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Biomedical subjects

C Galli

Publications and source records attributed to C Galli.

At least 127 records · Page 7Linked to original sources
PubMed1998

Effects of supplementation with unsaturated fatty acids on plasma and membrane lipid composition and platelet function in patients with cirrhosis and defective aggregation.

BACKGROUND/AIMS: Defective platelet aggregation and reduced platelet production of thromboxane A2, a metabolite of arachidonic acid, are common findings in patients with cirrhosis. We evaluated the effects of dietary supplementation with two combinations of unsaturated fatty acids on platelet function and plasma and membrane fatty acids in patients with liver cirrhosis. METHODS: In a double-blind study, 15 patients with cirrhosis and defective aggregation were randomized to receive a 6-week supplementation with gamma-linolenic and linoleic acid (1 g/day of each fatty acid) or with oleic acid and linoleic acid (groups GLA and OA, respectively). RESULTS: Under baseline conditions, patients showed elevated concentrations of monounsaturated fatty acids and a reduction in polyunsaturated fatty acids. The product/precursor ratios for delta6 and delta5 desaturases, two key enzymes in the pathway leading to arachidonic acid, were significantly reduced in the group of patients. In the GLA group, a significant increase in the levels of dihomo-gamma-linolenic acid (20:3omega6) was observed in plasma and membranes, together with a parallel decrease in the 20:4/20:3omega6 ratio after supplementation. No significant changes were observed in the OA group. The levels of arachidonic acid did not change significantly in either group of patients. Platelet aggregation to collagen was unchanged in the GLA group, but significantly improved in the OA group. CONCLUSIONS: These results show that supplementation with precursors of arachidonic acid is ineffective in elevating plasma or membrane arachidonate levels and does not improve platelet aggregation, suggesting that synthesis of arachidonic acid through the delta5 desaturase cannot be correspondingly activated or that incorporation/retention of the produced fatty acid into lipids is impaired. The increased platelet aggregation in the OA group is likely to be explained by the effect of oleic acid contained in the diet, the effects of which may have been counteracted by the elevation in 20:3omega6, a source of anti-aggregatory prostanoids, in the GLA group.

Aged↗
PubMed1998

Ethanol enhances cholesterol synthesis and secretion in human hepatomal cells.

Excessive consumption of alcohol leads to severe alterations of lipid metabolism, including hyperlipemia and hypercholesterolemia. Following these epidemiological observations, we investigated the effects of ethanol at the cellular level by employing a human hepatomal cell line (HepG2) and by evaluating the biosyntheses of lipid classes from different labeled precursors. Incubation of cells with 2% ethanol resulted in a decreased labeling of phospholipids and in an increase in cholesterol synthesis and secretion. Triglyceride synthesis was increased by ethanol but their secretion in the medium was reduced, suggesting that these alterations may be related to their accumulation in the liver. The alcohol-induced alterations of lipid metabolism are not due to its metabolite acetaldehyde and data suggest that alcohol enhances cholesterol synthesis by affecting the initial steps without increasing HMGCoA expression. The observed modifications of lipid metabolism in HepG2 may partially explain the enhanced incidence of cardiovascular disorders that has been associated with alcoholism.

Acetates↗
PubMed1998

Functional food science and the cardiovascular system.

Cardiovascular disease has a multifactorial aetiology, as is illustrated by the existence of numerous risk indicators, many of which can be influenced by dietary means. It should be recalled, however, that only after a cause-and-effect relationship has been established between the disease and a given risk indicator (called a risk factor in that case), can modifying this factor be expected to affect disease morbidity and mortality. In this paper, effects of diet on cardiovascular risk are reviewed, with special emphasis on modification of the plasma lipoprotein profile and of hypertension. In addition, dietary influences on arterial thrombotic processes, immunological interactions, insulin resistance and hyperhomocysteinaemia are discussed. Dietary lipids are able to affect lipoprotein metabolism in a significant way, thereby modifying the risk of cardiovascular disease. However, more research is required concerning the possible interactions between the various dietary fatty acids, and between fatty acids and dietary cholesterol. In addition, more studies are needed with respect to the possible importance of the postprandial state. Although in the aetiology of hypertension the genetic component is definitely stronger than environmental factors, some benefit in terms of the development and coronary complications of atherosclerosis in hypertensive patients can be expected from fatty acids such as alpha-linolenic acid, eicosapentaenoic acid and docosahexaenoic acid. This particularly holds for those subjects where the hypertensive mechanism involves the formation of thromboxane A2 and/or alpha 1-adrenergic activities. However, large-scale trials are required to test this contention. Certain aspects of blood platelet function, blood coagulability, and fibrinolytic activity are associated with cardiovascular risk, but causality has been insufficiently proven. Nonetheless, well-designed intervention studies should be initiated to further evaluate such promising dietary components as the various n-3 and n-6 fatty acids and their combination, antioxidants, fibre, etc. for their effect on processes participating in arterial thrombus formation. Long-chain polyenes of the n-3 family and antioxidants can modify the activity of immunocompetent cells, but we are at an early stage of examining the role of immune function on the development of atherosclerotic plaques. Actually, there is little, if any, evidence that dietary modulation of immune system responses of cells participating in atherogenesis exerts beneficial effects. Although it seems feasible to modulate insulin sensitivity and subsequent cardiovascular risk factors by decreasing the total amount of dietary fat and increasing the proportion of polyunsaturated fatty acids, additional studies on the efficacy of specific fatty acids, dietary fibre, and low-energy diets, as well as on the mechanisms involved are required to understand the real function of these dietary components. Finally, dietary supplements containing folate and vitamins B6 and/or B12 should be tested for their potential to reduce cardiovascular risk by lowering the plasma level of homocysteine.

Blood Coagulation↗
PubMed1998

The effect of minor constituents of olive oil on cardiovascular disease: new findings.

There has been much interest regarding the components that contribute to the beneficial health effects of the Mediterranean diet. Recent findings suggest that polyphenolic compounds found in olive oil are endowed with several biologic activities that may contribute to the lower incidence of coronary heart disease in the Mediterranean area.

Cardiovascular Diseases↗
PubMed1998

Psychiatric comorbidity in chronic daily headache.

Clinical evidence suggests that chronic daily headache (CDH) occurs in association with psychopathologies: previous studies have focused particularly on migraine. To evaluate this association, we studied, using the DSM-IIIR criteria, a population of 88 patients (18M, 70F) affected by CDH (mean duration 7.4 +/- 8.7 years). We documented the presence of a psychiatric disorder in 90% of this population. The most frequent diagnosis was a comorbidity of anxiety and mood disorders. The comorbidity of psychiatric disorders and headache has important implications as far as treatment is concerned.

Adult↗
PubMed1998

In vitro techniques for the assessment of neurotoxicity.

Risk assessment is a process often divided into the following steps: a) hazard identification, b) dose-response assessment, c) exposure assessment, and d) risk characterization. Regulatory toxicity studies usually are aimed at providing data for the first two steps. Human case reports, environmental research, and in vitro studies may also be used to identify or to further characterize a toxic hazard. In this report the strengths and limitations of in vitro techniques are discussed in light of their usefulness to identify neurotoxic hazards, as well as for the subsequent dose-response assessment. Because of the complexity of the nervous system, multiple functions of individual cells, and our limited knowledge of biochemical processes involved in neurotoxicity, it is not known how well any in vitro system would recapitulate the in vivo system. Thus, it would be difficult to design an in vitro test battery to replace in vivo test systems. In vitro systems are well suited to the study of biological processes in a more isolated context and have been most successfully used to elucidate mechanisms of toxicity, identify target cells of neurotoxicity, and delineate the development and intricate cellular changes induced by neurotoxicants. Both biochemical and morphological end points can be used, but many of the end points used can be altered by pharmacological actions as well as toxicity. Therefore, for many of these end points it is difficult or impossible to set a criterion that allows one to differentiate between a pharmacological and a neurotoxic effect. For the process of risk assessment such a discrimination is central. Therefore, end points used to determine potential neurotoxicity of a compound have to be carefully selected and evaluated with respect to their potential to discriminate between an adverse neurotoxic effect and a pharmacologic effect. It is obvious that for in vitro neurotoxicity studies the primary end points that can be used are those affected through specific mechanisms of neurotoxicity. For example, in vitro systems may be useful for certain structurally defined compounds and mechanisms of toxicity, such as organophosphorus compounds and delayed neuropathy, for which target cells and the biochemical processes involved in the neurotoxicity are well known. For other compounds and the different types of neurotoxicity, a mechanism of toxicity needs to be identified first. Once identified, by either in vivo or in vitro methods, a system can be developed to detect and to evaluate predictive ability for the type of in vivo neurotoxicity produced. Therefore, in vitro tests have their greatest potential in providing information on basic mechanistic processes in order to refine specific experimental questions to be addressed in the whole animal.

Animals↗
PubMed1998

Plasma arachidonic acid and serum thromboxane B2 concentrations in phenylketonuric children are correlated with dietary compliance.

Phenylketonurics display lower arachidonic acid levels in plasma lipids, reflecting the lower intake due to the dietary treatment poor in phenylalanine-rich animal foods. Plasma arachidonic acid levels and serum thromboxane B2 concentrations have been measured in 13 treated phenylketonuric children and compared with those of 12 healthy controls. A direct relationship between plasma arachidonic acid and thromboxane B2 concentrations has been observed only in phenylketonurics, whose plasma arachidonic acid status correlated negatively with their dietary compliance. These results suggest that the low consumption of animal fats may contribute to modulate the production of arachidonic acid-derived platelet eicosanoids.

Adolescent↗
PubMed1998

Evaluation of the Abbott LCx Mycobacterium tuberculosis assay in comparison with culture methods in selected Italian patients.

A ligase chain reaction (LCR) DNA amplification method for the molecular diagnosis of Mycobacterium tuberculosis (Abbott LCx MTB) was evaluated in comparison with solid and liquid phase culture on 622 selected samples collected in two large Italian hospitals, of which 310 obtained from HIV-1 positive patients and 312 from HIV-negative individuals. The overall prevalence of mycobacteria by culture was 22% (137/622), and the apparent sensitivity and specificity of LCx vs. culture were 87.6% and 98.2%. Of the 26 culture positive/LCx negative samples, 22 were positive for MOTT and 4 for M. tuberculosis. All 9 samples positive by LCx and negative by culture were classified as true positive by clinical criteria. The final values of sensitivity, specificity, positive predictive value and negative predictive value for LCx rose to 96.8%, 100%, 100% and 99.2%, respectively. The adjusted sensitivity of culture methods was 89.5% for solid phase and 92.7% for Bactec. In view of the high sensitivity on both smear-positive (100%) and smear-negative (92.4%) samples and of the high negative predictive value, the LCR-based amplification method appears suitable as a routine screening method for the rapid diagnosis of M. tuberculosis in high-risk patients.

DNA, Bacterial↗
PubMed1997

Vacuoles induced by Helicobacter pylori toxin contain both late endosomal and lysosomal markers.

Intoxication of mammalian cells with the vacuolating toxin (VacA) released by Helicobacter pylori causes the formation of large acidic vacuoles containing the vacuolar ATPase proton pump and Rab7, a late endosome marker. Here, we describe a novel subcellular fractionation procedure, and we show that nanomolar concentrations of VacA induce a clear redistribution of lysosomal membrane glycoproteins among endocytic compartments. This redistribution is an early event in the process of cellular intoxication by VacA and precedes the formation of macroscopic vacuoles. The absence of the cation independent mannose 6-P receptor and the presence of Rab7 and of lysosomal membrane proteins in the newly formed compartment suggest that the vacuolating toxin induces the accumulation of a post-endosomal hybrid compartment presenting both late endosomal and lysosomal features.

Animals↗
PubMed1997

Inhibition of leukocyte leukotriene B4 production by an olive oil-derived phenol identified by mass-spectrometry.

We have evaluated the effects of hydroxytyrosol (HT), a potent antioxidant present in olive oil, on the formation of arachidonic acid 5-lipoxygenase metabolites by leukocytes in vitro. HT, a simple phenolic compound, extracted from first-pressure oil, was isolated by HPLC and characterized by gas chromatography/mass spectrometry. HT inhibited in a dose-related manner the production of leukotriene B4 (LTB4) by calcium ionophore-stimulated leukocytes. As expected, similar inhibition was observed for omega-oxidized metabolites of LTB4, namely 20-hydroxy and 20-carboxy-LTB4. The results disclose a new biological activity of olive oil-derived phenols on leukocyte eicosanoid production.

Antioxidants↗
PubMed1997

Factors controlling haemopoiesis in ovine long-term bone marrow cultures.

We describe an adaptation of the Dexter technique for obtaining ovine long-term bone marrow cultures able to sustain haemopoiesis in vitro for long periods. Two inocula of bone marrow cells collected at three-five weeks interval, in IMDM supplemented with fetal calf serum (10%), horse serum (10%) and hydrocortisone (5 x 10(-7) M), gave rise to the growth of an adherent cell layer which supported, in most cases, active haemopoiesis for up to 15 weeks. The cell layer was composed of macrophages, fibroblasts and adipocytes. Haemopoietic cells formed large foci of "cobblestone" areas. Haemopoietic progenitors were also released into the supernatant medium and were detectable by clonogenic assay. Granulocytes and monocyte-macrophages differentiated in the cultures in constant proportion until week five, when the monocytic lineage superseded the myelocytic one. These cultures, between weeks five and twelve, produced colony forming cells in a constant pattern, indicating the presence and self renewing of early haemopoietic progenitor cells.

Animals↗
PubMed1997

Manipulation of the fate of long chain polyunsaturated fatty acids in cultured cells.

We have studied the biosynthesis of long chain polyunsaturated fatty acids (LC-PUFA) from their precursors in cultured cells undergoing physiological modifications, or under the influence of lipid-lowering drugs or ethanol. The formation of arachidonic acid (AA, 20:4 n-6) from the percursor linoleic acid (LA, 18:2 n-6) in the neuroblastoma cells SK-N-BE is enhanced at early stages of differentiation, and declines when differentiation is complete, in concomitance with maximal accumulation of AA in cell lipids. In the monocytic cells THP-1, the biosynthesis of LC-PUFA is also enhanced by treatment with the HMGCoA reductase inhibitor simvastatin (S), an effect which is reverted by mevalonate and other intermediates of cholesterol synthesis. Maximal activation of LC-PUFA synthesis by S occurs at concentrations lower than those required for maximal inhibition of cholesterol synthesis. In the hepatoma cells HepG2, ethanol decreases the biosynthesis of LC-PUFA while potentiating the incorporation of acetate into cholesterol. LC-PUFA synthesis appears thus to be modulated in the course of cell differentiation and complex interactions between LC-PUFA and cholesterol synthesis occur, as judged from data obtained through pharmacological manipulations.

Arachidonic Acid↗
PubMed1997

Plasma arachidonic acid and serum thromboxane B2 concentrations in phenylketonuric children negatively correlate with dietary compliance.

The study addresses the relationship of plasma arachidonic acid and thromboxane production with the dietary compliance in treated phenylketonuric patients, whose vegan-like dietary pattern makes them a useful model to evaluate the effects of the near-total avoidance of animal fats. Thirteen treated phenylketonuric children were compared with twelve healthy controls for arachidonic acid intake, plasma fatty acids and platelet thromboxane B2 production, assessed as accumulation of this eicosanoid in serum. The calculated intake of arachidonic acid was lower in phenylketonurics than in controls and this was associated with lower levels in plasma lipids. Plasma arachidonic acid concentrations and serum thromboxane B2 levels correlated with the last 12 months phenylalanine levels, taken as negative indicator of dietary compliance. A direct relationship between plasma arachidonic acid concentration and thromboxane B2 production was observed only in phenylketonuric patients (r = 0.74, P = 0.01). While well-compliant PKU subjects have low arachidonic acid and thromboxane concentrations in plasma, the low compliance with animal food avoidance, evoking higher phenylalanine levels, results in elevation of both plasma arachidonic acid and serum thromboxane B2. This gives support to the hypothesis that the consumption of animal fats may affect the production of arachidonic acid-derived platelet eicosanoids.

Adolescent↗
PubMed1997

Changes in right ventricular filling dynamics during left anterior descending, left circumflex and right coronary artery balloon occlusion.

AIM: Transient coronary artery occlusion during percutaneous transluminal coronary angioplasty may cause left ventricular diastolic dysfunction. The aim of this study was to evaluate the effect of left anterior descending, left circumflex and right coronary artery balloon occlusion on right ventricular diastolic function. METHODS: Thirty-five patients with single-vessel coronary artery disease and no previous myocardial infarction were selected. Left and right ventricular filling pressures were monitored by Doppler echocardiography and haemodynamic monitoring. This was performed during and immediately after 60 s of coronary balloon occlusion of the left anterior descending artery in 21 cases (Group 1), the left circumflex artery in eight cases (Group 2) and the right coronary artery in six cases (Group 3). Doppler analysis of left and right ventricular filling included peak velocity of early (PFVE) and late ventricular filling (PFVA) and PFVE to PFVA ratio (PFVE/PFVA). RESULTS: In all three groups, balloon inflation induced a significant increase in left and right filling pressures (P < 0.05). No qualitative difference in haemodynamic changes was found between groups during inflation. Significant impairment in the Doppler pattern of left and right ventricular filling occurred after 20 s of coronary occlusion: PFVE values in mitral and tricuspid valves decreased by 14% and 25% in Group 1, 13% and 25% in Group 2, and 10% and 21% in Group 3, respectively, as PFVA remained unchanged in all groups, the PFVE/PFVA ratio of mitral and tricuspid valve flows significantly decreased (Group 1: -12% and -20%, Group 2: -10% and -21%, Group 3: -14% and -21%, respectively). All parameters returned to baseline within 30 s after each balloon deflation. CONCLUSION: Our data suggest that brief episodes of acute myocardial ischaemia, such as those induced by 60 s of coronary artery occlusion during percutaneous transluminal coronary angioplasty, elicit simultaneous diastolic dysfunction of both ventricles, independent of the coronary artery involved.

Angioplasty, Balloon, Coronary↗
PubMed1997

Premenstrual dysphoric disorder and eating disorders.

UNLABELLED: Premenstrual Dysphoric Disorder (PMDD) can be differentiated from Premenstrual Syndrome (PMS) by the use of the research criteria provided by the Diagnostic and Statistical Manual (DSM) IV. Indeed, PMS corresponds to mild clinical symptoms, such as breast tenderness, bloating, headache and concomitant minor mood changes, while premenstrual magnification occurs when physical and psychological symptoms of a concurrent axis I disorder get worse during the late luteal phase. Changes in appetite and eating behavior have been documented in women suffering from PMS, with an increased food intake occurring during the luteal phase. Moreover, in women with PMS, a major effect of the phase of the menstrual cycle on appetite has been documented and a high correlation with self-ratings of mood, particularly depression, has been described only in such disturbance. The aim of the present study was to analyse the clinical similarities between PMDD and Eating Disorders (in particular Bulimia Nervosa and Binge Eating Disorder). Thus, we compared the DSM III-R comorbidity, the personality dimensions and the eating attitudes in these patients, attempting to identify any relationship between groups. Twelve PMDD women (mean age 28 years), diagnosed using DSM IV criteria and premenstrual assessor form, were compared with 10 eating disorder (ED) women (6 Bulimia Nervosa, 4 Binge Eating Disorder) (mean age 25 years) and with 10 control women matched for age. The following instruments were used: (i) clinical interview with DSM III-R criteria (SCID); (ii) a psychometric study with TPQ for the evaluation of three personality dimensions (novelty seeking, harm avoidance and reward dependence); (iii) EAT/26 for the evaluation of eating attitudes. Results show that a high comorbidity for mood and anxiety disorders in PMDD and ED is well documented. Our PMDD patients share a 16.6% of comorbidity with ED, whereas such an association is present only in 2.3% of the general population. In addition, as a common clue, the personality dimension, harm avoidance, linked to a serotonin mediation is significantly more frequent in PMDD and ED than in normal controls. IN CONCLUSION: from the present study it seems clear that a certain degree of similarity exists between the PMDD and ED. However, whether or not these two disorders really share common ground from a physiopathological point of view still has to be clarified by more extensive studies.

Adolescent↗
PubMed1997

Linoleic acid enhances the secretion of plasminogen activator inhibitor type 1 by HepG2 cells.

This study was undertaken in order to assess whether triglycerides and/or their fatty acids directly influence the secretion of plasminogen activator inhibitor type 1 (PAI-1) in HepG2 cells. To this end, subconfluent HepG2 cells were incubated with triglyceride-rich particles (TGRP) isolated from Intralipid for 16 h, and PAI-1 levels were determined in conditioned medium using a specific ELISA. TGRP (1 to 6 mg triglycerides/ml) concentration-dependently increased PAI-1 secretion by cells, concomitantly with significant increases in intracellular triglyceride (TG) levels. Fatty acid analysis indicated that the incubation of cells with 3 mg of TG per ml of TGRP induced significant accumulation of 18:2 n-6 (linoleic acid, LA) and 18:3 n-3 (linolenic acid) reflecting the fatty acid composition at the added triglycerides. We then tested the comparative effects on PAI-1 secretion by HepG2 cells of LA and 18:1 n-9 (oleic acid, OA). LA, as a bovine serum albumin (BSA) complex, concentration-dependently (1 to 35 mumol/L) increased the secretion of PAI-1 by cells, whereas OA-BSA only minimally affected it at the highest concentration used (35 mumol/L). Incorporation of LA into cell pools, in the presence of increasing concentration of the FA in the medium, was studied by the use of a preparation containing [14C]LA. LA accumulated in all lipid classes including diacylglycerol, the incorporated LA being converted into arachidonic acid (AA) as assessed by HPLC radiochromatography of the fatty acid methyl esters. It is concluded that PAI-1 secretion in HepG2 cells is modulated by triacylglycerols and by linoleic acid and/or its metabolic products.

Animals↗
PubMed1997

Effects of simvastatin on the metabolism of polyunsaturated fatty acids and on glycerolipid, cholesterol, and de novo lipid synthesis in THP-1 cells.

In the monocytic THP-1 cells, the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor simvastatin (5 microM) enhances the conversion of exogenous linoleic (18:2 n-6) and eicosapentaenoic (20:5 n-3) acids to their long-chain polyunsaturated fatty acid (LC-PUFA) derivatives, and this effect is associated with changes in the desaturation steps. In addition, formation of monounsaturated fatty acids from endogenously synthesized precursors is increased. These metabolic changes lead to elevated LC-PUFA and fatty acid (FA) unsaturation in cells. The effects of simvastatin on FA metabolism are associated with increased synthesis of triglycerides from glycerol. The dose-effect relationships for the activity of simvastatin on total linoleic acid (LA) conversion and cholesterol synthesis reveal that enhancement of PUFA metabolism is already maximal at 0.5 microM simvastatin, whereas cholesterol synthesis is further inhibited by concentrations of simvastatin up to 5 microM. The effects of 5 microM simvastatin on PUFA metabolism are partially prevented by mevalonate (1 mM) and geranylgeraniol (5 microM) but not by farnesol (10 microM). These data indicate that HMG-CoA inhibitors have profound effects on PUFA metabolism, and that the pathways for cholesterol and PUFA synthesis are mutually modulated.

Acetates↗