Biomedical subjects
E Nardi
Publications and source records attributed to E Nardi.
[Chromatographic study of lipids in normal human platelets].
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[Periodontal disease in children].
The authors analyze the most common periodontal diseases in pediatric age. They demonstrate that the control of the bacterial plaque is the determinant element to resolve these diseases.
Treatment of malignant hypertension with an angiotensin converting enzyme inhibitor.
Malignant hypertension developed in an 18-year-old man whose primary hypertension had been diagnosed by chance. Standing blood pressure was 290/170 mmHg. Tests of renal function revealed high blood urea nitrogen and creatinine levels and low levels of both effective renal plasma flow and the glomerular filtration rate. Plasma renin activity and levels of angiotensin II and aldosterone were greatly elevated. Severe concentric left ventricular hypertrophy was noted. The patient received standard antihypertensive treatment with furosemide, propranolol, nifedipine, and prazosin, but his blood pressure did not decrease and there was no improvement in the clinical or biochemical measures. The patient was then given 20 mg of enalapril daily for one year. The inhibition of angiotensin converting enzyme immediately reduced blood pressure. Angiotensin II and aldosterone levels became normal, kidney function and hemodynamics improved, and echocardiograms revealed that the left ventricular hypertrophy had regressed. The results confirm the pathogenetic role of angiotensin II in the development of the malignant phase of hypertension.
Lecithin: cholesterol-acyltransferase (LCAT) activity in alcoholic liver disease.
The activity of LCAT (the controlling enzyme for cholesterol esterification in plasma) is known to be reduced in alcoholic cirrhosis, while little is known about early stage (liver steatosis) alcoholics. In this study, LCAT activity was assayed by Stokke and Norum's method, before and after a 15-day sobriety period, in liver steatosis and in cirrhosis alcoholics. Before alcohol withdrawal, LCAT activity was depressed in both groups. After the sobriety period, LCAT activity was significantly raised in liver steatosis patients, but was still lower than in controls; in cirrhosis patients, it was increased, but not significantly. According to our results, LCAT activity impairment in alcoholic liver disease is sustained by both the hypothesized mechanisms, alcohol-related metabolic disorders and lowered LCAT-enzyme production, but to different degrees, depending on the stage of the disease. In liver steatosis, metabolic disorders play a major role, as a liver-impairment-induced decrease in LCAT production seems rather unlikely, and increased LCAT activity is more likely to be sustained by metabolic normalisation than by any recovery of the damaged liver. However, the lack of improvement in about 20% of patients, and the fairly wide scattering of individual data, suggest a minor LCAT production impairment in liver steatosis too. In cirrhosis, the major role seems to be played by a permanent decrease in LCAT production, as no significant rise in LCAT activity was observed after alcohol withdrawal. However the restored LCAT activity observed in some patients could be related to improvement in the metabolic disorder, thus confirming the effectiveness of this mechnism in cirrhosis too.(ABSTRACT TRUNCATED AT 250 WORDS)
High dose peptichemio in pretreated neuroblastoma.
The aim of this study was to evaluate the antitumor effect and toxicity of a single course of Peptichemio at high dose (450 mg/sq m) given to children with neuroblastoma resistant to first line treatment or at relapse. A total of 28 children were treated. Seven children showed partial response, 4 minor response, 8 had stable disease, and in 8 the tumor progressed. The principal toxic effect was myelosuppression. Hemorrhagic enteritis with liver failure and toxic death occurred in 1 patient. High dose Peptichemio can be administered with tolerable toxicity, inducing tumor regression in one third of previously treated patients.
Hyperprolactinemia and 5-alpha-reductase activity.
A number of experimental data indicate that hyperprolactinemia inhibits the activity of 5-alpha-reductase; however, no information is available about the time required for this enzyme to re-activate after prolactinemia has returned to normal values. In the present study, five normal caucasian men, whose fertility had previously been proven, were given HCG (5000 IU/day by intramuscular route for three days) both in basal conditions and after sulpiride-induced hyperprolactinemia (dosage = 200 mg/day for ten days). In both conditions, the plasma levels of prolactin (PRL), testosterone (T), dihydro-testosterone (DHT), 17-beta-estradiol (E2), and dehydroepiandrosterone sulfate (DHAS) were monitored during the treatment with HCG and for an additional 24 hrs after HCG discontinuation. All hormones were assayed by RIA. Our results demonstrate that hyperprolactinemia causes a marked decrease (58%) of DHT, a less marked decrease (39%) of T, an increase (43%) of DHAS whereas only a small increase (2%) of E2 was observed. Steroids were shown to behave differently after the HCG tests performed in the two experimental conditions. In particular, the levels of DHT had a much more pronounced increased after HCG in the second test than in the first; in contrast, both DHAS and E2 had a less marked response after the second test. Our data, on the one hand, confirm that 5-alpha-reductase is inhibited by hyperprolactinemia; on the other hand, the hyperprolactinemia-induced block of this enzyme appears to be rapidly reversible because the enzyme is reactivated within 48-72 hrs after normalization of prolactin levels. (Normal values of prolactin were on the average achieved on the 4th day after sulpiride discontinuation).(ABSTRACT TRUNCATED AT 250 WORDS)
Impairment of lecithin:cholesterol acyltransferase (LCAT) activity in hemodialyzed subjects. I. No evidence of plasma LCAT-inhibiting factors.
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Lecithin: cholesterol acyltransferase (LCAT) activity in long-term hemodialyzed subjects.
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The response of serum and seminal plasma prolactin to bromocriptine in normal men.
The Authors describe their experience with a group of twelve volunteer healthy men in order to evaluate if the bromocriptine inhibition of serum prolactin concentration also modifies seminal plasma PRL values. The results of this study lead us to suppose that PRL in semen could arrive from serum by a filtration process through the prostatovescicular apparatus.
[The certificate of delivery care (CEDAP): preliminary results in the city of Palermo].
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[Infant mortality in Palermo in 1994: a comparison among sources].
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