Somatosensory evoked potentials by median nerve stimulation in rabbits. I. Source localization by cortical and stereotaxic recordings.
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Biomedical subjects
Publications and source records attributed to A Romani.
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The relationships between Ca2+ transport and glucose-6-phosphatase activity, previously studied in isolated liver microsomes, were investigated in permeabilized hepatocytes in the presence of mitochondrial inhibitors. It was found that the addition of glucose 6-phosphate to the cells markedly stimulates the MgATP-dependent Ca2+ uptake. A progressive increase in the stimulation of Ca2+ uptake was seen with increasing amounts of glucose 6-phosphate up to 5 mM concentrations. Vanadate, when added in adequate concentrations (20-40 microM) to the hepatocytes inhibits both the glucose-6-phosphatase activity and the stimulation of Ca2+ uptake by glucose 6-phosphate, while not affecting the MgATP-dependent Ca2+ uptake. The addition of inositol 1,4,5-trisphosphate to permeabilized hepatocytes in which Ca2+ had been accumulated in the presence of MgATP and glucose 6-phosphate, results in a rapid release of Ca2+.
Cerebral ischemic lesions were induced in rabbits through internal carotid artery embolization by means of microspheres. Different models of stroke ranging from single focal cortical lesion to massive bilateral brain edema were reproduced and monitored up to the 24th hour by electroencephalogram (EEG and QEEG), somatosensory evoked potentials (SEPs), cerebral blood flow (CBF), platelet aggregation. The site and extent of the lesions were verified by histological examinations. Results obtained and physiopathological implications are discussed.
Twenty chronic male schizophrenic subjects aged 30-50 years were examined by an auditory event-related potential procedure for the evaluation of the P300 component, a CT scan and a neuropsychological test battery. The P300 latency was increased and its amplitude was reduced. CT scan measures showed lateral and third ventricle enlargement, and there was a global neuropsychological impairment. Poor neuropsychological performances were consistently associated with delayed P300 latencies, but not with CT scan measures. Ventricular enlargement was more pronounced among subjects with a negative family history for major psychiatric disorders.
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Lipid peroxidation in cellular membranes leads to the formation of toxic aldehydes. One product provided with particular reactivity has been identified as 4-hydroxynonenal and thoroughly studied as one of the possible mediators of the cellular injury induced by pro-oxidants. In the present study we have searched for the presence of 4-hydroxynonenal and other lipid peroxidation products in the liver of bromobenzene-poisoned mice, since under this experimental condition the level of lipid peroxidation is much greater than in the case of CCl4 or BrCCl3 hepatotoxicity. 4-Hydroxynonenal was looked for in liver extracts as either free aldehyde or its 2,4-dinitrophenylhydrazone derivative. In both cases, by means of thin-layer chromatography (TLC) and high-pressure liquid chromatography, a well resolved peak corresponding to the respective standards (free aldehyde or 2,4-dinitrophenylhydrazone derivative) was obtained. Total carbonyls present in the liver of intoxicated animals were detected as 2,4-dinitrophenylhydrazone derivatives. The hydrazones were pre-separated by TLC into three fractions according to different polarity (polar, non-polar, fraction I, and non-polar, fraction II). The amounts of carbonyls present in each fraction were determined by ultraviolet-visible spectroscopy. 'Non-polar carbonyls, fraction II' were further fractionated by TLC. The fraction containing alkanals and alk-2-enals was analyzed by high-pressure liquid chromatography and several aldehydes were identified. In addition, protein bound carbonyls were determined in the liver of bromobenzene-treated mice. The biological implications of the finding of 4-hydroxynonenal and other carbonyls in vivo in an experimental model of hepatotoxicity are discussed.
Divergence paralysis is a clinical syndrome that is characterized by esotropia and diplopia at distance fixation and fusion at near fixation. This syndrome is thought to result from a lesion in the brain stem, probably in the midbrain or in the pontine region. This paper reports a case in which ocular motility disturbances, simulating divergence paralysis, were caused by a bilateral and symmetrical restrictive syndrome involving the medial rectus muscles.
Seventy-two healthy volunteers aged 24-75 years were submitted to different auditory "oddball" ERP (Event Related Potential) paradigms which included an intensity discrimination and a right/left discrimination task. In both conditions, a late positive component (P3) of the vertex potential appeared. However its latency was about 30 msec greater and its amplitude was smaller in the intensity discrimination paradigm. Moreover, P3 latency increased with age in a strictly linear fashion in the intensity discrimination paradigm, whereas in the right/left discrimination paradigm an increase of latency with age was confined to the older age-groups, which is expressed by a quadratic latency/age function. A relation was found between the subjective feeling of difficulty in performing the tasks and P3 latency in the different paradigms.
Eighteen chronic schizophrenic subjects treated with a uniform dosage (4-6 mg/day p.o.) of haloperidol were submitted to computed tomography (CT) and to pattern reversal visual evoked potentials (VEPs). Compared to age-matched controls, schizophrenic patients showed lateral and third ventricular enlargement, greatly delayed VEP latencies and reduced amplitudes. These abnormalities were not related to diagnostic subgroups. Schizophrenic patients with a positive family history for major psychiatric disorders showed normal CT scan measures and greatly abnormal VEP measures, whereas patients with a negative family history showed CT scan signs of atrophy and less pronounced VEP abnormalities.
4-Hydroxynonenal (4-HNE) has been identified as one of the most reactive products in a series of toxic aldehydes originating from lipid peroxidation of cellular membranes. The possibility that this aldehyde plays a role as one of the mediators of the cellular injury induced by pro-oxidants is currently investigated. Mice intoxicated with bromobenzene showed levels of lipid peroxidation in the liver that exceed those induced by hepatotoxic haloalkanes CCl4 and BrCCl3. Hence, we have searched for the presence of 4-HNE and other lipid peroxidation products in the liver of bromobenzene-poisoned mice. We looked for 4-HNE in liver extracts as either free aldehyde or its 2,4-dinitrophenylhydrazone derivative. Using thin-layer chromatography (TLC) and high pressure liquid chromatography (HPLC) we obtained well resolved peaks, corresponding to the standard aldehyde or its 2,4-dinitrophenylhydrazone derivative, respectively. 2,4-dinitrophenylhydrazone derivatization was also used to determine the total carbonyl content in the liver of the intoxicated animals. Three fractions of hydrazones, according to their different polarity ("polar", "non-polar carbonyls, fraction I"; and "non-polar carbonyls, fraction II"), were obtained using TLC. The UV-visible spectra were recorded for quantitative evaluation. Further fractionation of "non-polar carbonyls, fraction II" provided a fraction containing several alkanals and alk-2-enals, which were analyzed and identified by HPLC. Furthermore, protein bound carbonyls were determined in the liver of the intoxicated animals.
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This work deals with the results of a clinical experience with viloxazine (VLZ) carried out on 43 depressed subjects of the female sex categorized with D.S.M. III criteria. Clinical ratings were made by means of the Hamilton Scale for depression and the Taylor self rating scale for anxiety. The results prove the efficacy of the drug in all the examined patients, along with the rapidity of effects in comparison with the tricyclic antidepressants. The elderly patients improved better than the adult subjects, especially when the depression was of the inhibited type.
20 normal subjects were submitted to seven auditory ERP paradigms in which they were required to count regularly presented cliks (A1, A2, A3), cliks presented in pseudorandom order (B) and in which they had to discriminate relevant from non relevant stimuli characterized by side of provenience (C1, C2) or intensity difference (D). In paradigms C and D a P 300 component was evoked. Age was significantly correlated with P 300 latency only in paradigm D. There was a significant relationship between differences in subjective feelings of difficulty or engagement in performing the counting tasks in C and D and P 300 latency.
Visual evoked potentials by flash (VEP-f) and pattern reversal (VEP-p) stimulation and BAEPs were performed in parkinsonian patients before and after 1 and 4 hours levodopa + Carbidopa administration in two separate experiments. In the first experiment (9 patients and 9 controls) an increase of latencies of peaks III and IV of VEP-f was observed in parkinsonian patients but not in controls. In the second experiment (6 patients) an increase of latencies of peaks N70 and P100 of VEP-p and an increase of latency of peak III and of III-V interval of BAEPs was observed. The results confirm the influence of dopaminergic systems on visual pathways and suggest that the effects of acute 1-DOPA administration may differ from those of chronic treatment. Moreover some evidence exists that dopaminergic systems are involved also in acoustic pathways.
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