[Glucide interconversion and glycogen synthesis by uridine-diphosphoglucose (UDPG), in cerebral tumors].
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Biomedical subjects
Publications and source records attributed to L Frattola.
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Short-duration cooling of the nerve to the extensor digitorum longus muscle of the rat in vivo induced partially reversible denervation of the muscle and atrophy in the type 2 muscle fibers. Increases in cyclic adenosine monophosphate, cyclic guanosine monophosphate phosphodiesterase, adenylate cyclase, and guanylate cyclase were observed in the denervated muscle. Treatment with gangliosides of the bovine brain cortex seemed to improve the excitability of the surviving motor units and to encourage recovery of neuromuscular trophic control, but it did not affect the nerve conduction velocity or the contractile properties of the denervated muscle.
A double-blind, randomized electromyographic investigation was conducted of the effects of cerebral ganglioside treatment on patients suffering from diabetic or alcoholic polyneuropathy. Cerebral gangliosides (50 mg once a day) administered to 15 diabetic and to 15 alcoholic neuropathic patients for 40 days, facilitated the reappearance of sensory potentials and significantly increased the MAP amplitude in median, ulnar, and peroneal nerves. In relation to ganglioside treatment, there was no significant change in the conduction velocities or in the distal latencies of these nerves, nor was there a change in the duration of the MAPs. On the basis of these results, it is suggested that the cerebral gangliosides are capable of inducing an improvement in the excitability of nerve fibers and of facilitating the processes of reinnervation, probably by means of an enhancement of fiber sprouting.
We examined cognitive functions and central conduction velocities in 20 patients, over 63-year old, with NIDDM compared with 20 normal, age-matched controls. Mean conduction velocity of median nerve, was significantly lower in diabetics than in controls, but absolute values were within normal range. Neurological examination showed clinical signs of lower limbs neuroperipheral involvement. Only one cognitive subtest performance was abnormal whereas there was no impairment in central conduction velocities. In our study population, although median nerve conduction velocity values may introduce a bias of low peripheral neuropathy incidence, there was no evidence of a massive or progressive specific central nervous system involvement caused by NIDDM.
The levels of the cyclic adenosine 3',5'-monophosphate (cyclic AMP)-phosphodiesterase (PDE) and the biochemical properties of its endogenous protein activator (PDEA) obtained from the human brain cortex and from different types of human cerebral tumours have been evaluated. The effects of the various PDEAs were studied measuring the activation of an activator-depleted cyclic AMP-PDE prepared from a normal brain cortex. The PDEA, obtained from normal and pathological tissues, did not change the affinity of the purified PDE for cyclic AMP, while it increased the Vmax of the enzyme. On the other hand, a cross-activation study showed that the PDEA lacked tissue specificity and was present in the tissue in excess over the enzyme. The levels of cyclic AMP-PDE and PDEA were much higher in normal than in tumoural tissues. The enzyme activity decreased in cerebral tumours more markedly than the protein activator. This biochemical pattern was more evident in the tumours of glial origin which are the most malignant.
In order to evaluate the efficacy of dihydroergokryptine mesylate (DEK) - a semisynthetic ergot alkaloid having a neuroprotective activity through the activation of antioxidant enzymatic systems - in dementia of Alzheimer type, a long-term, randomized, placebo-controlled, double-blind study was carried out. The interim analysis after 1-year follow-up is here reported. Two-hundred-and-fifteen patients fulfilling the NINCDS-ADRDA criteria for probable Alzheimer's disease were enrolled by 14 geriatric and neurologic Italian centers. The study design included a 1-month pre-treatment phase with placebo; 1-year double-blind treatment with DEK or placebo; a further 1-year open phase of treatment with DEK. The active drug dosage was 5 mg bid orally administered for the first 2 weeks, 10 mg bid for the following 2 weeks, 20 mg bid for the following 11 months. Efficacy was assessed by means of Gottfries-Bråne-Steen (GBS) Rating Scale for dementia and Mental Deterioration Battery. The univariate analysis showed a significant improvement of GBS subscales and factors (with the exception of the Factor III, depression-anxiety). Multivariate analysis showed a significant difference between treatments in GBS scale (P=0.002) without any influence of age and illness duration. These results were confirmed by the end-point analysis carried out on GBS scores using baseline value as covariate. Minor adverse events were observed in 9 out of 108 patients (8.3%) of the DEK group and in 7 out of 107 (6.5%) of the placebo group. No change in blood pressure, heart rate and routine laboratory tests was observed. These preliminary results suggest positive symptomatic effects of DEK on elderly patients with probable Alzheimer's disease indicating a slowing down of the cognitive decline.
One hundred forty-one adult patients treated for no less than 6 months with standard daily doses of the commonest antiepileptic drugs (AEDs) were recruited in five Italian centers and submitted to intensive clinical and electrophysiologic investigation to assess the effects of AEDs on peripheral nerves. Eighty percent of the patients were receiving monotherapy. Carbamazepine (CBZ) was the most common AED (51 cases), followed by phenytoin (PHT) (46), phenobarbital (PB) (42), and valproate (VPA) (25). Fifty-three percent of the patients had one or more symptoms of polyneuropathy (paresthesias being the most common complaint). The neurologic examination was abnormal in 32%. Electrophysiologic findings in two or more separate nerves were abnormal in 77 patients (54.6%); of these, 27 (19.1%) had abnormal neurologic findings and 21 (14.9%) also had symptoms of polyneuropathy. Sensory functions were most frequently impaired. Sural nerve biopsy was performed in 4 patients receiving monotherapy with CBZ, PHT, PB, and VPA. Except in patients receiving VPA (in whom no morphologic abnormalities were detected), mild predominantly axonal damage with secondary myelin changes was noted. A correlation was noted between polyneuropathy, age of the patient and, to a lesser extent, receipt of two or more AEDs.
beta-adrenergic receptors were measured in cerebral microvessels of gerbils and rats after ligature of the right or left common carotid artery. The results indicate a decrease in the number of beta-adrenergic receptors in brain microvessels of both ipsilateral and contralateral hemispheres. This event may reflect altered patterns of the neuronal regulation of brain microvasculature and may be related to cerebrovascular alterations which are concomitant with ischemia. Furthermore, the results show that the decrease in beta-receptor density is more pronounced in the left hemisphere, independently on the side of carotid occlusion. This finding suggests that microvessel function in the left side of the brain is more vulnerable to hypoxia effects.
The effect of short term and long term ischemia induced by right carotid occlusion was studied on beta-adrenergic receptor function in rat cerebral microvessels. The results show a different time-dependent responsiveness of the two hemispheres to ischemia, with a pronounced and more persistent decrease in the number of capillary beta-receptors in the left side of the brain. The data suggest the existence of asymmetries in the control of brain microvasculature which may mediate the different time-course of beta-receptor changes in response to ischemia.
Extra corporeal photochemotherapy (ECP) is an immunomodulating procedure used in several nonneurological diseases which, similarly to multiple sclerosis, are likely to be due to T-cell-mediated autoimmunity and it is probable that ECP can modulate the normal activity of peripheral blood mononuclear cells (PBMC). Using the Lewis rat experimental allergic encephalomyelitis (EAE) model of human multiple sclerosis (MS) we examined the effect of extracorporeal UV-A irradiation on psoralen-activated PBMC. In our experiment the comparison between the two groups of animals (ECP or sham-treatment) evidenced that the ECP treatment reduced the severity of EAE on clinical grounds and this result was confirmed by the pathological examination. The changes in the titers of anti-myelin antigen antibodies typical of EAE were also modulated by the procedure. Ex vivo examination evidenced a significant reduction in tumor-necrosis factor-alpha (TNF-alpha) released by PBMC after lipopolysaccharides (LPS) stimulation in culture. We conclude that ECP modifies the normal activity of PBMC during the course of EAE and it is possible that one of the anti-inflammatory mechanisms of action of ECP is correlated to a down-regulation of T-helper 1 lymphocytes activity.
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Adenyl-cyclase (A-C) and Phosphodiesterase (PDE) behaviour in a large number of human cerebral tumors is reported and compared with that of normal gray and white matter. PDE is much reduced in all oncotypes. Also A-C appears reduced in all tumors except astrocytomas where enzymatic activity is similar to that of gray matter. The Authors tried to explain these changes in activity by relating them to the malignancy of the oncotypes or to their different embryologic origin.
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