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Biomedical subjects

S Mazza

Publications and source records attributed to S Mazza.

At least 73 records · Page 4Linked to original sources
PubMed1978

Night sleep organization in patients with severe hepatic failure. Its modifications after L-dopa treatment.

20 subjects with severe hepatic failure have been studied by means of all night polygraphic sleep recordings. Base night recordings have been made, as well as registrations after treatment with drugs that are known to improve the clinical conditions of these patients, especially concerning the psychic performances. Base night recordings show sleep disruption, with a large amount of wakefulness at the beginning of the registrations and during the night itself; sleep stages are strongly reduced, especially REM sleep. After L-dopa treatment, these negative patterns are furthermore enhanced and the percentage incidence of the REM stage is very low; nevertheless, this behaviour goes side by side with a light improvement in psychological performances. On the contrary, therapy with lactulose seems to improve the neuropsychiatric state and the sleep organization; as a matter of fact, wakefulness is lower in the night records after lactulose treatment, whilst the percentage incidence of sleep stages tends back toward normality; REM sleep has clearly risen.

Adult↗
PubMed1976

Occult normal pressure hydrocephalus with parkinsonian symptomatology.

The authors describe a case where a parkinsonian symptomatology is associated with pneumoencephalographic and RISA-cisternographic findings typical of an occult normal pressure hydrocephalus. They discuss their personal contribution in the light of what has been already reported in the literature on the same subject. They conclude that a CSF dynamics disturbance among the possible physiopathogenetic mechanisms of an extrapyramidal syndrome in young subjects should be considered. On the other hand, they also emphasize the possibility that the occult normal pressure hydrocephalus may have syndromical expression which are different from the typical one initially described.

Adult↗
PubMedDate not supplied

Central sensory and motor conduction in vitamin B12 deficiency.

Four patients with subacute combined degeneration were studied through upper and lower limb SEPs recorded with a non-cephalic reference montage and through cortical and spinal magnetic stimulation. Clinical signs were confined to the lower limbs in 3 patients; the remaining patient presented only paraesthesiae in 4 limbs. Median nerve SEPs showed a normal cervical N13 response with a significant increase of central conduction time concerning exclusively the P9-P14 interpeak interval. Central motor conduction to upper and lower limb muscles was abnormal. Nerve conduction studies provided no evidence of peripheral nerve involvement. These electrophysiological findings suggest that in vitamin B12 deficiency the higher segments of the cervical cord are usually affected first and that central sensory and motor conduction studies are sensitive methods for detecting such damage.

Action Potentials↗
PubMedDate not supplied

Sleep microstructure and EEG epileptiform activity in patients with juvenile myoclonic epilepsy.

Clinical and EEG manifestations of juvenile myoclonic epilepsy (JME) occur in a strict relationship to the sleep-wake cycle, particularly to transition phases (awakening, falling asleep, afternoon relaxation after work). JME manifestations are deactivated during sleep. Because arousal fluctuations during NREM sleep may be controlled by the same neurophysiologic mechanisms regulating awakening, we studied the relationship between the cyclic alternating pattern (CAP) and JME manifestations. All-night polysomnographic recordings of 10 JME patients were analyzed for variations of epileptiform EEG abnormalities in relation to sleep stages and to different microstructural variables (NCAP, CAP, phases A and B). CAP rates (ratio between total CAP duration and total NREM sleep duration) were also calculated. Average CAP rate was 46.70%, significantly higher than that (23%) of an age-matched control group. Macrostructural analysis showed only a trend toward a slight predominance of EEG epileptiform activity during slow wave sleep but no significant correlation between spiking rates and sleep stages. Microstructural analysis confirmed the CAP modulation of EEG epileptiform activity, with maximum appearance of epileptiform abnormalities during phase A CAP (normalized spiking rate = 4.00 +/- 0.98) and strong inhibition during phase B (0.06 +/- 00.6). Intermediate values were noted during NCAP (0.54 +/- 0.27). No correlation was noted between spiking rates during NREM sleep and CAP rates, possibly indicating that in JME patients the increased CAP rate may be partially independent of epileptiform EEG activity. Our data suggest that in JME patients CAP may be a neurophysiologic oscillator organizing expression of the epileptiform discharges independent of the tendency of the individual patient to produce epileptiform EEG discharges.

Activity Cycles↗
PubMedDate not supplied

CD44v10: an antimetastatic membrane glycoprotein for pancreatic cancer.

AIMS: The aims of this study were 1) to investigate the mRNA pattern of CD44 variants in three primary (MIA PaCa 2, PANC-1, PSN-1) and two metastatic (CAPAN-1, SUIT-2) pancreatic cancer (PC) cell lines; 2) to ascertain whether the genetic transfer of CD44s and CD44v10 modifies the adhesion of PC cells to the extracellular matrix (ECM) in vitro and their metastatic behavior in vivo. METHODS: CD44 mRNA analysis was done by means of RT-PCR. Adhesion to ECM the was assessed using coated microtiter plates. For the study of CD44v10 insertion in the CAPAN-1 line, liposome-mediated DNA transfer was used. SCID mice were employed for in vivo experiments. RESULTS: CD44v10 mRNA was not expressed by the CAPAN-1 nor by four of the six SUIT-2-derived clones. The stable expression of CD44v10 by modified CAPAN-1 significantly enhanced fibronectin adhesion. Mice without either liver or pancreatic metastases were more frequently found among the animals injected with modified (CD44v10 expressing) than with non-modified CAPAN-1. CONCLUSIONS: 1) It is possible to differentiate between metastatic and non-metastatic PC cells on the basis of CD44v10 expression; 2) CD44v10 seems to be involved in mediating fibronectin adhesion in vitro and in counteracting metastases in vivo.

Animals↗
PubMedDate not supplied

Pancreatic cancer cells invasiveness is mainly affected by interleukin-1beta not by transforming growth factor-beta1.

BACKGROUND: We investigated in vitro whether IL-1beta and TGF-beta1 affect pancreatic cancer cell growth, adhesion to the extracellular matrix and Matrigel invasion. MATERIALS AND METHODS: Adhesion to fibronectin, laminin and type I collagen, and Matrigel invasion after stimulation with saline, IL-1beta and TGF-beta1 were evaluated using three primary and three metastatic pancreatic cancer cell lines. RESULTS: Extracellular matrix adhesion of control cells varied independently of the metastatic characteristics of the studied cell lines, whereas Matrigel invasion of control cells was partly correlated with the in vivo metastatic potential. IL-1beta did not influence extracellular matrix adhesion, whereas it significantly enhanced the invasiveness of three of the six cell lines. TGF-beta1 affected the adhesion of one cell line, and exerted contrasting effects on Matrigel invasion of different cell lines. CONCLUSIONS: IL-1beta enhances the invasive capacity of pancreatic cancer cells, whereas TGF-beta1 has paradoxical effects on pancreatic cancer cells; this makes it difficult to interfere with TGF-beta1 signaling in pancreatic cancer treatment.

Cell Adhesion↗
PubMedDate not supplied

Gabapentin in the prophylaxis of migraine: a double-blind randomized placebo-controlled study.

OBJECTIVE: Gabapentin is an antiepileptic drug of new generation that increases brain GABA levels. We report the results of a three-month randomised double-blind placebo-controlled study on the effects of gabapentin in the prophylaxis of patients with migraine meeting the IHS criteria. PATIENTS AND METHODS: We treated 63 patients suffering from migraine with or without aura. Patients treated their attack at home using symptomatic drugs and clinical assessment was recorded on a diary. After a washout of 8 week from any other prophylactic treatment, all patients were treated with 1200 mg/day of gabapentin; this is our therapeutic plan: 400 mg/day from 1st to 3rd day, 800 mg/day from 4th to 6th day and 1200 mg/day from 7th day. RESULTS: No patients withdrew, gabapentin was well tolerated; adverse events (somnolence, dizziness, tremor, fatigue and ataxia) generally were transient and mild to moderate in severity and in 13 patients (27%) only occurred. At the end of treatment, in such case, we reported a significative reduction of frequency and intensity of migraine in 30 patients treated with gabapentin. DISCUSSION: Our observations indicate that gabapentin is well tolerated by patients and that reduces headache frequency and use of symptomatic drugs in both groups. Gabapentin shows to have an effective therapeutic action in the prophylactic treatment of migraine.

Acetates↗
PubMedDate not supplied

[New perspectives in the diagnosis and therapy of narcolepsy].

Narcolepsy syndrome is a common, although often misdiagnosed, neurological disorder, whose clinical features are excessive daytime somnolence with sleep attacks, caplexy, sleep paralysis and hypnagogic hallucinations. The clinical manifestation have been interpreted as the expression of a sudden intrusion of dissociated REM phenomena in wakefulness. Sometimes the clinical manifestations may include only some of the symptoms: in particular, the cases in which the only symptom is excessive daytime somnolence may be difficult to diagnose. The etiopathogenesis of narcolepsy syndrome is still poorly understood. Recent experimental evidences suggest that a protein, called "orexin", which is supposed to play a role in the control mechanisms of both sleep and eating behaviour, is involved in its pathogenesis. The treatment of narcolepsy has been, up to now, exclusively symptomatic, and in some way empirical and unsatisfactory, especially regarding to daytime sleepiness. Recently, new pharmacological agents, acting on the serotoninergic and/or noradrenergic systems, allow a better control of the cataplectic attacks. The recent development of modafinil, a central nervous system stimulant, devoid of the serious side effects of amphetamines and other compounds, allows to hope in a better control of daytime somnolence and sleep attacks. The aim of the paper is to describe the recent advances in the diagnosis and treatment of narcolepsy.

Catalepsy↗
PubMedDate not supplied

Metastatic colorectal cancer stimulates collagen synthesis by fibroblasts.

BACKGROUND: We ascertained in vitro whether there were any differences in the growth of fibroblasts and the production of collagen (PIIIP), in relation to the presence of conditioning sera or tumor tissues from colorectal cancer (CRC) patients with disease progression or regression after surgery. PATIENTS AND METHODS: Fibroblasts were conditioned with: 1) 10% of control (n=20) or CRC patients' (n=57) sera; 2) 10% of tumor tissue homogenates obtained from CRC patients without (group A, n=6) or with (group B, n=5) liver metastases. After surgery, 29/57 patients (group 1) developed while 28/57 (group 2) did not develop a recurrent disease. RESULTS: The ratio between cell growth and PIIIP production increases when fibroblasts were conditioned by group I (p<0.05), but not by controls or group 2 sera. Tumor homogenates from group B inhibited cell growth (p<0.001), while they induced PIIIP production (p<0.001) in comparison with results from group A. CONCLUSION: CRC non-metastatic cancer cells induce mainly fibroblasts growth, while metastatic cells mainly induce collagen synthesis. This effect is probably caused by soluble mediators, which partly pass into the systemic circulation.

Adult↗
PubMedDate not supplied

Sleep disorders in childhood: a review.

Several studies in the last ten years have been directed towards a better understanding of sleep disorders in childhood. Defining sleep disorders in this age is difficult in dependence of relevant differences in sleep patterns at subsequent developmental stages. In new-borns total sleep time is fairly equal during night and day. Normally, day-time sleep gradually decreases over the first three years of life, such that night-time sleep progressively increases till the age of four, and similar to adult sleep-time by adolescence. The most frequent sleep disorders observed in childhood are parasomnias, that, thought to be a CNS sign of immaturity, tend to be quite predictable, recurring in the same families and not even influenced by environmental stimuli. These disorders included: a) arousal disorders, that generally emerge from delta sleep or relate to arousals occurring during NREM sleep, very common in childhood and fairly common in adulthood either; b) somnambulism and somniloquy, that have many common characteristics: first of all, they have the potential to generate a great sense of discomfort and fear in parents watching a child who suddenly sits up in bed eyes-opened but 'unseeing'; c) nocturnal enuresis, that is substantially not a problem of depth of sleep, despite many parents believe. Although narcolepsy is more common in adolescence, many studies have demonstrated that narcoleptic symptoms may begin in childhood. Narcoleptic symptoms in children are similar in their appearance to those predominant in adults, but their expression may be different because of CNS maturational factors. Historical descriptions of the OSAS evidenced since the beginning the importance of neurobehavioral complications associated with the cessation of airflow at the nose and mouth accompanied by respiratory effort, deriving from upper airway obstruction which occurs during sleep.

Adolescent↗
PubMedDate not supplied

[Neuropathological study of a case of progressive familial myoclonic epilepsy (author's transl)].

We previously reported (Europ, Neurol., 3, 347-364, 1970) on two clinical observations of progressive myoclonus epilepsy in the same family. Now, we complete the clinical study showing the neuropathological findings concerning one of the two patients who died at the age of twenty. Degenerative neuronal alterations were found involving the olivo-cerebello-rubral system and, in a minor degree, the brain stem and thalamic structures. No Lafora bodies were found. These pathological features make it possible to suggest a differentiation from a first group of progressive myoclonus epilepsy (Unverricht-Lundborg) and another group (with epileptic manifestations) of dyssynergia cerebellaris myoclonica (Ramsay Hunt). We agree with the suggestion of other authors that it is difficult to establish precise differentiations between these groups at neuropathological level. We think however that the distinction is still possible on the basis of the clinical picture. Our observations cupport the hypothesis that our patient is an "abiotrophic" case of Unverricth-Lundborg syndrome, as we previously had suggested on clinical and especially neurophysiological findings.

Adult↗
PubMedDate not supplied

[Depression in epilepsy: symptom or syndrome?].

An occurrence of depression or depressive symptomatology has been reported in 30% of patients with epilepsy. Depression has been reported peri- and interictally. To make a differentiation may be difficult in patients with frequent seizures. However, complex partial seizures, particularly if are located on temporal lobe, appear to be etiologic factors, especially in men with left-sided epileptic foci. Depression is also more frequent in patients treated with polytherapy, particularly with phenobarbital and vigabatrin. The depression appears to be endogenous and has also been described in patients with temporal lobectomy. Underlying risk factors (genetic, metabolic, etc) and some psychosocial condition also play a part and may explain the increased rates of depression in patients with epilepsy. Treatment approaches include psychotherapy, rationalization of antiepileptic drug medication and antidepressant treatment. The use of antidepressant treatment, in these patients, still raises uncertainties because of the widespread persuasion that this drugs exacerbated seizures. This adverse event is relatively uncommon at therapeutic dosages, and its incidence with some of most frequently used antidepressant drugs is close to that of spontaneous seizures calculated for the general population, but the incidence may rise up to 30-40% after overdosage. On the basis of the data reported in literature, it appears fair to say that maprotiline and amoxapine show the greatest seizure risk, whereas trazodone, fluoxetine and fluvoxamine show the least. The data also showed that antidepressant drugs may display both convulsant and anticonvulsant effect and it is likely that the most important factor to assess the effect of a given antidepressant drug in terms of inhibition-excitation is drug dosage. Nevertheless, further studies are needed in this field, both to clarify the complex modulating effects of antidepressants on seizure threshold and to identify clearer and safer guidelines to manage the treatment of patients with epilepsy and concomitant depression.

Anticonvulsants↗