On a further case of radiation meningioma.
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Biomedical subjects
Publications and source records attributed to S Vitali.
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The aim of our study was to investigate the mechanisms involved in hypoglycemia-induced platelet activation. Sixteen healthy male subjects received a 60-min intravenous infusion of human regular insulin at the rate of 64 mU . m-2 . min-1: throughout 150 min, we serially measured plasma concentrations of glucose, insulin, and counterregulatory hormones; platelet sensitivity to ADP, thrombin and platelet-activating factor; plasma concentrations of platelet markers for specific proteins of in vivo release reaction (beta-thromboglobulin and platelet factor 4). Our study showed that insulin-induced hypoglycemia causes a significant increase in platelet sensitivity to aggregating agents in vitro and a platelet release reaction in vivo. Hypoglycemia-induced platelet activation was not correlated with plasma glucose concentrations at nadir and occurred before the increase of plasma growth hormone and cortisol. To further elucidate the mechanisms of hypoglycemia-induced platelet activation, we incubated in vitro platelet-rich plasma (PRP) of seven fasting healthy subjects with the same concentrations of insulin, epinephrine, glucagon, growth hormone, and cortisol measured in vivo during insulin-induced hypoglycemia. Only epinephrine was able to increase platelet sensitivity to aggregating agents. To investigate the role of alpha-adrenergic receptors in this phenomenon, we also studied four healthy subjects on another occasion, repeating the above-described insulin infusion together with intravenous infusion of phentolamine (-15 to +150 min), 5 mg over 2 min followed by 500 micrograms/min. alpha-Blockade was able to suppress hypoglycemia-induced increase of platelet sensitivity to aggregating agents.(ABSTRACT TRUNCATED AT 250 WORDS)
The present study was carried out in order to verify whether, in benzodiazepine-medicated healthy volunteers, oxiracetam retained the properties already observed after administration in normal volunteers. In a cross-over study, 12 volunteers, medicated the night before with 5 mg diazepam, were i.v. treated with 1 g oxiracetam or saline. An electroencephalogram (EEG) was performed before, and 15 and 120 min after, nootropic or saline injection. Computerized examination of the EEG traces showed an increase of the alpha- and a decrease of the delta-relative activities, particularly in the fronto-temporal regions. These preliminary results suggest that oxiracetam might be useful in benzodiazepine-treated patients by improving their cognitive activities without nullifying the sedation of anxiety and neurotic behavior.
The article deals with 6 patients operated on for meningioma many years after they had undergone X-ray therapy because of an epidemic of tinea capitis in their community. One of the patients developed another meningioma 13 years after the operation. A causal connexion between radiation and tumors is supported by the patient linkage and by the similarity of tumor type, site and latency (36.14 +/- 7.51 years).
This work aims to study the exercise-induced changes of Factor VIII Complex both in healthy subjects and in type I diabetics without vascular complications, and to investigate the possible relations between growth hormone and Von Willebrand's Factor response to exercise. Results show that maximal exercise performed by cycle ergometer causes a significant increment of the procoagulant subunit (VIII:C) and of Von Willebrand Factor (VIII:RiCoF) both in healthy controls and in type I diabetics, whereas a slight increment of Factor VIII-Related antigen (VIIIR:Ag) is observed only in diabetics. The shape of the mean GH response to exercise parallels the one of Von Willebrand's Factor: however, the presence of VIII:RiCoF increments also in GH non-responders supports the conclusion that growth hormone is not the only factor involved in the regulation of Von Willebrand's Factor exercise-induced increase.
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Fifty-one alcoholics, previously admitted to the hospital for medical care and treated with disulfiram, were re-examinated after 1-3 years. In thirty of them (58%) total abstinence was found; eighteen patients (35%) behaved so in spite of disulfiram withhold during the first year of self-administration. No side-effects were reported. General behaviour, mood, work, interest and familiar relationships improved. The treatment generally failed in the cases of secondary alcoholism as in marked neurosis or psychosis. The research proved the main role of family and environment in the successful cases. The treatment with disulfiram is useful but incomplete.
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HbA1 levels were determined by a rapid chromatographic column test in 15 healthy subjects (HS) and in 15 maturity-onset diabetics (MOD), fasting and 2 h after glucose ingestion (100 g for HS, 50 g for MOD). Chromatography was carried out both before and after 6 h of red cell incubation in saline at 37 degrees C. HbA1 in HS at 0 and 120 min of OGTT was not significantly different, either before (6.24 +/- 0.61% and 6.22 +/- 0.62%) or after red cell incubation in saline (5.85 +/- 0.61% and 5.87 +/- 0.55%). Red cell incubation in saline significantly reduced HbA1 levels both at 0 and 120 min (2p less than 0.001). HbA1 in MOD before red cell incubation in saline, was slightly but significantly higher at 120 min (8.61 +/- 1.03%) than at 0 min (8.39 +/- 1.01%): 2p less than 0.001. After incubation in saline, this difference was cancelled (7.86 +/- 0.85% at 0 min and 7.97 +/- 0.83% at 120 min: n.s.). Post-incubation levels were lower than pre-incubation ones both at 0 and 120 min (2p less than 0.001). The HbA1 increment observed in MOD is significantly correlated (p less than 0.01; r=0.64) to the blood glucose increment observed at the glycemic peak. We conclude that hemoglobin glycosylation may show rapid changes also in MOD, reflecting blood glucose changes, whereas in HS the physiological glycemic excursions are not wide enough to produce rapid HbA1 changes. Since labile and stable HbA1 co-elute in the rapid chromatographic methods, red cell incubation in saline for 6 h at 37 degrees C is recommended as a simple procedure which allows the measurement of the stable fraction alone, i.e. the real index of long-term glycemic control, independent of rapid glycemic fluctuations.
The patient study has been performed in order to evaluate the usefulness of the artificial pancreas in the surgical management of previously not localized insulinomas. In the 4 patients studied, blood glucose was maintained both overnight and during surgery up to a preselected individualized level in order to avoid hypoglycemia. During surgery, only one patient required dextrose infusion. The continuous intrasurgical monitoring of blood glucose in the 4 cases examined showed that: (1) anesthesia induction, surgical incision and viscera mobilization were accompanied by a rise in blood glucose (10.30 mg/dl), reaching the highest levels 30-40 min after the start of the operation; (2) adenoma manipulation was followed by a drop in blood glucose (10.40 mg/dl), reaching the lowest level after 30-40 min; (3) adenoma resection was followed by a rise in blood glucose (25-40 mg/dl), particularly evident after 30-40 min. It is concluded that the artificial pancreas is certainly useful during surgery of insulin-producing tumors, allowing continuous monitoring of glycemia and avoiding dangerous blood glucose excursions: however, when the insulinoma is not identified during surgery, the periods elapsing between the surgical phases and the blood glucose changes observed can be too prolonged to ensure successful conservative serial pancreatectomy in all cases.
The aim of this study was to investigate the influence of short-term submaximal postprandial exercise on plasma glucose concentrations in tightly controlled insulin-dependent diabetic patients treated by means of continuous subcutaneous insulin infusion (CSII). Two hours after breakfast, five diabetic patients and five healthy control subjects followed this protocol: 30 min of mild exercise, 30 min rest, 30 min of moderate exercise, 150 min rest. Serial determinations of plasma glucose, free insulin, and growth hormone (GH) were made. Similar control studies without exercise were also performed. In the diabetic patients, analysis of variance and covariance did not reveal any significant difference between the 2-h postbreakfast concentrations of plasma glucose and free insulin and postexercise values. A significant GH increase was observed after the exercise periods. Plasma glucose and insulin concentrations throughout the exercise study were not significantly different from the control study concentrations. Plasma free insulin concentrations of the diabetic patients were higher than the concentrations of healthy subjects. We conclude that CSII-treated, tightly controlled, insulin-dependent diabetic patients performing short-term mild and moderate exercises 2 and 3 h after breakfast do not have a high risk of hypoglycemia in spite of mild hyperinsulinemia.
This study has been designed to investigate, in five non-insulin-dependent diabetic patients, the influence of physical training (1 h a day, 7 days a wk for 6 wk, at 50-60% maximum oxygen uptake) on blood glucose control, glucose tolerance, insulin secretion, and insulin action. Physical training resulted in a significant improvement in blood glucose control, glucose tolerance, and insulin action. These results suggest that short-term intense physical training ameliorates the main metabolic derangements of non-insulin-dependent diabetes mellitus.
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