RingDings market analysis

A Work Project, presented as part of the requirements for the Award of a Masters Degree in Management from the NOVA – School of Business and Economics

A onda de calor de Agosto de 2003 e os seus efeitos sobre a mortalidade da população portuguesa

RESUMO - Portugal continental, como outros países europeus, foi afectado por uma onda de calor de grande intensidade no Verão de 2003, com efeitos na mortalidade da população. O excesso de óbitos associados à onda de calor foi estimado pela comparação do número de óbitos observados entre 30 de Julho e 15 de Agosto de 2003 e o número de óbitos esperados se a população tivesse estado exposta às taxas de mortalidade médias do biénio 2000-2001 no respectivo período homólogo. Os óbitos esperados foram calculados com ajustamento para a idade. O número de óbitos observados (O) foi superior ao número esperado (E) em todos os dias do período estudado e o seu excesso global foi estimado em 1953 óbitos (excesso relativo de 43%), dos quais 1317 (61%) ocorreram no sexo feminino e 1742 no grupo de 75 e + anos (89%). A nível distrital, Portalegre teve o maior aumento relativo do número de óbitos (+89%) e Aveiro o menor (+18%). Numa área geográfica contínua do interior do território (Guarda, Castelo Branco, Portalegre e Évora) houve aumentos relativos superiores a 80%. Em termos absolutos, o maior excesso de óbitos ocorreu no distrito de Lisboa (mais cerca de 396) e no do Porto (mais cerca de 183). As causas de morte «golpe de calor» e «desidratação e outros distúrbios metabólicos» tiveram os aumentos relativos mais elevados (razões O/E de, respectivamente, 70 e 8,65). Os maiores aumentos absolutos do número de óbitos ocorreram no grupo das «doenças do aparelho circulatório» (mais 758), nas «doenças do aparelho respiratório» (mais 255) e no conjunto de «todas as neoplasias malignas» (mais 131). No período da onda de calor e no período de comparação, a percentagem dos óbitos que ocorreu nos hospitais (52% e 56%), no domicílio (32 e 33%) e em «outros locais» foi semelhante. A discussão sobre os factores que condicionaram a obtenção dos valores apresentados, relativos ao excesso de óbitos por sexo, grupo etário, distrito, causa e local da morte, permite concluir que os mesmos se afiguram adequados para medir a ordem de grandeza e caracterizar o efeito da onda de calor na mortalidade. O erro aleatório, medido pelos intervalos de confiança, e alguns possíveis erros sistemáticos associados ao período de comparação escolhido não deverão afectar de modo relevante as estimativas.

PET Molecular Imaging of Hypoxia in Ischemic Stroke: An Update.

Hypoxia, a condition of insufficient oxygen availability to support metabolism, occurs when the vascular supply is interrupted, as in stroke. The identification of the hypoxic and viable tissue in stroke as compared with irreversible lesions (necrosis) has relevant implications for the treatment of ischemic stroke. Traditionally, imaging by positron emission tomography (PET), using 15O-based radiotracers, allowed the measurement of perfusion and oxygen extraction in stroke, providing important insights in its pathophysiology. However, these multitracer evaluations are of limited applicability in clinical settings. More recently, specific tracers have been developed, which accumulate with an inverse relationship to oxygen concentration and thus allow visualizing the hypoxic tissue non invasively. These belong to two main groups: nitroimidazoles, and among these the 18F-Fluoroimidazole (18F-FMISO) is the most widely used, and the copper-based tracers, represented mainly by Cu-ATSM. While these tracers have been at first developed and tested in order to image hypoxia in tumors, they have also shown promising results in stroke models and preliminary clinical studies in patients with cardiovascular disorders, allowing the detection of hypoxic tissue and the prediction of the extent of subsequent ischemia and clinical outcome. These tracers have therefore the potential to select an appropriate subgroup of patients who could benefit from a hypoxia-directed treatment and provide prognosis relevant imaging. The molecular imaging of hypoxia made important progress over the last decade and has a potential for integration into the diagnostic and therapeutic workup of patients with ischemic stroke.

Intraoperative cerebral perfusion and postoperative cognitive dysfunction in geriatric patients

Background: Inadequate intraoperative cerebral perfusion has been suggested as a possible cause of postoperative cognitive dysfunction (POCD). Methods: We investigated 35 patients aged 65 or older undergoing elective major non-cardiac surgery under standardized general anaesthesia (thiopental, sevoflurane, fentanyl, atracurium). Intraoperative cerebral perfusion was monitored with transcranial Doppler, and near-infrared spectroscopy (NIRS). Arterial blood pressure was monitored continuously with a Finapres device. Mx, an index allowing continuous monitoring of cerebrovascular autoregulation based on the changes in mean arterial blood pressure (MAP) and cerebral blood flow velocity was calculated. Mx >0.5 was defined as disturbed cerebrovascular autoregulation. Cognitive function was measured preoperatively and 7 days postoperatively using the CERAD-NAB Plus test battery. A postoperative decline >1 z-score in at least two of the tested domains was defined as POCD. Data are shown as mean } SD. Results: Mean age was 75 } 7 yrs. Sixteen patients (46%) developed POCD. These patients were older (77 } 8 vs 73 } 7 yrs), had lower MAP (77 } 12 vs 81 } 11 mm Hg), lower cerebral tissue oxygenation indices measured by NIRS (66.8 } 6.0 vs 68.6 } 4.3%) and less efficient cerebrovascular autoregulation (Mx 0.54 } 0.17 and 0.44 } 0.22) than patients without POCD. Disturbed intraoperative cerebrovascular autoregulation was found more often (56 vs 37%) in patients with POCD. However, none of these differences reached statistical significance. Conclusions: Our data show a trend towards subtle changes in intraoperative cerebral perfusion in elderly patients who develop POCD. However, a cause effect relationship must not be assumed and a greater number of patients needs to be investigated patients. However, more patients need to be investigated to confirm and characterize these differences.

PFO closure vs. medical therapy in cryptogenic stroke or transient ischemic attack: A systematic review and meta-analysis.

BACKGROUND/OBJECTIVES: This study aims to assess whether patent foramen ovale (PFO) closure is superior to medical therapy in preventing recurrence of cryptogenic ischemic stroke or transient ischemic attack (TIA). METHODS: We searched PubMed for randomized trials which compared PFO closure with medical therapy in cryptogenic stroke/TIA using the items: "stroke or cerebrovascular accident or TIA" and "patent foramen ovale or paradoxical embolism" and "trial or study". RESULTS: Among 650 potentially eligible articles, 3 were included including 2303 patients. There was no statistically significant difference between PFO-closure and medical therapy in ischemic stroke recurrence (1.91% vs. 2.94% respectively, OR: 0.64, 95%CI: 0.37-1.10), TIA (2.08% vs. 2.42% respectively, OR: 0.87, 95%CI: 0.50-1.51) and death (0.60% vs. 0.86% respectively, OR: 0.71, 95%CI: 0.28-1.82). In subgroup analysis, there was significant reduction of ischemic strokes in the AMPLATZER PFO Occluder arm vs. medical therapy (1.4% vs. 3.04% respectively, OR: 0.46, 95%CI: 0.21-0.98, relative-risk-reduction: 53.2%, absolute-risk-reduction: 1.6%, number-needed-to-treat: 61.8) but not in the STARFlex device (2.7% vs. 2.8% with medical therapy, OR: 0.93, 95%CI: 0.45-2.11). Compared to medical therapy, the number of patients with new-onset atrial fibrillation (AF) was similar in the AMPLATZER PFO Occluder arm (0.72% vs. 1.28% respectively, OR: 1.81, 95%CI: 0.60-5.42) but higher in the STARFlex device (0.64% vs. 5.14% respectively, OR: 8.30, 95%CI: 2.47-27.84). CONCLUSIONS: This meta-analysis does not support PFO closure for secondary prevention with unselected devices in cryptogenic stroke/TIA. In subgroup analysis, selected closure devices may be superior to medical therapy without increasing the risk of new-onset AF, however. This observation should be confirmed in further trials using inclusion criteria for patients with high likelihood of PFO-related stroke recurrence.

Cerebral perfusion CT: Current state of the art : P44

Purpose: The aim of this educational poster is to introduce the technical principles of cerebral perfusion CT and to provide examples of its clinical applications and potential limitations in the everyday emergency practice. Methods and materials: Cerebral perfusion CT is a well established investigatory tool for many vascular and parenchymal brain dysfunctions. CT perfusion maps allow a semiquantitative assessment of cerebral perfusion. Results: Currently, cerebral perfusion CT has a pivotal role in differentiating reversible from irreversible ischemic parenchymal insult besides its integral role in grading vasospasm after subarachnoid hemorrhage. Furthermore, cerebral perfusion CT can be coupled to acetazolamide administration in order to assess the cerebrovascular reserve capacity before performing extra-/intra-cranial bypass surgery in patients with cerebral vascular insufficiency. Cerebral perfusion CT can also identify diffuse abnormalities of cerebral perfusion in children with traumatic brain injury showing a low initial GCS in order to predict the final outcome regarding the late occurrence of irreversible parenchymal damage. Cerebral Perfusion CT is also able to detect focal parenchymal perfusion abnormalities in acute epileptic seizures. Conclusion: Cerebral perfusion CT can be integrated in the management of many vascular, traumatic and functional disorders of the brain.

Impaired left ventricular function as a predictive factor for mid-term survival in octogenarians after primary coronary artery bypass surgery.

BACKGROUND: The impact of preoperative impaired left ventricular ejection fraction (EF) in octogenarians following coronary bypass surgery on short-term survival was evaluated in this study. METHODS: A total of 147 octogenarians (mean age 82.1 ± 1.9 years) with coronary artery diseases underwent elective coronary artery bypass graft between January 2000 and December 2009. Patients were stratified into: Group I (n = 59) with EF >50%, Group II (n = 59) with 50% > EF >30% and in Group III (n = 29) with 30% > EF. RESULTS: There was no difference among the three groups regarding incidence of COPD, renal failure, congestive heart failure, diabetes, and preoperative cerebrovascular events. Postoperative atrial fibrillation was the sole independent predictive factor for in-hospital mortality (odds ratio (OR), 18.1); this was 8.5% in Group I, 15.3% in Group II and 10.3% in Group III. Independent predictive factors for mortality during follow up were: decrease of EF during follow-up for more that 5% (OR, 5.2), usage of left internal mammary artery as free graft (OR, 18.1), and EF in follow-up lower than 40% (OR, 4.8). CONCLUSIONS: The results herein suggest acceptable in-hospital as well short-term mortality in octogenarians with impaired EF following coronary artery bypass grafting (CABG) and are comparable to recent literature where the mortality of younger patients was up to 15% and short-term mortality up to 40%, respectively. Accordingly, we can also state that in an octogenarian cohort with impaired EF, CABG is a viable treatment with acceptable mortality.

Total aortic arch stenting--hemodynamical impact of carotid artery perfusion.

The aim of this experimental study is to evaluate the feasibility and the outcome of total endovascular stent implantation in the aortic arch. Indications for this operation-technique would be acute or chronic dissection of the aortic arch (non-A-non-B dissection) or type B dissection with retrograde extension. Four pigs were canulated via the distal abdominal aorta and a retrograde placement of a Djumbodis arch stent (4-9 cm) was controlled by using intravascular ultrasound and intracardiac ultrasound by the inferior cava vein and under radioscopic control. Cerebral perfusion, by using a flow meter placed on one prepared carotid artery, were controlled before, immediate post-procedural (<1 min), and in the early follow-up after aortic arch stent implantation. During the implantation process, especially during balloon inflation and deflation, mean carotid perfusion decreases slightly. A reactive increase of carotid perfusion after stent placements indicates transitory cerebral hypo-perfusion. Non-covered aortic arch stent implantation is technically feasible and could be a potential treatment option in otherwise inoperable arch dissections. The time required for balloon inflation and deflation causes an important risk of cerebral ischemia. The latter can be reduced by transaxillary perfusion.

Asymptomatic high flow subclavian steal in a patient with hemodialysis access.

Subclavian steal phenomenon due to proximal subclavian artery stenosis or occlusion is not un-common but often remains asymptomatic. We describe the case of a 66-year-old man with end-stage renal disease hemodialysed through a brachio-brachial loop graft of the left forearm. Echo-Doppler precerebral examination showed a high reversed flow of 570 ml/min in the ipsilateral vertebral artery. After successful endovascular recanalization of the subclavian artery, access blood flow increased and vertebral flow decreased to 30 ml/min. Complete neurological examination was normal both before and after endovascular treatment. This case demonstrates how high a subclavian steal can be without causing symptoms and how well precerbral and cerebral circulation can adapt to hemodynamic changes.

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

ERP and cardiovascular correlates of source memory discrimination in older and younger adults /

There is much evidence to support an age-related decline in source memory ability. However, the underlying mechanisms responsible for this decline are not well understood. The current study was carried out to determine the electrophysiological correlates of source memory discrimination in younger and older adults. Event-related potentials (ERPs) and continuous electrocardiographic (ECG) data were collected from younger (M= 21 years) and older (M= 71 years) adults during a source memory task. Older adults were more likely to make source memory errors for recently repeated, non-target words than were younger adults. Moreover, their ERP records for correct trials showed an increased amplitude in the late positive (LP) component (400-800 msec) for the most recently presented, non-target stimuli relative to the LP noted for target items. Younger adults showed an opposite pattern, with a large LP component for target items, and a much smaller LP component for the recently repeated non-target items. Computation of parasympathetic activity in the vagus nerve was performed on the ECG data (Porges, 1985). The resulting measure, vagal tone, was used as an index of physiological responsivity. The vagal tone index of physiological responsivity was negatively related to the LP amplitude for the most recently repeated, non-target words in both groups, after accounting for age effects. The ERP data support the hypothesis that the tendency to make source memory errors on the part of older adults is related to the ability to selectively control attentional processes during task performance. Furthermore, the relationship between vagal tone and ERP reactivity suggests that there is a physiological basis to the heightened reactivity measured in the LP response to recently repeated non-target items such that, under decreased physiological resources, there is an impairment in the ability to selectively inhibit bottom-up, stimulus based properties in favour of task-related goals in older adults. The inconsistency of these results with other explanatory models of source memory deficits is discussed. It is concluded that the data are consistent with a physiological reactivity model requiring inhibition of reactivity to irrelevant, but perceptually-fluent, stimuli.

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.

The roles of ERK1/2 and PI3K in abnormal vascular functions in angiotensin II-infused hypertensive rats

Background: Ang II plays a major role in cardiovascular regulation. Recently, it has become apparent that vascular superoxide anion may play an important role in hypertension development. Treatment with antisense NAD(P)H oxidase or SOD decreased BP in Ang II-infused rats. Wang et al recently reported mice which lack one of the subunits of NAD(P)H oxidase developed hypertension at a much lower extent when compared to the wild type animals infused with Ang II, indicating that superoxide anion contributes to elevation in BP in the Ang II-infused hypertensive model. In the Ang II-infused hypertensive model, altered reactivity of blood vessels is often associated with the elevation of systolic blood pressure. We have observed abnormal tension development and impaired endothelium-dependent relaxation in the isolated aorta of Ang II-infused and DOCA-salt hypertensive rats. Recently, several other cellular signal molecules, including ERK1I2 and PI3K, have been determined to play important roles in the regulation of smooth muscle contraction and relaxation. ERKl/2 and PI3K pathways are also reported to contribute to Ang II induced cell growth, hypertrophy, remodeling and contraction. Moreover, these signaling pathways have shown ROS-sensitive properties. Therefore, the aim of the present study is to investigate the roles of ERKl12 and PI3K in vascular oxidative stress, spontaneous tone and impaired endothelium relaxation in Ang II-infused hypertensive model. Hypothesis: We hypothesize that the activation of ERKl12 and PI3K are elevated in response to an Ang II infusion for 6 days. The elevated activation of phospho-ERKl/2 and PI3K mediated the increased level of vascular superoxide anion, the abnormal vascular contraction and impaired endothelium-dependent vascular relaxation in Ang II-infused hypertensive rats. Methods: Vascular superoxide anion level is measured by lucigenin chemiluminescence. Spontaneous tone and ACh-induced endothelium-dependent relaxation was measured by isometric tension recording in organ chamber. The activity of ERK pathway will be measured by its Western blot of phosphorylation of ERK. PI3K activity was evaluated indirectly by Western blot of the phosphorylation of PDKl, a downstream protein of PI3K signaling pathway. The role of each pathway was also addressed via comparing the responses to the specific inhibitors. Results: Superoxide anion was markedly increased in the isolated thoracic aorta from Ang II-infused rats. There was spontaneous tone developed in rings from Ang II-induced hypertensive but not sham-operated normotensive rats. ACh-induced endothelium-dependent relaxation function is impaired in Ang II-infused hypertensive rats. Superoxide dismutase and NAD(P)H oxidase inhibitor, apocynin, inhibited the abnormal spontaneous tone and ameliorated impaired endothelium-dependent relaxation. The expression of phopho-ERKII2 was enhanced in Ang II-infused rats, indicating the activity of ERK1I2 could be increased. MEK1I2 inhibitors, PD98059 and U126, but not their inactive analogues, SB203580 and U124, significantly reduced the vascular superoxide anion in aortas from Ang II-infused rats. The MEK1I2 inhibitors reduced the spontaneous tone and improved the impaired endothelium-dependent relaxation in aorta of hypertension. These findings supported the role of ERKII2 signaling pathway in vascular oxidative stress, spontaneous tone and impaired endothelium-dependent relaxation in Ang II-infused hypertensive rats. The amount of phospho-PDK, a downstream protein of PI3K was increased in Ang II rats indicating the activity of PI3K activity was elevated. Strikingly, PI3K significantly inhibited the increase of superoxide anion level, abnormal spontaneous tone and restored endothelium-dependent relaxation in Ang II-infused hypertensive rats. These findings indicated the important role of PI3K in Ang II-infused hypertensive rats. Conclusion: ERKII2 and PI3K signaling pathways are sustained activated in Ang II-infused hypertensive rats. The activated ERKII2 and PI3K mediate the increase of vascular superoxide anion level, vascular abnormal spontaneous tone and impaired endothelium-dependent relaxation.