406 research outputs found

    Gli stereotipi e la tensione tra vulnerabilità e autonomia

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    This commentary on the essay proposed by Federico José Arena aims to deepen the analysis of stereotypes as generalizations offered by the Author from a cognitive perspective. Then, it presents a discussion of the Author’s approach to stereotypes, in particular regarding the limitation of the ‘legitimacy control’ only to vulnerable groups. Lastly, it highlights some of the difficulties on the use of the concept of autonomy associated with the phenomena of oppression and social influence

    Temporal relations of the endocrine response to hypotension with sodium nitroprusside

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    Sodium nitroprusside was infused intravenously for 10 minutes in normal men, reclining at 45 degrees, in a dose sufficient to decrease the arterial pressure by 10 mmHg. The effect on a variety of plasma hormones was measured during the infusion and for 20 minutes afterwards. The heart rate increased to a maximum of 149\%. Norepinephrine rose to a maximum of 196\% in 5 minutes. Epinephrine reached a peak of 207\% after 10 minutes. Plasma renin activity reached a peak of 449\% at 10 minutes. Aldosterone did not change during the infusion, but increased to a maximum of 145\% 10 minutes later. Vasopressin increased sharply at the end of the infusion to 893\% and then rapidly decreased. Corticotropin, prolactin and growth hormone started to increase toward the end of the infusion, but reached their maxima during recovery. Corticotropin (225\%) and prolactin (288\%) peaked 10 minutes after the infusion, while growth hormone (414\%) appeared still to be rising 20 minutes after the end of the infusion. Cortisol also rose progressively during recovery to a level of 138\%. No significant changes were seen in the concentrations of insulin, glucagon, atrial natriuretic peptide, bombesin or neurotensin

    Incidence and outcome of persons with a clinical diagnosis of heart failure in a general practice population of 696,884 in the United Kingdom

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    Background: There are few large population-based studies of the incidence and outcome of heart failure where the diagnosis of heart failure (HF) has been made by a General Practitioner (GP) in the community. Methods: From the General Practice Research Database in the UK, we selected a population of 686,884 people 45 years or older. Incident cases of HF in 1991 were classified definite HF, possible HF, or a first prescription of diuretics without a diagnosis of HF. The population was followed for 3-year mortality. Results: A total of 6478 patients had definite HF (mean age 77.2 years, 55.5% women), 14,050 had possible HF and 6076 persons were prescribed diuretics without a definite or possible diagnosis of HF. The overall incidence of definite HF was 9.3/1000 persons/year and of possible HF 20.2/1000 persons/year. Diuretics were prescribed for the first time for other reasons for 8.7 persons/1000/year. The incidence of HF was higher in men. The incidence of definite HF increased with age. Survival curves showed higher mortality rates in the first 3 months after the diagnosis of HF. One-year cumulative probability of death for patients with definite HF was 15.9 times higher in men and 14.7 times higher in women in comparison with the UK population. Conclusion: The diagnosis of HF by a GP successfully identifies patients at high risk of death, comparable to patients with HF identified by cardiologists on the basis of defined diagnostic criteria. HF is common in the general population, increases sharply with age, and has a poor prognosis

    Temporal relations of the endocrine response to exercise

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    We have followed the hormonal response to exercise in twelve normal males cycling at a constant moderate load for ten minutes. Plasma concentrations of a variety of hormones were measured at set times before and during exercise and for twenty minutes afterward. The plasma concentration of norepinephrine and epinephrine and plasma activity of renin rose to a maximum at the end of exercise and then declined. The plasma concentrations of neurotensin and atrial natriuretic peptide followed a similar course. Plasma vasopressin rose to a peak at the end of exercise and then fell transiently below the initial value ten minutes after exercise. The plasma concentrations of aldosterone, prolactin and adrenocorticotropin increased during exercise but continued to do so, reaching a peak at ten minutes after exercise. Plasma growth hormone increased during exercise and continued to increase throughout the period of twenty minutes' recovery. Cortisol did not change during exercise but rose progressively during the recovery period. Plasma concentrations of glucagon did not change while that of insulin decreased during exercise. The plasma concentration of bombesin slowly increased during exercise and declined during recovery, reaching a basal value 10 minutes later

    Neuroendocrine response to standing and mild exercise in patients with untreated severe congestive heart failure and chronic constrictive pericarditis

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    OBJECTIVES: Plasma hormones at rest in patients with untreated severe congestive cardiac failure are similar to those occurring during heavy exercise in healthy people. This study examines the hypothesis that the neuroendocrine effects of exercise are modified in untreated congestive cardiac failure. DESIGN: The effect of lying, standing, upright exercise, and recovery on several plasma hormones was measured in healthy controls and 2 groups of patients with severe untreated heart failure. The level of exercise was the same in all groups and low enough to be within the capacity of patients with severe failure. PATIENTS: There were 12 healthy controls, 9 patients with untreated severe congestive cardiac failure caused by myocardial disease, and 12 patients with untreated constrictive pericarditis. SETTING: A tertiary referral centre in North India. RESULTS: Heart rate, noradrenaline, renin activity, aldosterone, cortisol, growth hormone and atrial natriuretic peptide (ANP) were higher in the 2 groups of patients than in the healthy controls during both rest and exercise (P < 0.01 for both comparisons). In general, the effects of this mild degree of exercise were no greater than those of standing. The increase in heart rate during exercise was greater in the group with constrictive pericarditis than in the controls (P = 0.04) and (non-significantly) in congestive heart failure. Apart from these differences the pattern of responses to standing and exercise was similar in the three groups. CONCLUSIONS: While there was evidence of a broad neuroendocrine activation in patients with congestive cardiac failure, the only abnormal increase during exercise (of marginal significance) was found for renin activity in those with myocardial disease. In patients with untreated congestive failure, a substantially normal endocrine response to exercise was superimposed on abnormal resting concentrations

    Occurrence of oxidative stress during myocardial reperfusion

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    Reperfusion, without doubt, is the most effective way to treat the ischaemic myocardium. Late reperfusion may however cause further damage. Myocardial production of oxygen free radicals above the neutralizing capacity of the myocytes is an important cause of this reperfusion damage. There is evidence that prolonged ischaemia reduces the naturally occurring defence mechanisms of the heart against oxygen free radicals, particularly mitochondrial manganese superoxide dismutase, and intracellular pool of reduced glutathione. Consequently, reperfusion results in a severe oxidative damage, as evidenced by tissue accumulation and release of oxidized glutathione. An oxygen free radical-mediated impairment of mechanical function also occurs during reperfusion of human heart. In fact we observed during surgical reperfusion of coronary artery disease (CAD) patients, a prolonged and sustained release of oxidized glutathione; the degree of oxidative stress was inversely correlated with recovery of mechanical and haemodynamic function. These findings represent the rationale for therapeutic interventions which increase the cellular antioxidant capacities and improve the efficacy of myocardial reperfusion

    Role of oxygen free radicals in ischemic and reperfused myocardium

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    In recent years there has been considerable interest concerning the role of oxygen radicals in myocardial ischemia and reperfusion injury. The sequential univalent reduction of oxygen gives rise to very reactive intermediate products. Normally, the tissue concentration of these intermediate products of oxygen is limited and the aerobic myocardium survives because of the existence of a delicate balance between the generation of the various oxidants and the maintenance of the antioxidant defense mechanism. Several possible sources have been identified for the production of active oxygen species after ischemia and reperfusion and these sources may be mutually interactive. The ability of scavengers of oxygen free radicals, including vitamin E, to improve mechanical, mitochondrial, and sarcoplasmic reticulum function in animal models of ischemic-reperfusion injury also suggests that oxygen free radicals are partly responsible for myocardial damage in these models, although caution in the interpretation of these data is necessary

    Left ventricular dysfunction due to stunning and hibernation in patients

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    Left ventricular dysfunction is in most cases the consequence of myocardial ischemia. It may occur transiently during an attack of angina and usually it is reversible. It may persist over hours or even days in patients after an episode of ischemia followed by reperfusion, leading to the so-called condition of stunning. In patients with persistent limitation of coronary flow, left ventricular dysfunction may be present over months and years, or indefinitely in subjects with fibrosis, scar formation, and remodeling after myocardial infarction. However, chronic left ventricular dysfunction does not mean permanent or irreversible cell damage. Hypoperfused myocytes can remain viable but akinetic. This type of dysfunction has been called hibernating myocardium. The dysfunction due to hibernation can be partially or completely restored to normal by reperfusion. It is, therefore, important to clinically recognize a hibernating myocardium. In the present article we evaluate stunning and hibernation with respect to clinical decision making and, when possible, we refer to our ongoing clinical experience

    Left ventricular dysfunction due to stunning and hibernation in patients.

    No full text
    Left ventricular dysfunction is in most cases the consequence of myocardial ischemia. It may occur transiently during an attack of angina and usually it is reversible. It may persist over hours or even days in patients after an episode of ischemia followed by reperfusion, leading to the so-called condition of stunning. In patients with persistent limitation of coronary flow, left ventricular dysfunction may be present over months and years, or indefinitely in subjects with fibrosis, scar formation, and remodeling after myocardial infarction. However, chronic left ventricular dysfunction does not mean permanent or irreversible cell damage. Hypoperfused myocytes can remain viable but akinetic. This type of dysfunction has been called hibernating myocardium. The dysfunction due to hibernation can be partially or completely restored to normal by reperfusion. It is, therefore, important to clinically recognize a hibernating myocardium. In the present article we evaluate stunning and hibernation with respect to clinical decision making and, when possible, we refer to our ongoing clinical experience
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