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Biomedical subjects

A Bruni

Publications and source records attributed to A Bruni.

At least 19 recordsLinked to original sources
PubMed1992

Phospholipid metabolism in rat intestinal mucosa after oral administration of lysophospholipids.

The present results indicate that PS, a phospholipid contained in small amounts in the human diet and not included in plasma lipoproteins, may be used to influence phospholipid metabolism in intestinal mucosal cells. Since PS influx into absorptive cells occurs after its hydrolysis to lysoPS, this metabolite may be used to increase the absorption of this phospholipid. These data show that lysoPS, after diffusion into intestinal cells, is sequentially converted into PS and PE (which make up a minor fraction of the lipids present in lipoproteins). As expected, lysoPS given together with radiolabeled unsaturated fatty acids was unable to promote their transfer into plasma lipoproteins. In this respect lysoPS differed from lysoPC, the latter increasing the appearance of dietary fatty acids in plasma. When given together, lysoPS decreased the lysoPC-induced transfer of unsaturated fatty acids into plasma. This effect required addition of triglycerides to the lipid mixture. In attempting to explain this triacylglycerol-dependent inhibition by lysoPS, we found that this phospholipid increased the incorporation of glycerol into mucosal cell PC. In contrast, lysoPC was inhibitory. Furthermore, in the presence of labeled inositol, lysoPC (but not lysoPS) promoted the appearance of labeled phosphatidylinositol. The data thus suggest that the two lysophospholipids differ in promoting the two main pathways of PC synthesis in the intestinal cells. While lysoPC favors PC synthesis by reacylation, lysoPS enhances the CDP-choline pathway of PC synthesis.

Administration, Oral↗
PubMed1992

Genetic evidence for a novel familial Alzheimer's disease locus on chromosome 14.

Familial Alzheimer's disease (FAD) has been shown to be genetically heterogeneous, with a very small proportion of early onset pedigrees being associated with mutations in the amyloid precursor protein (APP) gene on chromosome 21, and some late onset pedigrees showing associations with markers on chromosome 19. We now provide evidence for a major early onset FAD locus on the long arm of chromosome 14 near the markers D14S43 and D14S53 (multipoint lod score z = 23.4) and suggest that the inheritance of FAD may be more complex than had initially been suspected.

Aged↗
PubMed1992

Transesophageal echocardiographic findings in partial and complete papillary muscle rupture complicating acute myocardial infarction.

Papillary muscle rupture occurred in two patients with recent inferior myocardial infarction. In one case with partial rupture transesophageal echocardiography in the standard four-chamber view did not visualize the rupture and in the second case with complete rupture it provided incomplete diagnostic information. A not previously described transgastric longitudinal scanning of the left ventricle provided complete delineation of the lesion and it was of great value in the diagnosis and management of this potentially lethal complication. Both patients were operated upon and had a favourable outcome.

Echocardiography↗
PubMed1992

Decreased serum level of tumor necrosis factor in animals treated with lipopolysaccharide and liposomes containing phosphatidylserine.

The rise in serum level of tumor necrosis factor (TNF), produced by lipopolysaccharide, has been measured in mice and rabbits treated with phospholipid liposomes. After 3 daily ip injection (mice) or 5 daily i.v. injections (rabbits) of 30 mg/kg of a phospholipid mixture enriched in phosphatidylserine, the action of lipopolysaccharide was 80-90% reduced. The phospholipid effect is dose dependent, requires a minimum of two daily injections before the administration of lipopolysaccharide, and is still manifest 2 days after the last phospholipid dose. Among individual purified phospholipids, phosphatidylserine and phosphatidylethanolamine were effective whereas phosphatidylinositol, phosphatidylglycerol, and phosphatidylcholine did not show significant activity. The data indicate that the parenteral administration of liposomes containing the aminophospholipids phosphatidylserine, and phosphatidylethanolamine is an efficient mode to reduce the endotoxin-induced production of TNF. As suggested by liposome pharmacokinetics, this effect may be related to phospholipid accumulation in the mononuclear phagocyte system of liver and spleen.

Animals↗
PubMed1991

Pharmacokinetic characterization of phosphatidylserine liposomes in the rat.

1. The plasma decay, tissue uptake and biotransformation of radiolabelled phosphatidylserine (PS) liposomes have been investigated in rats following bolus i.v. injection (2 mg kg-1). 2. PS plasma concentration showed a biexponential decay with half-lives of 0.85 and 40 min. The following interpretation of the biphasic decay is proposed: (1) The rapid initial decline is due to the irreversible uptake of PS liposomes by the mononuclear phagocyte system, as demonstrated by the almost exclusive accumulation of PS in liver and spleen. (2) The slow decay phase reflects the elimination of that fraction of PS that has been incorporated into high density plasma lipoproteins (HDL). A kinetic model has been developed to describe these phenomena and a good agreement has been observed between experimental data and theoretical values. 3. Evidence has been obtained that a large fraction of PS is hydrolyzed at the injection site, probably by phospholipase A2 and other hydrolytic enzymes released by platelets. Hydrolysis at the injection site has also been observed following intraperitoneal and intramuscular injections. 4. As shown by the comparative analysis of the biotransformation products found in tissues after administration of either [3H]-glycerol-PS or [14C]-serine-PS, parenterally administered PS follows two distinct metabolic pathways: (1) decarboxylation to phosphatidylethanolamine and (2) extensive hydrolytic degradation with release of the individual components of the molecule. These pathways probably reflect the two main mechanisms of PS uptake, incorporation into the plasma membrane and internalization by endocytosis, respectively.

Animals↗
PubMed1990

Signalling mechanism in the lysophosphatidylserine-induced activation of mouse mast cells.

Lysophosphatidylserine (0.1-1 microM) elicits histamine release in isolated mouse peritoneal mast cells. The effect becomes manifest after a lag of 30 s and reaches completion in 5 min. Maximal activity is observed when serine is in L-configuration. As shown by the activity of a lysophosphatidylserine analogue lacking the OH group in C2 position of glycerol, conversion into phosphatidylserine is not required. When 32PO4-labeled mast cells are challenged 2-5 min with lysophosphatidylserine, the labeling of phosphatidate, phosphatidylinositol and phosphatidylcholine is increased. When [3H]arachidonate-labeled mast cells are used, lysophosphatidylserine increases the appearance of isotopic diacylglycerol and phosphatidate. Like the secretory response, these effects are independent of the presence of extracellular Ca2+. Incubations in the presence of [3H]glycerol show that lysophosphatidylserine does not activate the de novo synthesis of phospholipids. In agreement with a participation of phosphoinositidase C in the action of lysophosphatidylserine, we observe accumulation of inositol phosphates in [3H]inositol labeled mast cells incubated in the presence of Li+. The results suggest that lysophosphatidylserine delivers its stimulus to mast cells, by the activation of phosphoinositide-dependent signalling mechanism.

Acylation↗
PubMed1990

Ultraviolet-mediated antimycotic activity of alpha-terthienyl on Microsporum cookei.

Alpha-terthienyl (alpha-T) in the presence of UV-A irradiation reduced the growth rate of Microsporum cookei. In the dark, alpha-T accumulated in small diffuse vacuoles within the hyphae. After UV-A treatment, alpha-T caused damage to the membranes of the nucleus, mitochondria and endoplasmic reticulum. Plasmolytic and autolytic changes occurred resulting in plasma membrane breakage and cell wall aberrations. UV-A activated alpha-T would appear to target membrane proteins.

Microscopy, Electron↗
PubMed1990

[Prognostic stratification of survivors of lst myocardial infarction: evaluation of regional kinetics and ejection fraction by bidimensional echocardiography].

To determine the prognostic value of some echocardiographic indices of left ventricular function (ejection fraction, wall motion score index, left ventricular dimension) in the first year after acute myocardial infarction, we studied prospectively 162 consecutive patients (mean age: 61 +/- 11) who survived the hospital phase of a first acute myocardial infarction. Two-dimensional echocardiography was performed at hospital discharge (mean: 20 +/- 3 days after admission). For the analysis of wall motion, an 11 segment model of the left ventricle was used; from the scoring system of segmental ventricular function (1 = normal, 2 = hypokinetic, 3 = akinetic, 4 = dyskinetic, 5 = aneurysmal) we derived the wall motion score index (sum of assigned number to each segment/11). The echocardiographic ejection fraction was determined using the monoplane ellipsoid formula for the calculation of end diastolic and end systolic volumes in apical four-chamber and two-chamber views; the assumed ejection fraction was the mean value resulting from values of ejection fraction calculated in the two views. The follow-up was protracted from 13 to 36 months (mean: 22 months). Fourteen patients (9%) died as a result of cardiac events within 13 months of myocardial infarction. Of the patients with ejection fraction greater than or equal to 45% (81/162 = 50%) two died (first year mortality = 2.4%); of those with 35-45% ejection fraction (58/162 = 35%) two died (first year mortality = 3.5%); while of those with less than or equal to 35% ejection fraction (25/162 = 15%) ten died (first year mortality = 40%). Of the patients with wall motion score index less than 1.5 (76/162 = 47%) none died in the follow-up period; of those with score index between 1.5 and 1.9 (61/162 = 37%) four died (first year mortality = 7%); of those with score index greater than or equal to 1.9 (25/162 = 15%) ten died (first year mortality = 40%). Thus, ejection fraction and score index have the same predictive value for mortality in the first year after a first acute myocardial infarction. However, an interesting datum is that in the sub-group of patients with less than or equal to 35% ejection fraction and score index less than 1.9 the first year mortality was 15%, while in the sub-group with less than or equal to 35% but score index greater than or equal to 1.9 the first year mortality was 57%.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1979

F1-ATPase from different submitochondrial particles.

1. F1-ATPase has been extracted by the diphosphatidylglycerol procedure from mitochondrial ATPase complexes that differ in ATPase activity, cold stability, ATPase inhibitor and magnesium content. 2. The ATPase activity of the isolated enzymes was dependent upon the activity of the original particles. In this respect, F1-ATPase extracted from submitochondrial particles prepared in ammonia (pH 9.2) and filtered through Sephadex G-50 was comparable to the enzyme purified by conventional procedures (Horstman, L.L. and Racker, E. (1970) J. Biol. Chem. 245, 1336--1344), whereas F1-ATPase extracted from submitochondrial particles prepared in the presence of magnesium and ATP at neutral pH was similar to factor A (Andreoli, T.E., Lam, K.W. and Sanadi, D.R. (1965) J. Biol. Chem. 240, 2644--2653). 3. No systematic relationship has been found in these F1-ATPase preparations between their ATPase inhibitor content and ATPase activity. Rather, a relationship has been observed between this activity and the efficiency of the ATPase inhibitor-F1-ATPase association within the membrane. 4. It is concluded that the ATPase activity of isolated F1-ATPase reflects the properties of original ATPase complex provided a rapid and not denaturing procedure of isolation is employed.

Adenosine Triphosphatases↗
PubMed1979

Pharmacological effects of phosphatidylserine liposomes: the role of lysophosphatidylserine.

1. Unique among the phospholipids, phosphatidylserine depresses brain energy metabolism when injected intravenously into mice in the form of sonicated liposomes. The possibility that this effect results from a metabolic transformation of phosphatidylserine is examined in this paper. 2. A strong enhancement of the phosphatidylserine effect is induced by the incubation of liposomes with rat serum. Similar phosphatidylserine activation is observed after the incubation of the phospholipid with purified phospholipase A2 from pancreas. In both cases phosphatidylserine is split into the deacylated derivative, lysophosphatidylserine. 3. Lysophosphatidylserine reproduces with greater efficacy the effect of phosphatidylserine on brain energy metabolism. Other lysophospholipids are not effective. 4. It is concluded that the pharmacological effects of phosphatidylserine liposomes is due to the generation of lysophosphatidylserine.

Animals↗
PubMed1979

Pharmacological effects of phosphatidylserine liposomes: regulation of gylcolysis and energy level in brain.

1 The accumulation of glucose in the brain produced by the administration of phosphatidylserine liposomes into mice has been studied by measurement of the cerebral contents of glycolytic intermediates and high-energy compounds. 2 With a normal supply of oxygen to the brain, inhibition of glycolysis is indicated mainly at the phosphofructokinase step. The ratio of glucose-6-phosphate to fructose-1,6-diphosphate increased, whereas the levels of pyruvate and especially lactate decreased. 3 Under conditions of cerebral ischaemia, the administration of phosphatidylserine delays glycogen mobilization and ATP use. As a consequence of decreased energy utilization, the brain adenylate energy charge remains at a high level. 4 It is concluded that the phosphatidylserine-induced glucose accumulation in the brain is due to reduced energy expenditure and therefore to a decrease in carbohydrate consumption. The inhibition of glycolysis by the high level of adenylate energy charge is probably the control mechanism explaining the decreased carbohydrate utilization.

Adenine Nucleotides↗
PubMed1977

Cold lability of membrane-bound F1-ATPase.

1. Preincubation of MgATP submitochondrial particles with EDTA or Tris.HCl liberated a measurable amount of ATPase inhibitor that could be rapidly purified using only trichloroacetic acid precipitation and heat treatment. 2. In spite of the emergence of high ATPase activity, a considerable amount of ATPase inhibitor was left in the particles. Comparative analysis of other submitochondrial preparations indicated that only AS-particles were effectively depleted. 3. The high ATPase activity of inhibitor-deficient particles, was labile at low temperature provided that the exposure to cold was done in the presence of MgATP. Other nucleotides could not substitute for ATP. Glycerol inhibited and salts enhanced the cold inactivation of membrane-bound F1-ATPase. Isolation of F1-ATPase from cold-inactivated particles yielded a soluble preparation of correspondingly lower activity. 4. It is concluded that together with the increase of ATPase activity, the ATP-dependent cold lability of membrane-bound F1-ATPase and the dislocation of ATPase inhibitor at non operative sites reveal the extent of ATPase complex disorganization.

Adenosine Triphosphatases↗
PubMed1977

[Absence of cutaneous phenomena of delayed hypersensitivity in the use of zymosan as adjuvant in comparison with Freund's complete adjuvant in autoimmune experimental orchitis].

In previous researches some of the Authors proved that Zymosan acts as adjuvant in determining the experimental autoimmune aspermatogenesis, in absence of skin reactivity of delayed type. The aim of the present investigations was to ascertain if Zymosan possess some components analogous to those of mycobacteria, which can be considered responsible in determining hypersensitivity reactions of delayed type. The results, obtained also in cross experiments, don't confirm this hypothesis.

Adjuvants, Immunologic↗
PubMed1977

Submicroscopic morphology of Trichophyton mentagrophytes grown at different temperatures.

Several modifications were observed in Trichophyton mentagrophytes cultivated at 19 degrees and 37 degrees C, i.e. nine degrees below and above the optimum of 28 degrees C. The phenomena included inhibition of the growth rate, changes in the gross aspects of the cultures as well as of the microscopic and submicroscopic morphology of the hyphal cells. At the ultrastructural level, in particular, it was shown that, at the suboptimal temperature, although the organelle structure in both young and aged hyphal cells remained nearly unchanged, unusual bodies of probable storage significance and plasmalemmasomes were formed. At the supraoptimal temperature, the youngest cells showed a normal organization but were richer in glycogen clusters and enveloped by a cell wall thicker than the ones at the optimal condition. In the cells far from the apex, the endomembrane integrity was lost and consequently an autolytic activity occurred. Degradation phenomena were detectable also at cell wall level. The cytological changes observed were tentatively correlated with a possible different sensitivity of the membrane system at the experimented temperature conditions.

Cell Membrane↗
PubMed1977

Activation of (Na+ + K+)-dependent ATPase by lipid vesicles of negative phospholipids.

1. Kidney (Na+ + K+)-stimulated ATPase was depleted of phospholipids by extraction with lubrol and inserted in lipid structures of known composition. Both ouabain-sensitive ATPase and phosphatase reactions could be partially restored by lipid replacement. 2. Lipid vesicles of natural and synthetic negative phospholipids proved to be effective. The low activity of uncharged liposomes was increased when negative charges were included into the bilayer structure. 3. Reactivation by negative phospholipids was accompanied by spontaneous re-assembly of a stable lipid-protein complex. By contrast, the interaction of lipid deficient ATPase complex with uncharged lamellae was possible only after sonication of lipid-protein suspension. Reactivation did not ensue. 4. The ouabain-sensitive ATPase reactivated by synthetic dioleoylphosphatidylglycerol yielded curvilinear Arrhenius plots. The same pattern was seen with the original undepleted microsomal preparation. A discontinuity close to the temperature of fluid-order transition was found with dimyristoyl phosphatidylglycerol. 5. It is concluded that reassembly of lipid-deficient (Na+ + K+)-stimulated ATPase requires the addition of diacylphospholipids with fluid acyl-chains and negatively charged polar heads able to assemble in an expanded lamellar configuration.

Adenosine Triphosphatases↗