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Biomedical subjects

E Ferrari

Publications and source records attributed to E Ferrari.

At least 235 records · Page 13Linked to original sources
PubMed1991

[Influence of sex hormones on hemorrheology and plasma proteins during the menstrual cycle].

Our study was undertaken to verify the relation among sex hormone profile, hemorheologic pattern, blood lipids and plasma proteins throughout the menstrual cycle. In effect, the estrogenic activity has been related to blood hypercoagulability, thromboembolic disorders and to cardiovascular complications in normal women and in several diseases. The protocol study concerns 15 healthy young women (mean age 25 years), with normal body weight, investigated on day 7 (follicular phase), day 14 (ovulatory phase), and days 21, 25, 27 (mid-and late luteal phase) of menstrual cycle. We evaluated: blood, plasma and serum viscosity (at shear-rate of 450; 90; 4.5; 2.25 s-1), erythrocyte deformability, haematocrit, plasma fibrinogen and fibronectin, apolipoprotein A-A1-B, triglycerides, total-HDL and LDL-cholesterol, FSH, LH, 17-beta-estradiol, progesterone, testosterone, androstenedione, DHEA, DHEA-sulfate and the estradiol/progesterone ratio (E2/P ratio). Higher blood, serum and plasma viscosity (p less than 0.01), and lower erythrocyte deformability (p less than 0.01) were demonstrated during follicular and ovulatory phase, than in mid- and late luteal phases of menstrual cycle. Plasma fibrinogen (p less than 0.01) and fibronectin (p less than 0.001) were also significantly increased in ovulatory and follicular phases; whereas haematocrit, blood lipids and apolipoproteins remained unchanged throughout the menstrual cycle. Positive correlations among E2/P ratio, plasma viscosity, fibrinogen and fibronectin, and negative correlations between E2/P ratio and erythrocyte deformability, were found on day 21 (p less than 0.05) and day 25 (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Brain excitability and long latency muscular arm responses: non-invasive evaluation in healthy and parkinsonian subjects.

Thirty healthy and 35 volunteers affected by Parkinson's disease (PD) were examined. Long latency responses (LLRs) and short latency somatosensory evoked potentials (SEPs) after median nerve stimulation were respectively recorded from forearm flexor muscles, and from 19 scalp electrodes, during relaxation (condition 1), light and maximal muscle contraction (conditions 2 and 3). Linear interpolation of SEPs was performed to produce isopotential colour maps. Latencies and amplitudes of the V1-V2 component in LLR, as well as of parietal, central and frontal scalp SEPs were analysed in the 3 experimental conditions. Highly significant inverse correlation matched the frontal SEP to the LLR V2 component amplitudes, both in healthy and in PD subjects. However, the V2 component--which in the former group was reliably identifiable only in condition 3--was presented in conditions 1 and 2 in a high percentage of PD subjects who also showed an abnormally reduced frontal SEP during complete relaxation. Excitability changes of brain motor areas induced by a sensory input were tested as follows: the motor cortex was transcranially stimulated (TCS) by magnetic pulses with an intensity 10% below (A) or above (B) the threshold for twitch elicitation during complete relaxation of forearm muscles; TCS was randomly preceded (range 14-32 msec) by a shock to the median or ulnar nerve at the elbow with identical characteristics as for LLR elicitation. An initial epoch of 'inhibition' followed by a peak of 'facilitation' of the amplitude of motor responses to TCS was observed when conditioning stimuli to the median nerve preceded TCS by 14-20 and by 24-32 msec, respectively. Contrary to normals, conditioning stimulation of the median nerve did not significantly influence the excitability threshold to TCS in those parkinsonians with depressed frontal N30.

Adult↗
PubMed1991

Peripheral opioid secretory pattern in anorexia nervosa.

The peripheral secretion of endogenous opioids was studied in 10 women with restrictive anorexia nervosa and 10 age- and sex-matched healthy controls. The circadian rhythm of beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH), and their responses to the administration of corticotropin releasing hormone (CRH, 1 micrograms/kg body weight, i.v.), clonidine (150 microgram, i.v.), domperidone (10 mg, i.v.), and 5-hydroxytryptophan (5-HTP, 200 mg, p.o.) were examined in patients and controls. The results revealed increased nocturnal secretion of beta-EP and diurnal-nocturnal secretion of beta-LPH with loss of circadian rhythmicity of both peptides, normal response to CRH stimulation, blunted response to clonidine and domperidine, and normal beta-EP and blunted beta-LPH response to 5-HTP stimulation. The data suggest a complex alteration of peripheral opioids and of central aminergic mechanisms that regulate proopiomelanocortin-derived peptide secretion and eating behavior.

5-Hydroxytryptophan↗
PubMed1991

[Ischemic clinical forms of hypertrophic cardiomyopathies: differential diagnosis with myocardial infarction. Apropos of 15 cases].

This study reports 15 cases of ischaemic clinical forms of hypertrophic cardiomyopathy (HCM). In this retrospective study over a 3 year period, 15 patients with HCM presented with clinical and electrocardiographic signs simulating unstable angina (N = 5) or myocardial infarction (N = 10). All patients had chest pain lasting at least 20 minutes with pseudo-ischaemic ECG changes. Two patients were given thrombolytic therapy. The clinical and enzymatic outcome and results of complementary investigations (including coronary angiography) confirmed the absence of coronary artery disease. The diagnostic of HCM was made by echocardiography. These cases were all apparently primary forms of HCM without intraventricular pressure gradient under basal conditions. Three of the patients were known cases of HCM but the condition was diagnosed after the ischaemic presentation in the other cases. Eight of them had however been considered to have had coronary insufficiency for an average of 5 years. The clinical presentation of HCM represents a difficult differential diagnostic problem with myocardial infarction. Echocardiography is of little help in distinguishing the 2 diseases as septal hypokinesis is often observed in HCM. The clinical course usually reestablishes the diagnosis within a few hours but the delay is often too long in this situation of therapeutic emergency and the indications of thrombolysis may be wrongly posed. Although there is no available formal means of distinguishing the two conditions, this study underlines that this clinical form of HCM is not rare and that the diagnosis should be keep in mind with the other differential diagnoses of myocardial infarction.

Adult↗
PubMed1991

Clinical and biological evaluation of dilevalol vasodilating properties in mild to moderate hypertension.

Dilevalol is a vasodilating beta-blocker with proven antihypertensive activity. In this study, 28 patients with mild-to-moderate uncomplicated hypertension underwent 2 submaximal exercise tests, each consisting of progressive steps of 20 watts for 2 minutes or up to 85% theoretical maximum heart rate. Five minutes after the first test, patients received either placebo or dilevalol 200 mg, 400 mg or 600 mg. The second exercise test was performed 3 hours later. Diastolic blood pressure, systolic blood pressure, heart rate and norepinephrine plasma levels were assessed before and after exercise. Dilevalol at all doses caused a significant decrease in heart rate and blood pressure both at rest and during exercise, compared to placebo. Dilevalol 600 mg had a greater effect on diastolic blood pressure than dilevalol 200 mg and 400 mg. Administration of dilevalol 200 mg and 400 mg enabled 42% of patients to increase their maximal exercise level by 20 to 60 watts. Dilevalol increased plasma norepinephrine levels at the 100 watts exercise levels from 5.1 +/- 4.0 nmol/l to 7.6 +/- 4.3 nmol/l (p less than 0.05). No adverse effects were observed during dilevalol treatment. This study shows that dilevalol is an effective antihypertensive agent that blunts heart rate and blood pressure risings during exercise.

Administration, Oral↗
PubMed1991

[Value of the replacement of intravenous trinitrin by oral trinitrin in the acute phase of myocardial infarction complicated by regressive left ventricular insufficiency].

Left ventricular failure is a common complication of the acute phase of myocardial infarction. The most appropriate current treatment, when an increase in preload is the predominant or sole feature, involves nitroglycerin by infusion combined in varying degrees with diuretics. The aim of this study was to assess the value of maintenance treatment following intravenous nitroglycerin based upon a long acting nitrate derivative designed to achieve a hemodynamic result. Twenty patients with a mean age of 62 and with left ventricular failure during the acute phase of a myocardial infarction were studied. They were all treated with IV nitroglycerin using an automatic pump syringe. Pulmonary artery diastolic pressure, cardiac output, blood pressure and heart rate were measured hourly for six hours then every 6 hours. When PADP fell to below 18 mmHg, maintenance treatment with placebo or long acting nitroglycerin was given double-blind (10 patients were given long acting nitroglycerin and 10 patients the placebo). Pulmonary artery pressures, blood pressure and heart rate were measured every 2 hours for 8 hours, then at 12 and 24 hours. No significant difference was found in heart rate, blood pressure, cardiac output nor PADP (10 +/- 3.5 mmHg cf. 12 +/- 2.8 mmHg; NS) between the two groups. In total, maintenance treatment with long acting nitrate derivatives following IV nitroglycerin for hemodynamic purposes in patients with an acute myocardial infarction complicated by regressive cardiac failure would no appear to be necessary.

Administration, Oral↗
PubMed1991

[Apical hypertrophic pseudocardiomyopathy: nosological problems].

The classification of hypertrophic cardiomyopathies remains a thorny nosological problem. Within this extensive diagnostic group, it is felt that the very special sub-group of "Japanese" apical hypertrophic forms must be subject to the strictest possible criteria in order to avoid improper use. The case reported here of biventricular apical hypertrophic cardiomyopathy in a 60-year-old woman with a family history of HCM, in whom the clinical, ECG and above all angiographic features were typically those of AHCM but where the existence of an intraventricular gradient was found during challenge manoeuvres emphasises this classification problem. Pseudo-AHCM in a context of OCM or pseudo-OCM in a context of AHCM? The discussion is not merely of nosological interest in view of the recently documented clear prognostic differences between these two conditions. Main series from the literature are reviewed.

Cardiomyopathy, Hypertrophic↗
PubMed1991

[Short term post-surgical prophylaxis in gynecology. Use of cefonicid].

In this study the Authors have evaluated the use of cefonicid in "short-term" post-surgical prophylaxis in gynecology. No effects, nor alteration to hematochemical parameters related to the administration of this medicine have been observed and the analysis of data shows that the use of cefonicid contributes to reducing the incidence of post-surgical infections in hospital in a cure group compared to a control group.

Cefonicid↗
PubMed1990

Hormonal circadian rhythms in eating disorders.

The circadian rhythm of several plasma hormones (prolactin, growth hormone, adrenocorticotropic hormone (ACTH), cortisol, and melatonin) was simultaneously evaluated in 23 women with anorexia nervosa (AN), in 27 obese (OB) women, and in gender and age-matched healthy controls. A trend toward similar alterations of the circadian pattern of the different hormones was observed in the two groups of patients, with the exception of plasma growth hormone (GH), which exhibited nutrition-dependent impairments. The timing of the peaks for each hormonal rhythm revealed the existence of an internal desynchronization in both eating disorders.

Adult↗