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M Calvani

Publications and source records attributed to M Calvani.

At least 73 records · Page 4Linked to original sources
PubMed1996

High performance liquid chromatography of long-chain acylcarnitine and phospholipids in fatty acid turnover studies.

In this paper we describe a rapid, isocratic high performance liquid chromatography (HPLC) method for the study of radioactive fatty acid incorporation into complex lipids of human erythrocytes, which allows the simultaneous separation of the major phospholipid classes and long-chain acylcarnitines. The lipid extract of erythrocytes pulsed with radioactive fatty acids was injected into an HPLC system equipped with a silica column. The individual components eluted were monitored by ultraviolet absorption and radioactive emission. With respect to the UV profile, the radioactive profile showed an additional peak between phosphatidyl-choline and phosphatidylethanolamine, which was identified as long-chain acylcarnitine by different experimental approaches. The radioactivity recovered in the long-chain acylcarnitines contains essential information enabling definition of acyl trafficking in red cells.

Carnitine↗
PubMed1996

[Hepatic abscesses caused by Streptococcus intermedius].

Pyogenic abscess of the liver is uncommon child's pathology. The authors briefly describe a clinical picture characterized by beginning of an hepatic abscess dues to a germ that is not usually pathogen for men. It is often a mouth saprophyte.

Child↗
PubMed1995

Effect of propionyl-L-carnitine treatment on membrane phospholipid fatty acid turnover in diabetic rat erythrocytes.

In this work we have examined the effect of the oral administration of propionyl-L-carnitine (PLC) on the membrane phospholipid fatty acid turnover of erythrocytes from streptozotocin-induced diabetic rats. A statistically significant reduction in radioactive palmitate, oleate, and linoleate, but not arachidonate, incorporation into membrane phosphatidylcholine (PC) of diabetic rat erythrocytes with respect to control animals was found. Changes in radioactive fatty acid incorporation were also found in diabetic red cell phosphatidylethanolamine (PE), though they were not statistically significant. Oral propionyl-L-carnitine (PLC) treatment of diabetic rats partially restored the ability of intact red cells to reacylate membrane PC with palmitate and oleate, and reacylation with linoleate was fully restored. The analysis of the membrane phospholipid fatty acid composition revealed a consistent increase of linoleate levels in diabetic rat red cells, a modest decrease of palmitate, oleate and arachidonate. The phospholipid fatty acid composition of diabetic red blood cells was not affected by the PLC treatment. Lysophosphatidylcholine acyl-CoA transferase (LAT) specific activity measured with either palmitoyl-CoA or oleyl-CoA was significantly reduced in diabetic erythrocyte membranes in comparison to controls. In addition, LAT kinetic parameters of diabetic erythrocytes were altered. The reduced LAT activity could be partially corrected by PLC treatment of diabetic rats. Our data suggest that the impaired erythrocyte membrane physiological expression induced by the diabetic disease may be attenuated by the beneficial activity of PLC on the red cell membrane phospholipid fatty acid turnover.

Administration, Oral↗
PubMed1995

Cardiac and renal endothelin-1 binding sites in streptozotocin-induced diabetic rats.

UNLABELLED: The aim of this work was to study cardiac and renal endothelin binding sites during the progression of diabetes. Male Crl:CD (BR) rats were made diabetic by injection of streptozotocin (STZ, 45 mg kg-1 i.v.). Only rats with a glycaemia of 500 mg per 100 ml or higher, were used. The hearts were taken at 2, 4 or 6 weeks and kidneys at 2 and 6 weeks, after diabetes induction, for binding studies. In the heart, the number of Et-1 binding sites was significantly increased 2 weeks after STZ-induction of diabetes (449 +/- 13 vs. 345 +/- 18 fmol (mg protein) -1, in controls; p < 0.05) without modification of KD value (104 +/- 5 vs 101 +/- 7 pM). Comparable results were obtained 4 and 6 weeks after STZ-induction. In the kidney both the parameters were unchanged at all the times tested. IN CONCLUSION: a specific increase in cardiac Et-1 binding sites, without change in affinity of the peptide, was found 2, 4 and 6 weeks after diabetes induction; while renal Et-1 binding sites were not modified.

Animals↗
PubMed1995

Protective actions of L-carnitine and acetyl-L-carnitine on the neurotoxicity evoked by mitochondrial uncoupling or inhibitors.

The mechanism for the pathological increase in cell death in various disease states e.g. HIV immunodefficiency or even ageing or Alzheimer's disease, occurs by complex and as yet undefined mechanism(s) related to immunological, virological or biochemical disturbances (i.e. energy depletion, oxidative stress, increased protein degradation). We have studied mitochondrial uncoupling or inhibitor toxicity on neurones at the cellular level and at the mitochondrial level using rhodamine (Rh123) and 10-nonylacridine orange (NAO) fluorescence with confocal microscopy. Blockade of the mitochondrial chain complexes at various points was studied. The possible protective effects of the compound L-carnitine, which plays a central role in mitochondrial function, was tested in this form of neurotoxicity. It appears that L-carnitine and its acetylated form, acetyl-L-carnitine, can attenuate the cell damage, as assessed by lactate dehydrogenase (LDH) release, evoked by the uncoupler, p-(trifluoromethoxy)phenylhdyrazone (FCCP), or by the inhibitors, 3-nitropropionic acid (3-NPA) or rotenone. Further, the FCCP-induced inhibition of Rh123 uptake was antagonized by the preincubation of cells with L-carnitine. Since such neurotoxic mechanisms may be operating in the various pathological forms of myotoxicity and neurotoxicity, these observations suggest potential for a therapeutic approach.

Acetylcarnitine↗
PubMed1994

The aging process of skin and the increase in size of subcutaneous adipocytes.

The aging of skin has been associated with an increase in size of the adipocytes located within the subcutaneous tissue. This topic is the subject of our study conducted on rats clinically treated with L-acetyl-carnitine (LAC) at 4, 8, 16, and 21 months of age and on a control group. Normal rats showed a significant increase in adipocyte diameter between four and eight months, and between sixteen and twenty-one months of age. Rats treated with L-acetyl-carnitine did not show significant changes up to the age of sixteen months, but did so between sixteen and twenty-one months of age. Four-month-old rats, both those under treatment and controls, did not show a significant change in adipocyte diameter. On the other hand, rats receiving L-acetyl-carnitine showed significantly smaller adipocyte diameters than those of the control group. Our results demonstrate that the long-term administration of L-acetyl-carnitine blocks the progressive increase in size of the subcutaneous adipocytes present in the rat's aging skin. We hypothesize that L-acetyl-carnitine reequilibrates the catabolic deficit of fats in the skin of the elderly.

Acetylcarnitine↗
PubMed1994

[The role of endomysium antibodies in the diagnosis and monitoring of celiac disease].

Coeliac disease is a common cause of chronic diarrhea in children and adults. It is also frequently detected in children exclusively affected by iron deficiency anemia, hypocalcemia, short stature, dental enamel defects, epilepsy and intracranial calcifications, etc. The coeliac disease diagnosis may be facilitated by the use of some immunological tests like anti endomysial (AEA) or anti gliadin (AGA) antibodies detection. From December 1990 to September 1992 anti endomysial IgA and anti gliadin IgG antibodies were respectively detected in 1680 and 1598 sera from children and adults affected by chronic diarrhea, failure to thrive or other symptoms compatible with coeliac disease diagnosis. According to ESPGAN criteria at that time coeliac disease diagnosis was made in 73 cases. In our experience AEA IgA show to have a better sensitivity and specificity in the diagnosis of coeliac disease rather than AGA IgG (97.5% vs 95.1% and 99.5% vs 98.3% respectively).

Adolescent↗
PubMed1994

[Atherosclerosis and juvenile dyslipidemias].

Large-scale and systemic epidemiological, pathological and experimental studies emphasized and documented the childhood origin of atherosclerosis. There is increasing consensus that lipid levels in children to a large extent determine the rate of coronary artery disease (CAD) in the adult population. Minimal sudanophilic intimal deposits, and the presence of intracellular and extracellular lipid, and a slight increase in interstitial ground substance in 3 years of age or older patients are found. In the Bogalusa Hearth Study aortic fatty streaks were strongly related the antemortem levels of both total cholesterol and low-density lipoprotein cholesterol (LDL-C) independent of race, sex, and age, and were negatively correlated with the ratio of high-density lipoprotein (HDL-C) to low-density plus very-low-density lipoprotein cholesterol (LDL-C+VLDL-C). The potential for primary prevention is real and the strongest piece of evidence for its is the remarkable trend in CHD mortality rates in recent times, rapidly downward in many western countries. A number of factors influence plasma levels of lipid and lipoproteins in newborn, in infants, in children and adolescents and their relevance as possible predictors of adult coronary artery disease. They are certain inherited disorders of dyslipoproteinemia (familial hypercholesterolemia, familial combined hyperlipidemia, hyperapobetalipoproteinemia, and hypoalphalipoproteinemia) and secondary causes of hyperlipidemia (congenital biliary atresia, glycogen storage diseases, hypothyroidism, diabetes mellitus and nephrotic syndrome, etc).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Acetyl-L-carnitine and Alzheimer's disease: pharmacological considerations beyond the cholinergic sphere.

Since ALCAR and L-carnitine are "shuttles" of long chain fatty acids between the cytosol and the mitochondria to undergo beta-oxidation, they play an essential role in energy production and in clearing toxic accumulations of fatty acids in the mitochondria. ALCAR has been considered of potential use in senile dementia of the Alzheimer type (SDAT) because of its ability to serve as a precursor for acetylcholine. However, pharmacological studies with ALCAR in animals have demonstrated its facility to maximize energy production and promote cellular membrane stability, particularly its ability to restore membranal changes that are age-related. Since recent investigations have implicated abnormal energy processing leading to cell death, and severity-dependent membrane disruption in the pathology of Alzheimer's disease, we speculate that the beneficial effects associated with ALCAR administration in Alzheimer patients are due not only to its cholinergic properties, but also to its ability to support physiological cellular functioning at the mitochondrial level. This hypothetical mechanism of action is discussed with respect to compelling supportive animal studies and recent observations of significant decrease of carnitine acetyltransferase (the catalyst of L-carnitine acylation to acetyl-L-carnitine) in autopsied Alzheimer brains.

Acetylcarnitine↗
PubMed1992

Idiopathic facial paralysis: new therapeutic prospects with acetyl-L-carnitine.

The study population was composed of 43 patients affected by idiopathic facial paralysis (20 males and 23 females), aged between 11 and 67. The study was carried out in a double-blind, randomized, placebo controlled manner. Acetyl-L-carnitine was given in an oral dose of 3 x 1 g daily for 1 month, along with a daily oral administration of 50 mg of methylprednisolone for 14 days. The evaluation was made by means of electromyograms (EMG) of the orbicularis oculi and oris muscles, by the Schirmes lacrimation test, by stapedial reflex test and a score scale for clinical assessment of paralysis. Results so far obtained have shown an earlier functional recovery of the nerve in those patients treated with acetyl-L-carnitine. Comparison between the affected and unaffected sides of the face revealed a statistical significance in the treated group (p < 0.05) as well as the amplitudes of the muscle action potentials (MAP) between the affected sides (p < 0.01).

Acetylcarnitine↗
PubMed1992

Metabolic aspects of acute cerebral hypoxia during extracorporeal circulation and their modification induced by acetyl-carnitine treatment.

Following their previous research experiences in human tissue hypoxia, in the present study the authors. investigated the metabolic effects of acute brain hypoxia in a group of patients in course of extracorporeal circulation for aorto-pulmonary bypass. One hundred subjects were treated, half with a placebo and half with acetyl-carnitine to evaluate the effects of oxidative stress in some brain plasmatic metabolites and to verify the effect of acetyl-carnitine on the tissue energy capacity. The levels of lactate, pyruvate, succinate and fumarate showed a significant imbalance due to hypoxia, while the acetyl-carnitine treatment confined the metabolic gradients within physiological limits. This means that during the course of extracorporeal circulation brain hypoxia plays a pathological role assuming the typical picture of cellular oxidative damage and the acetyl-carnitine antagonizes these deleterious effects of hypoxia by a protective mechanism on the energy processes and then on the cellular enzymic activities. In this regard, the d-tyrosine levels, considered as a proteolytic index, confirm the action of acetyl-carnitine on the cell morpho-functional integrity.

Acetylcarnitine↗
PubMed1992

Influence of acetyl-carnitine on some mitochondrial enzymic activities in the human cerebral tissue in conditions of acute hypoxia.

Following previous research on human tissue in conditions of acute and massive hypoxia, in the present work the authors compared the cellular enzymic response to oxidative stress in normoxic (perifocal) and hypoxic (focal) areas in human brain affected by regional acute vasculopathies. Two homogeneous groups of patients were selected following strict clinical inclusion/exclusion criteria. The groups of patients were treated with a placebo or acetyl-carnitine at same doses and following randomized, double-blind procedures. The focal areas showed a significant functional damage in lactate, pyruvate and succinate dehydrogenases and in the cytochrome oxidase activity when compared with the enzymic capacities of perifocal areas (normoxic as controls). The pretreatment with acetyl-carnitine antagonized the above-mentioned enzymic damage by a protective action linked to the endocellular energy restoration. In accordance with these data, the therapeutic role played by acetyl-carnitine in the cerebral focal hypoxia appeared to be a determinant for the cell survival mainly in the reversible phase of oxidative damage.

Acetylcarnitine↗
PubMed1991

Clinical issues of cognitive enhancers in Alzheimer disease.

Cognitive enhancers is a provocative and vague label for drugs used to treat dementia of the Alzheimer type. Several issues have to be carefully considered in order to perform reliable clinical trials with such compounds. The lack of an animal model appropriately matching the human pathology, the difficulty in finding worldwide criteria for clinical diagnosis and determining which patients are eligible and how they are best tested, methods of treatment, and interpreting results are undoubtedly the major problems to be solved. A review of the literature points out that the "day-after" approach of treatment (once severe neuropathological damage has been established) is no longer feasible, or has limited advantages. A different pharmacological approach, based on preventive measures during the first stages of the neurodegeneration, seems mandatory.

Alzheimer Disease↗
PubMed1991

Acetyl-L-carnitine: a drug able to slow the progress of Alzheimer's disease?

Defects in cholinergic neurotransmission do not, by themselves, constitute the sole pathophysiologic concomitants of Alzheimer's disease (AD). Recent findings point out that abnormalities in membrane phospholipid turnover and in brain energy metabolism may also characterize AD. Acetyl-L-carnitine (ALC) is an endogenous substance that, acting as an energy carrier at the mitochondrial level, controls the availability of acetyl-L-CoA. ALC has a variety of pharmacologic properties that exhibit restorative or even protective actions against aging processes and neurodegeneration. A review of a series of controlled clinical studies suggests that ALC may also slow the natural course of AD.

Acetylcarnitine↗
PubMed1991

Acetyl-l-carnitine as possible drug in the treatment of hypothalamic amenorrhea.

Several neuroendocrine disregulations have been demonstrated in patients with hypothalamic amenorrhea, but a definite therapeutic strategy has not yet been found. Since acetyl-l-carnitine (ALC) has been reported to have a specific effect on central cholinergic, serotoninergic, dopaminergic and opioidergic systems, 20 patients with hypothalamic amenorrhea were treated with ALC (2 g/day, per os). Both the clinical efficacy and the endocrine parameters were evaluated after 6 months. The patients were subdivided in two groups according to their LH plasma levels: A) hypogonadotropic: 10 subjects with plasma LH less than 3 mIU/ml, and B) normogonadotropic: 10 subjects with plasma LH greater than 3 mIU/ml. All subjects underwent: 1) a pulsatility study (4 h sampling every 10 min), 2) GnRH test (two bolus injections of 10 micrograms at time 0 and +120), 3) TRH test (200 micrograms). These parameters were evaluated before and after 6 months of ALC administration. The occurrence of a spontaneous menstruation was observed in 6 out of 10 hypogonadotropinemic and in 4 out of 10 normogonadotropinemic patients. Menstrual bleeding occurred between the 3rd and the 6th month of therapy. Major hormonal changes after ALC administration were observed in the hypogonadotropic subjects. They showed a significant increase in baseline plasma LH levels (from 0.9 +/- 0.1 to 3.5 +/- 0.7 mIU/ml, p less than 0.05) (mean +/- SEM), a significant increase in LH pulse amplitude (p less than 0.01) with no changes in LH pulse frequency, and a significantly increased response of LH to the latter GnRH bolus during the GnRH test. Hypogonadotropic patients also showed a significant increase in both estradiol (from 18.8 +/- 2.5 to 48 +/- 3.3 pg/ml, p less than 0.05) and PRL (from 6 +/- 1 to 11.4 +/- 1.7 ng/ml, p less than 0.05). No significant differences were observed in the hormonal parameters of normogonadotropic patients after 6 months of ALC therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcarnitine↗
PubMed1991

[Asymptomatic congenital cytomegalovirus infection].

Congenital cytomegalovirus infection occurs in about 1% of live births. Although 10% of these develop severe central nervous system impairment, the remainder have asymptomatic infection. However among the asymptomatic, 10% have some problems, mainly neurosensory hearing loss. The case of an infant affected by cytomegalovirus infection who developed neurological signs and impairment in auditory brain stem response is described.

Brain↗