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Biomedical subjects

A Bruni

Publications and source records attributed to A Bruni.

At least 55 records · Page 3Linked to original sources
PubMed1994

Epstein-Barr virus infection in sinonasal non-Hodgkin's lymphomas.

Sinonasal non-Hodgkin's lymphomas (SNHLs) of B- or T-cell immunophenotype have been associated with Epstein-Barr virus (EBV) infection of neoplastic lymphoid tissue. Nine SNHLs were investigated using immunohistochemistry, the polymerase chain reaction (PCR) for EBV genome and in situ hybridization (ISH) for EBV encoded RNAs (EBER), immunoglobulin (CI-gHR) and clonal T-cell receptor (CTC beta R) gene rearrangements. Eight cases were diagnosed as peripheral pleomorphic T-cell lymphomas (pPTCL). PCR showed the presence of EBV genome in eight cases; ISH for EBER led to the detection of positive cells in five cases. Late membrane protein (LMP) immunostaining was observed in three cases. No EBV positivity has been detected in control cases. The frequent association with EBV infection in the cases illustrated confirms the previous suggestions that EBV may have a role in the genesis of lymphomas of the sinonasal region.

Adult↗
PubMed1994

Lipid mediators of immune reactions: effect of a linked phosphorylserine group.

Immunoregulation by lipids containing the phosphorylserine (PHS) group has been studied in rodent peritoneal mast cells and human peripheral blood lymphocytes. When PHS is linked to a phospholipid backbone (mono- and diacylglycerol), mast cell activation is produced. However, the effect decreases linking the PHS group to long chain alkanols and is abolished in cholesteryl-PHS, showing that the acylglycerol moiety participates in mast cell activation. Phospholipids containing the PHS group inhibit proliferation of activated peripheral blood lymphocytes. In contrast to mast cells, this effect is retained in alkyl-PHS and is enhanced in cholesteryl-PHS, indicating that in this case the PHS group is the main effector. Among non-phospholipid PHSs, cholesteryl-PHS has been the most interesting since it associates lack of mast cell activation and high inhibitory activity on peripheral blood lymphocytes. This selectivity suggests that this compound may have a potential as an immunosuppressive agent.

Animals↗
PubMed1994

Interaction of monensin on dimorphic transition and hyphal growth in Candida albicans.

Monensin, an exocytosis perturber, was assayed on the dimorphic fungus Candida albicans in order to study its effects on wall synthesis and morphogenesis. In the presence of the drug, both germ-tube formation and hyphal elongation were markedly inhibited according to the dose and exposure time. The effect was accompanied by morphogenetic malformations which could be detected under UV light and by transmission electron microscopy. Enormous wall and septa thickenings revealed by cytochemical tests indicated an abnormal deposition of chitin. Since chitin synthase is inserted in the plasma membrane in a latent state and its activation depends on regulatory factors reaching the cell periphery through an orderly exocytosis, it is assumed that monensin affects the vesicular traffic leading to a prevalence of activators over inhibitors of the enzyme.

Candida albicans↗
PubMed1993

Role of a serum phospholipase A1 in the phosphatidylserine-induced T cell inhibition.

We have previously shown that unsaturated phosphatidylserines inhibit mitogen-induced T cell activation. We now report that the inhibitory action requires a protein present in bovine and human serum. Partial purification and phospholipase assay show that this protein has phospholipase A activity on phosphatidylserine but not phosphatidylethanolamine, phosphatidylcholine and phosphatidylinositol. In short incubations (1-3 h)2-acyl lysophosphatidylserine is produced but in longer incubations the cis-unsaturated fatty acid is also released. Experiments on peripheral blood mononuclear cells indicate that the unsaturated fatty acid becomes the main responsible for the PS-induced inhibition and that 2-acyl lysophosphatidylserine enhances the inhibitory effect of fatty acid.

Animals↗
PubMed1993

Dopamine receptors on human T- and B-lymphocytes.

The presence of functional dopamine receptors on differentiated cells of the mammalian immune system is still under discussion. This study has utilized (-)-[3H]sulpiride as a ligand, to detect the presence of recognition sites of the dopamine D2 receptor family on human T- and B-lymphocytes. The (-)-[3H]sulpiride binding was of high affinity (Kd 0.9 nM +/- 0.2 nM), specific, saturable (Bmax 10.2 +/- 1.4 fmol/10(6) cells) and reversible. The pharmacological characterization of the recognition site suggests similarities mainly with the D2 and D4 rather than D3 subtype of dopamine receptor. Furthermore, dopamine treatment was able to reduce the intracellular cAMP levels of lymphocytes stimulated with forskolin, thus suggesting a potential functional significance of this dopamine receptor in mediating neural-immune interactions.

Adult↗
PubMed1993

Longitudinal transgastric echocardiographic views utilizing a single-plane probe: anatomic correlations and clinical applications.

In order to widen the diagnostic capability of single-plane transesophageal echocardiography, which has been so far confined to transverse imaging planes, we obtained four transgastric longitudinal echocardiographic views which have not been previously described. These views can image structures such as superior and inferior vena cava, the right ventricular inflow and outflow tract, the mitral apparatus and the ascending aorta, which are poorly visualized by transesophageal transverse single-plane echocardiography. Among 400 consecutive patients these scans gave relevant additional diagnostic information in 62 cases (15.5%) and provided the correct diagnosis in 37 (9.2%). There were no complications related to the longer gastric manipulation of the probe and the quality of the images was high. We conclude that longitudinal echotomographic scanning of the heart is not exclusively confined to the use of biplane or omniplane probes, but longitudinal views can be consistently obtained with a single-plane instrument.

Aorta↗
PubMed1993

Phosphatidylserine, a putative inhibitor of tumor necrosis factor, prevents autoimmune demyelination.

We tested the effect of bovine cortex phosphatidylserine (BC-PS), a membrane phospholipid known to inhibit the release of the cytokine tumor necrosis factor (TNF), in SJL/J mice sensitized for adoptively transferred experimental autoimmune encephalomyelitis (EAE). Control, sensitized mice developed severe clinical and histologic EAE within 6 to 9 days, whereas only 20% of mice given BC-PS displayed clinical signs that were much less severe and minimal CNS pathology. Cessation of BC-PS treatment after 15 to 40 days led to disease within 1 to 2 weeks, but when treatment was more prolonged, animals remained healthy after cessation. Serial transfer of spleen cells (SC) from BC-PS-treated and control animals into naive recipients resulted in acute EAE within 6 to 7 days with cells from either donor type. Animals treated late with BC-PS failed to relapse and generally remained healthier than controls did over a 40-day period of observation. Cultures of lymph node cells or SC from BC-PS-treated and control animals showed an 80 to 90% reduction in TNF production in the BC-PS-treated group. Thus, we demonstrate that PS can abrogate or significantly reduce the severity of EAE without permanently inhibiting effector T cells. The approach might be considered a candidate for future therapies of relevance to MS.

Animals↗
PubMed1993

Absorption and distribution of arachidonate in rats receiving lysophospholipids by oral route.

Absorption and distribution of polyunsaturated fatty acids was investigated in rats receiving lysophospholipids per os (30 mg kg-1). Lysophosphatidylcholine (lysoPC) increased [3H]arachidonate absorption and its incorporation into mucosal phosphatidylcholine. Transport of [3H]arachidonate by the phospholipid fraction of lymph lipoproteins and the level of [3H]arachidonate in plasma and liver lipids was also increased by lyso PC. Lysophosphatidylserine also increased [3H]arachidonate absorption but channeled the fatty acids into the aminophospholipid fraction of mucosal phospholipids, thus decreasing its efflux in lymph lipoproteins. As a consequence, lysophosphatidylserine caused [3H]arachidonate accumulation in mucosa. As similar results were obtained with [14C]linoleate, the data suggest that the addition of an appropriate lysophospholipid to the diet may direct absorption and distribution of polyunsaturated fatty acids.

Absorption↗
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↗