secretion after sympathetic stimulation. The main objective of this study was to clarify the mechanisms of noradrenergic neuron NPY in the development of obesity. The metabolic phenotype of a homozygous mouse overexpressing NPY in the brain noradrenergic neurons and sympathetic nervous system (OE-NPYDβH mouse) was characterized. OE-NPYDβH mice had an increased fat mass and body weight, which caused impairments of glucose metabolism and hyperinsulinaemia with age. There were no differences in energy intake or expenditure, but the sympathetic tone was down-regulated and the endocannabinoid system activated. Furthermore, peripheral Y2-receptors in energy-rich conditions played an important role in mediating the fat-accumulating effect of NPY. These results indicate that noradrenergic neuron NPY promotes obesity via direct effects in the periphery and by modulating the sympatho-adrenal and endocannabinoid systems. Additionally, NPY in the central noradrenergic neurons is believed to possess many important roles. The phenotype of the OE-NPYDβH mouse resembles the situations of chronic stress and Npy gene polymorphism and thus these mice may be exploited in testing novel drug candidates for the treatment of obesity.

Recueil de lettres originales.

Contient : 1 Lettre du roi « CHARLES » IX aux « ducz de Nemours et d'Aumalle,... A Verdun, le XXIIe jour d'avril 1569 » ; 2 Lettre du roi « CHARLES » IX au « duc de Nemours,... A Reyns, le XIIe jour de may 1569 » ; 3 Lettre du roi « CHARLES » IX au « duc de Nemoux,... De Verdun, ce XXe jour d'avril 1569 » ; 4 Lettre du roi « CHARLES » IX au « duc de Nemours,... A Verdun, le XXIIIIe jour d'avril 1569 » ; 5 Lettre de « CATERINE » DE MEDICIS au « duc de Nemours,... De Verdun, cet XXIIIme d'avril 1569 » ; 6 Lettre du roi « CHARLES » IX au « duc de Nemours,... De Soully, le XXIXe jour d'avril 1569 » ; 7 Lettre de « CATERINE [DE MEDICIS]... à... monsieur le duc de Nemours,... De Penney, cet XIIIIme de may 1569 » ; 8 Lettre du roi « CHARLES » IX au « duc de Nemours,... A Montceaulx, le XIXe jour de may 1569 » ; 9 Lettre du roi « CHARLES » IX au « duc de Nemours,... A Montceaulx, le XIXe jour de may 1569 » ; 10 Lettre de « CATERINE [DE MEDICIS]... à... madame de Nemours,... De Chenonseaulx, cet XXIme jour de may 157II » ; 11 Lettre d'ALFONSE II, « duca DI FERRARA », au « duca di Nemours,... Di Ferrara, a XX di maggio M.D.LXIX » ; 12 Lettre d'« E[MMANUEL] PHILIBERT [duc DE SAVOIE]... à... monseigneur [le duc de] Genevoys et de Nemours,... De Thurin, le XXIe may 1569 » ; 13 Lettre de « HENRIETTE DE CLEVES [duchesse DE NEVERS]... à monsieur le duc de Nemours,... De Nevers, ce XXIe may 1569 » ; 14 Lettre de « ALFONSO D'ORNANO,... all' illustrissimo... duca di Namors,... Da Cuers in Provenza, il XXII magio 1569 » ; 15 Lettre de « GUILLAUME DE MONTMORENCY,... à monsieur le duc de Nemoux,... Au camp de Ste Gemes, ce XXIIe may 1569 » ; 16 Lettre de « MARGUERITE DE FRANCE,... à... monseigneur le duc de Nemours,... De Thurin, ce XXIIIIe jour de may 1569 » ; 17 Lettre de « CLAUDE DE LORRAINE,... à monsieur le duc de Nemoux,... De camp pres Bourges, ce XXVe may 1569 » ; 18 Lettre de « BELLIEVRE,... à monseigneur le duc de Genevois et de Nemours,... De Solleurre, le XXVe jour de may 1569 » ; 19 Lettre de « HENRIETTE DE CLEVES,... à monsieur le duc de Nemours,... De Nevers, ce XXVe may 1569 » ; 20 Lettre de « FRANÇOYS [duc D'ALENÇON]... à madame... de Ferrare,... De Paris, ce XXIIIIme juing 1569 » ; 21 Lettre de « CATERINE [DE MEDICIS]... à... madame de Nemours,... D'Orleans, cet premier jour de joulet 1569 » ; 22 Lettre de « CATERINE [DE MEDICIS]... D'Orleans, cet VIIIme de joulet 1569 » ; 23 Lettre de « JAQUELINE DE ROHAN,... à madame de Nemours,... De Blandi, ce 27e juillet 1569 » ; 24 Lettre de « LEONOR D'ORLEANS [duc DE LONGUEVILLE]... à monsieur le duc de Nemours,... De Gallon, ce IIe d'aoust 1569 » ; 25 Lettre de « Don FRANCES DE ALAVA,... à madame la duchesse de Ferrare,... De Paris, le IIIe d'aoust 1569 » ; 26 Lettre d'« ENTRAIGUES,... à madame la duchesse de Ferrare,... D'Orleans, le XVIe jour d'aoust 1569 » ; 27 Lettre de FRANÇOIS DE « MONTMORENCY,... à monsieur... le duc de Nemoux,... D'Amboize, le XIIIIme jour d'aoust 1569 » ; 28 Lettre de « FRANÇOYS », duc D'ALENÇON, au « duc de Nemours,... De Paris, le XXe jour d'aoust 1569 » ; 29 Lettre de « FRANÇOYS [duc D'ALENÇON]... à... madame de Ferrare,... A Paris, le XXIIIIe jour d'aoust 1569 » ; 30 Lettre de « FRANÇOYS [duc D'ALENÇON]... à... monsieur le duc de Nemours,... De Paris, ce XXVIme jour d'aoust 1569 » ; 31 Lettre de « BASTIEN DE LUXAMBOURG,... à monsieur... le duc d'Annemours,... Au camp de Chynon, ce XXIe jour de septembre 1569 » ; 32 Lettre de « ROGIER DE BELLEGARDE,... à monseigneur... le duc de Nemours... 1569 » ; 33 Lettre de « CATERINE [DE MEDICIS]... à... madame de Nemours,... Du Plesis, cet Xme d'octobre 1569 » ; 34 Lettre d'« E[MMANUEL] PHILIBERT [duc DE SAVOIE]... à madame... la duchesse de Genevoys et d'Anemours,... De Chambery, ce 26 octobre 1569 » ; 35 Lettre de « CATERINE [DE MEDICIS]... à... madame de Nemours,... De Tone Botone, cet VIme de novembre 1569 » ; 36 Lettre de « CLAUDE DE LORRAINE,... à monsieur... le duc de Nemours,... De Tonne et Boutonne pres St Jehan d'Angely, le XVe novembre 1569 » ; 37 Lettre du roi « CHARLES » IX au « duc de Nemoux,... Au camp de Tonne Boutonne, le XVIIe jour de novembre 1569 » ; 38 Lettre de « BASTIEN DE LUXAMBOURG,... à monsieur... le duc de Nemours et de Gennevoys,... Au camp de Tonné Boutonne, ce XVIIme jour de novembre 1569 » ; 39 Lettre de « CHARLES, e[vêque] du Mans... à monseigneur... le duc de Genevoys et de Nemours,... De Romme, ce XXIme de novembre 1569 » ; 40 Lettre, en espagnol, de « Don FRANCES DE ALAVA,... al illmo... duque de Nevers,... Metz, 8 decembris 1569 » ; 41 Lettre de « MARGUERITE DE FRANCE,... à... monsieur le duc de Nemours,... De Thurin, ce VIe jour de decembre 1569 » ; 42 Lettre de « C., conte DE ROGENDORFF,... à monseigneur... le duc de Nemours,... De Montereau Faut Yone, le VIIIe de decembre 1569 » ; 43 Lettre de « CATERINE [DE MEDICIS]... à... monsieur de Nemours,... De Tonay Botone, cet XI de decembre 1569 » ; 44 Lettre de « CATERINE [DE MEDICIS]... à... madame de Nemours,... De Colonge La Reau, cete nuit de Noel 1569 » ; 45 Lettre de « LEONOR D'ORLEANS [duc DE LONGUEVILLE]... à monsieur... de Nemoux,... De Blandy, ce XXIIIIe jour de decembre 1569 » ; 46 Lettre, en italien, de « FRANCESCO MARIA, principeD'URBINO », à Renée de France, duchesse de Ferrare. « Di Pesaro, alli XXVIII Xbre M.D.LXIX » ; 47 Lettre de « JAQUES DE SAVOYE [duc DE NEMOURS]... à madame... la duchesse de Ferrare » ; 48 Lettre, en italien, de l'évêque de Sinigaglia « a... madama la duchessa di Ferrara,... Da Sinigaglia, il XV di genaro 1570 » ; 49 Lettre, en italien, d'« ALESSANDRO RANGONE,... a... madama Rhenea di Franza,... Di Modena, li XXI di genaro M.D.LXX » ; 50 Lettre, en italien, de FRANÇOIS MARIE, « principe D'URBINO,... a... madama Renea di Francia, duchessa di Ferrara,... Di Pesaro, a XXII di genaro del LXX » ; 51 Lettre, en italien, du « duca D'URBINO,... a... madama Renea di Francia, duchessa di Ferrara,... Di Pesaro, il di III di genaro del LXX »

Men's Basketball Team (1988-89)

Coach: Garney Henley Team (Alphabetically): Bruce Adams, Frank Capretta, Kevin Farrow, David Dennis, Rob Demott, Brian Hayden, Peter Kaija, Steve Kolenko, Leacoft Panton, Kevin Rome, Kevin Stevinson, Glen Tone, Moe Willoughby

Cortical and autonomic modulation of attentional control /

Whereas the role of the anterior cingulate cortex (ACC) in cognitive control has received considerable attention, much less work has been done on the role of the ACC in autonomic regulation. Its connections through the vagus nerve to the sinoatrial node of the heart are thought to exert modulatory control over cardiovascular arousal. Therefore, ACC is not only responsible for the implementation of cognitive control, but also for the dynamic regulation of cardiovascular activity that characterizes healthy heart rate and adaptive behaviour. However, cognitive control and autonomic regulation are rarely examined together. Moreover, those studies that have examined the role of phasic vagal cardiac control in conjunction with cognitive performance have produced mixed results, finding relations for specific age groups and types of tasks but not consistently. So, while autonomic regulatory control appears to support effective cognitive performance under some conditions, it is not presently clear just what factors contribute to these relations. The goal of the present study was, therefore, to examine the relations between autonomic arousal, neural responsivity, and cognitive performance in the context of a task that required ACC support. Participants completed a primary inhibitory control task with a working memory load embedded. Pre-test cardiovascular measures were obtained, and ontask ERPs associated with response control (N2/P3) and error-related processes (ERN/Pe) were analyzed. Results indicated that response inhibition was unrelated to phasic vagal cardiac control, as indexed by respiratory sinus arrhythmia (RSA). However, higher resting RSA was associated with larger ERN ampUtude for the highest working memory load condition. This finding suggests that those individuals with greater autonomic regulatory control exhibited more robust ACC error-related responses on the most challenging task condition. On the other hand, exploratory analyses with rate pressure product (RPP), a measure of sympathetic arousal, indicated that higher pre-test RPP (i.e., more sympathetic influence) was associated with more errors on "catch" NoGo trials, i.e., NoGo trials that simultaneously followed other NoGo trials, and consequently, reqviired enhanced response control. Higher pre-test RPP was also associated with smaller amplitude ERNs for all three working memory loads and smaller ampUtude P3s for the low and medium working memory load conditions. Thus, higher pretest sympathetic arousal was associated with poorer performance on more demanding "catch" NoGo trials and less robust ACC-related electrocortical responses. The findings firom the present study highlight tiie interdependence of electrocortical and cardiovascular processes. While higher pre-test parasympathetic control seemed to relate to more robust ACC error-related responses, higher pre-test sympathetic arousal resulted in poorer inhibitory control performance and smaller ACC-generated electrocortical responses. Furthermore, these results provide a base from which to explore the relation between ACC and neuro/cardiac responses in older adults who may display greater variance due to the vulnerabihty of these systems to the normal aging process.

Information processing in sleep-onset insomnia : a test of the neurocognitive model /

The present thesis study is a systematic investigation of information processing at sleep onset, using auditory event-related potentials (ERPs) as a test of the neurocognitive model of insomnia. Insomnia is an extremely prevalent disorder in society resulting in problems with daytime functioning (e.g., memory, concentration, job performance, mood, job and driving safety). Various models have been put forth in an effort to better understand the etiology and pathophysiology of this disorder. One of the newer models, the neurocognitive model of insomnia, suggests that chronic insomnia occurs through conditioned central nervous system arousal. This arousal is reflected through increased information processing which may interfere with sleep initiation or maintenance. The present thesis employed event-related potentials as a direct method to test information processing during the sleep-onset period. Thirteen poor sleepers with sleep-onset insomnia and 1 2 good sleepers participated in the present study. All poor sleepers met the diagnostic criteria for psychophysiological insomnia and had a complaint of problems with sleep initiation. All good sleepers reported no trouble sleeping and no excessive daytime sleepiness. Good and poor sleepers spent two nights at the Brock University Sleep Research Laboratory. The first night was used to screen for sleep disorders; the second night was used to investigate information processing during the sleep-onset period. Both groups underwent a repeated sleep-onsets task during which an auditory oddball paradigm was delivered. Participants signalled detection of a higher pitch target tone with a button press as they fell asleep. In addition, waking alert ERPs were recorded 1 hour before and after sleep on both Nights 1 and 2.As predicted by the neurocognitive model of insomnia, increased CNS activity was found in the poor sleepers; this was reflected by their smaller amplitude P2 component seen during wake of the sleep-onset period. Unlike the P2 component, the Nl, N350, and P300 did not vary between the groups. The smaller P2 seen in our poor sleepers indicates that they have a deficit in the sleep initiation processes. Specifically, poor sleepers do not disengage their attention from the outside environment to the same extent as good sleepers during the sleep-onset period. The lack of findings for the N350 suggest that this sleep component may be intact in those with insomnia and that it is the waking components (i.e., Nl, P2) that may be leading to the deficit in sleep initiation. Further, it may be that the mechanism responsible for the disruption of sleep initiation in the poor sleepers is most reflected by the P2 component. Future research investigating ERPs in insomnia should focus on the identification of the components most sensitive to sleep disruption. As well, methods should be developed in order to more clearly identify the various types of insomnia populations in research contexts (e.g., psychophysiological vs. sleep-state misperception) and the various individual (personality characteristics, motivation) and environmental factors (arousal-related variables) that influence particular ERP components. Insomnia has serious consequences for health, safety, and daytime functioning, thus research efforts should continue in order to help alleviate this highly prevalent condition.

Moral reasoning and ethics in educational leadership /

School leaders face difficult decisions regarding discipline matters. Often, such decisions play an important role in determining the moral tone of the school and the health of the school community. Many stakeholders are affected by the outcome of such decisions. Codes of conduct, board and school policies, and discipline meetings are often shrouded under secrecy, making the discipline process mysterious. .; In this study I examined the process of moral reasoning. I sought to determine the extent to which school leaders were aware that they were involved in a process of moral reasoning, and ftirthermore, what kind of moral reasoning they practiced. As well, I investigated the ethical grounds and foundations underlying moral reasoning. Thus, in this study I probed the awareness of the process of moral reasoning and sought to find the ethical grounding of decision making. This qualitative study featured short field research. The process involved individual interviews with three different participants: school leaders of a public. Catholic, and an independent school. It found that each school leader practiced moral reasoning to varying degrees through the discipline process. It also explored the possible democratization of moral reasoning by linking to concepts such as fairness, due process, public accountability, and greater participation in the administering of discipline. This study has implications for practice, theory, and future research. The examination of school leaders as the primary focus for discipline matters opens the door to future research that could explore differences between the school systems and possibly other parties affected by moral reasoning in discipline cases.