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Biomedical subjects

G Sechi

Publications and source records attributed to G Sechi.

At least 19 recordsLinked to original sources
PubMed2002

Multiple sclerosis-associated retrovirus (MSRV) in Sardinian MS patients.

Blood and CSF of Sardinian patients with MS and neurologic control subjects were tested for MS-associated retrovirus (MSRV). CSF detection in MS was 50% at clinical onset, increasing with temporal disease progression, and 40% in control subjects. In blood, MSRV was detected in all MS patients, in most patients with inflammatory neurologic diseases, and rarely in healthy blood donors. MSRV may represent a marker of neurologic diseases of inflammatory origin.

Adult↗
PubMed2001

Epileptic seizures after treatment with thiocolchicoside.

PURPOSE: To report the occurrence of epileptic seizures in humans, closely related to the use of the centrally acting muscle relaxant thiocolchicoside. METHODS: Description of three case histories. RESULTS: Two patients, affected with complex-partial seizures, sometimes secondarily generalized, receiving antiepileptic therapy, were seizure free for 7 and 9 years, respectively. They had the reappearance of tonic-clonic seizures few days after the continued use of thiocolchicoside, at a cumulative dose of the drug of 52 mg and 76 mg, respectively. The third patient was brain damaged and without a history of seizures. He had a sudden, convulsive seizure a few minutes after 4 mg intramuscular thiocolchicoside. CONCLUSIONS: Our case histories indicate that thiocolchicoside has a powerful epileptogenic activity. This drug should be avoided in patients with epilepsy or acute brain injury and possible disruption of the blood-brain barrier.

Adult↗
PubMed2000

Risperidone, neuroleptic malignant syndrome and probable dementia with Lewy bodies.

1. Conflicting reports are available regarding the sensitivity of patients with Dementia with Lewy bodies (DLB) to risperidone. 2. The authors studied a rare familial case of probable DLB, who developed a documented episode of neuroleptic malignant syndrome (NMS) following the exposure to risperidone. Previously, the patient had had an episode of NMS on trifluoperazine. 3. The discontinuance of risperidone, in combination with a mild increase of dopaminergic therapy, led to a complete recovery in few days. 4. In patients with DLB, a continued vigilance for extrapyramidal side effects, including NMS, would be advisable during the use of risperidone.

Antipsychotic Agents↗
PubMed1999

Do acute lesions of Wernicke's encephalopathy show contrast enhancement? Report of three cases and review of the literature.

Contrast medium was given intravenously to three nonalcoholic patients who underwent MRI or CT in the acute stage of Wernicke's encephalopathy. Lesions enhancement was not seen in one patient examined within 4 days of clinical onset, was mild in a another 3 days after clinical deterioration and marked in a patient examined 12 days after admission. Contrast enhancement of lesions was present in half of 12 cases of acute disease reported previously. There was a substantial overlap in the time interval between clinical onset and contrast-enhanced CT or MRI in the groups of enhancing and nonenhancing lesions. Since contrast enhancement may be absent in acute WE, proton-density and T2-weighted images are more useful for diagnosis of this reversible but potentially fatal condition.

Acute Disease↗
PubMed1998

Increased serum lipoprotein(a) levels in patients with early renal failure.

BACKGROUND: Elevated serum lipoprotein(a) levels have been found in patients with end-stage renal disease and in patients undergoing dialysis, suggesting that this lipoprotein contributes to the increased cardiovascular risk seen in these patients. It is not known whether lipoprotein(a) levels are elevated in the early phases of renal disease. OBJECTIVE: To evaluate levels of lipoprotein(a) and other lipids and the prevalence of atherosclerotic disease in patients with early renal failure. DESIGN: Cross-sectional study. SETTING: Hypertension clinic of a university medical center. PATIENTS: 257 patients with normal renal function and 160 patients with early impairment of renal function (creatinine clearance, 30 to 89 mL/min per 1.73 m2 of body surface area). MEASUREMENTS: Renal function was assessed by 24-hour creatinine clearance, proteinuria, and microalbuminuria. Cardiovascular disease status was also assessed. Serum lipoprotein(a), lipids, apolipoproteins, and apolipoprotein(a) isoforms were measured. RESULTS: Age, blood pressure, and serum lipoprotein(a) levels were greater in patients with early renal failure than in those with normal renal function and were independently associated with the presence of decreased creatinine clearance. Serum lipoprotein(a) and creatinine clearance were inversely correlated. The prevalence of coronary artery, cerebrovascular, and peripheral vascular disease was greater in patients with early renal failure than in those with normal renal function. The frequency distribution of apolipoprotein(a) isoforms was similar in patients with normal and those with impaired renal function. CONCLUSIONS: Serum lipoprotein(a) levels are elevated in patients with early impairment of renal function and are associated with greater prevalence of cardiovascular disease. An inverse correlation between serum lipoprotein(a) level and creatinine clearance and a frequency distribution of apolipoprotein(a) isoforms similar to that of normal patients point to decreased renal catabolism as a probable mechanism of lipoprotein(a) elevation in patients with early renal failure.

Adult↗
PubMed1997

Co-variation of free amino acids in brain interstitial fluid during pentylenetetrazole-induced convulsive status epilepticus.

Effects of pentylenetetrazole (PTZ)-induced convulsive status epilepticus on free amino acids changes in venous blood, CSF and interstitial fluid (IF) of the brain were examined in dogs. A volume of brain IF sufficient for analysis was obtained by chronically implanted tissue cages. The onset of PTZ-induced convulsive seizures seemed mainly related to a marked increase of glutamate, aspartate, taurine, glycine and phosphoserine while, the maintenance and frequency of seizures seemed related to a marked increase of serine and glycine, in combination with a moderate rise of glutamate. L-alpha-Aminoadipate was recovered in moderate amount in epileptic brain IF, while, in controls, this compound was present in minimal amount. The observed complex temporal variation of the amino acidic pattern may play a role in PTZ-induced seizures and, possibly, in pharmacological kindling and brain structural alterations induced by PTZ.

Amino Acids↗
PubMed1996

Acute hyponatremia and neuroleptic malignant syndrome in Parkinson's disease.

1. The neuroleptic malignant syndrome (NMS) may occur, occasionally, in Parkinson's disease (PD) after withdrawal of antiparkinsonian drugs. However, the circumstances in which the NMS occurs and the pathophysiologic mechanisms remain uncertain. 2. The authors studied a woman with PD, who developed hyperthermia, increased muscular tone, tremor, signs of autonomic dysfunction and stupor as symptoms of acute hyponatremia due to gastrointestinal loss of sodium in excess of water. 3. The correction of hyponatremia led to a complete recovery after about 6 hours. During this period the antiparkinsonian therapy was not modified. 4. An acute imbalance of sodium in the central nervous system may play a role in the pathophysiology of NMS.

Aged↗
PubMed1996

Reduced intravenous glutathione in the treatment of early Parkinson's disease.

1. Several studies have demonstrated a deficiency in reduced glutathione (GSH) in the nigra of patients with Parkinson's Disease (PD). In particular, the magnitude of reduction in GSH seems to parallel the severity of the disease. This finding may indicate a means by which the nigra cells could be therapeutically supported. 2. The authors studied the effects of GSH in nine patients with early, untreated PD. GSH was administered intravenous, 600 mg twice daily, for 30 days, in an open label fashion. Then, the drug was discontinued and a follow-up examination carried-out at 1-month interval for 2-4 months. Thereafter, the patients were treated with carbidopa-levodopa. 3. The clinical disability was assessed by using two different rating scale and the Webster Step-Second Test at baseline and at 1-month interval for 4-6 months. All patients improved significantly after GSH therapy, with a 42% decline in disability. Once GSH was stopped the therapeutic effect lasted for 2-4 months. 4. Our data indicate that in untreated PD patients GSH has symptomatic efficacy and possibly retards the progression of the disease.

Aged↗
PubMed1995

Cerebral and cerebellar diaschisis following carbamazepine therapy.

1. The regional cerebral blood flow was studied by SPECT in patients with partial epilepsy before and after 30 days of monotherapy with carbamazepine (CBZ). 2. Both a qualitative visual interpretation and a semiquantitative analysis of SPECT was performed. All patients underwent EEG, CT scan, and MRI studies. The CBZ serum concentrations were assayed. 3. After therapy, in three patients with focal epilepsy, both a crossed cerebral and cerebellar diaschisis were observed, with respect to the side of the epileptic focus in the opposite hemisphere. No morphologic changes were detected at MRI in the cerebral or cerebellar remote hypometabolic areas found at SPECT. 4. CBZ may have a depressant action on the corticopontocerebellar pathways and on the corticocallosal connections.

Adolescent↗
PubMed1995

Hyperinsulinemia and hypertension. Do intestinal hormones play a role?

Gastric inhibitory polypeptide (GIP) is one of the strongest insulinotropic gut factors. Its secretion is induced by oral (but not intravenous) glucose and it has been implicated in the pathogenesis of hyperinsulinemic states (NIDDM, obesity). To determine its relevance to hypertension, 54 subjects were studied: 26 normotensives (12 with and 14 without family history of essential hypertension), and 28 essential hypertensive subjects. Plasma glucose, serum insulin (IRI), and GIP were evaluated after a mixed meal containing a total of 82 g of carbohydrates, and 2 g sodium chloride. Venous blood was collected at baseline and every 15 min during a 3-h period. Baseline levels of glucose, IRI, and GIP were comparable in the three groups. At 30 min, however, IRI and GIP were higher in normotensives with a family history of hypertension and in established hypertensive versus control subjects. Both in normotensive and in hypertensive groups, glucose, IRI, and GIP responses to the meal were significantly correlated. Our data suggest the contribution of altered GIP secretion in the pathogenesis of hyperinsulinemia in essential hypertension.

Adult↗
PubMed1993

[Angiotensin II receptors in the heart conduction tissue].

Angiotensin II exerts a positive chronotropic effect on mammalian heart. This effect can be mediated either by activation of the sympathetic nervous system or binding to specific receptors located in cardiac conduction tissue. Recently, two angiotensin II receptor subtypes have been identified in rat tissues. In the present study, we have investigated tissue distribution of angiotensin II receptor subtypes in conduction tissue obtained from rat hearts, employing an in situ autoradiographic technique. Receptor subtypes were identified by use of the peptide antagonists losartan (AT1) and PD123,177 (AT2). Angiotensin II binding was homogeneously distributed in right and left ventricle, and interventricular septum, with each subtype accounting for approximately 50% of the specific binding. Receptor density in the conduction tissue, identified by acetylcholinesterase histochemistry, was quantitated by counting the silver grains on tissue sections which, following incubation, were dipped in photographic emulsion and developed. In both sinoatrial and atrioventricular node AT1 and AT2 receptors were homogeneously distributed. Receptor density in sinoatrial node was comparable to myocardium, whereas it was significantly higher (p < 0.02) in atrioventricular node. In conclusion, both AT1 and AT2 receptors are homogeneously distributed in cardiac conduction tissue. Binding density is higher in the atrioventricular node than in the other structures examined in our study, suggesting a possible role of angiotensin II in the atrioventricular conduction.

Angiotensin II↗
PubMed1993

[Angiotensin receptors in the rat myocardium during pre- and postnatal development].

Angiotensin II exerts positive inotropic and chronotropic effects on mammalian heart by binding to specific membrane receptors. Recently, 2 subtypes of angiotensin II receptors (AT1 and AT2) have been distinguished using the nonpeptide antagonists losartan and PD123177. Because angiotensin II has been reported to have growth potentiating effects in several tissues, we examined angiotensin II receptors in fetal (embryonic day 16 and 19), neonatal (1, 2, 3 and 10 days), and adult (10 and 16 weeks) rats. We performed an 125I-[Sar1,Ile8]-angiotensin II in situ binding assay on tissue sections obtained from Sprague-Dawley rats. Binding specificity was verified by competition with unlabeled [Sar1]-angiotensin II. Distribution of AT1 and AT2 receptors was determined by competition with losartan and PD123177, respectively, and the density of receptors quantitated by emulsion autoradiography. Angiotensin II receptors were widely distributed throughout the heart, with each receptor subtype accounting for approximately 50% of the specific binding. Binding density was comparable in right and left ventricles, and interventricular septum. Throughout cardiac development a significant increase (p < 0.005) in the density of both receptor subtypes was found immediately after birth, reaching a maximum on day 2, and decreasing toward prenatal values thereafter. No variation in the proportion of the 2 receptor subtypes was observed during development. Thus, in rat heart, AT1 and AT2 receptors are equally distributed over the myocardium. The density of these angiotensin II receptors is developmentally regulated, suggesting a possible role of the cardiac renin-angiotensin system in heart growth and in the adaptation of the heart to postnatal circulatory conditions.

Analysis of Variance↗
PubMed1993

[The role of G-regulatory proteins in the intracellular mechanism of cardiac angiotensin-II receptors].

High-affinity angiotensin II receptors have been identified in cardiac tissue of many animal species. In the heart, angiotensin II exerts positive inotropic and chronotropic effects, constricts coronary vessels, and stimulates cell growth. In vascular smooth muscle and adrenal cortex angiotensin II interacts with guanidine nucleotide regulatory proteins because GTP-gamma-S causes dissociation of the radioligand from its receptor. To investigate whether angiotensin II interacts with guanidine nucleotide regulatory proteins also in cardiac tissue, we studied the effects of GTP-gamma-S on [Sar1, Ile8]-angiotensin II binding to angiotensin II receptor subtypes (AT1 and AT2) in hearts obtained from 16- to 20-week-old Sprague-Dawley rats. We employed an in situ technique performed on frozen tissue sections. Competition experiments performed with the nonpeptide inhibitors losartan and PD123177 allowed identification of both AT1 and AT2 angiotensin II receptors in rat heart. These receptors were present in comparable amounts. In a different set of experiments the effects of GTP-gamma-S (100 microM) on radioligand displacement from AT1 and AT2 receptors were studied. GTP-gamma-S caused a progressive dissociation of the radioligand from the AT1 receptor indicating that this receptor interacts with guanidine nucleotide regulatory proteins. In contrast, the AT2 receptor does not appear to directly interact with guanidine nucleotide regulatory proteins. In summary, the study shows that both angiotensin II receptor subtypes are present in rat heart and that guanidine nucleotide regulatory proteins are implicated in the signal transduction mechanism of the cardiac AT1 receptor.

Angiotensin II↗
PubMed1991

Serum insulin, insulin sensitivity, and erythrocyte sodium metabolism in normotensive and essential hypertensive subjects with and without overweight.

Increased insulin circulating levels and perturbations of intracellular sodium metabolism have been reported in essential hypertensive patients, leading to postulate their involvement in the pathophysiology of the disease. In-vitro studies have shown that insulin modulates the activity of some transmembrane sodium transporters. The aim of this investigation was to assess in subjects with essential hypertension and/or overweight, the levels of fasting serum insulin, the activity of sodium transporters and their possible relationships. In 18 lean normotensive, 12 overweight normotensive, 18 untreated lean essential hypertensive, and 16 untreated overweight essential hypertensive subjects, we measured the fasting levels of blood glucose and serum insulin, and calculated the glucose/insulin ratio as an index of sensitivity to insulin. In addition, in the red blood cells of these subjects, we evaluated the maximal rate of ouabain-sensitive Na/K pump, furosemide-sensitive outward Na/K cotransport, Nai/Lio countertransport, and the constant rate of passive permeability to Na. When compared to lean normotensive, overweight normotensive, lean hypertensive, and overweight hypertensive subjects exhibited significantly higher fasting insulin levels, with lower glucose/insulin ratio. No significant difference was found in the activity of Na/K pump, Na/K cotransport, and passive permeability to Na. The Nai/Lio exchange was significantly increased in both hypertensive groups. Mean blood pressure correlated positively and independently with body mass index and fasting insulinemia, and inversely with the glucose/insulin ratio. No relationships were found between blood pressure, fasting insulin levels or glucose/insulin ratio and the activity of sodium transport systems. We conclude that hyperinsulinemia and insulin resistance are associated with essential hypertension independently of overweight. These data lend support to the hypothesis that insulin is involved, concurrently with other factors, in the pathogenesis of essential hypertension in both lean and obese subjects.

Biological Transport↗