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Biomedical subjects

R Landolfi

Publications and source records attributed to R Landolfi.

At least 73 records · Page 4Linked to original sources
PubMed1988

Meningeal hematopoiesis causing exophthalmus and hemiparesis in myelofibrosis: effect of radiotherapy. A case report.

Meningeal myeloid metaplasia (MM) is very rarely observed in patients with myelofibrosis. We report the occurrence of meningeal MM causing exophthalmus and fever in a patient with myelofibrosis secondary to polycythemia vera. A computerized tomography (CT) scan showed multiple intracranial and intraorbital enhancing masses. A needle aspirate of retrobulbar space confirmed the diagnosis of extramedullary hematopoiesis. The patient subsequently developed a rapidly worsening tumor-like syndrome with hemiparesis, aphasia, and loss of sphinteric control. The administration of radiotherapy caused a complete and stable regression of clinical symptoms and a marked reduction of MM masses.

Adult↗
PubMed1988

High-performance liquid chromatography in protein sequence determinations.

The use of reversed-phase high-performance liquid chromatography (RP-HPLC) for the determination of protein sequences is reported. Topics considered include the peptide separation of endoprotease digestion mixtures, the application of HPLC peptide mapping as an efficient system to check the accuracy of an assumed protein sequence, obtained indirectly by DNA sequencing and the use of HPLC for amino acid analysis in the Edman sequence strategy. The use of RP-HPLC for an unconventional sequence strategy is demonstrated; HPLC exopeptidase mapping appears to be particularly useful as a future technique for small terminal sequence analysis. Finally, the coupling of HPLC with fast atom bombardment mass spectrometry is discussed.

Acetates↗
PubMed1988

Allosteric equilibria in the binding of fibrinogen to platelets.

The binding of fibrinogen to platelets occurs according to the law of mass action. The platelet receptor binds reversibly a single fibrinogen molecule and undergoes a conformational transition between two allosteric states, T and R, that differ in their affinity for fibrinogen. The equilibrium between the two forms is shifted by ADP toward the R (high-affinity) state, thus promoting the aggregation process. This model opens the way to consideration of allosteric modulation of the binding of fibrinogen to its platelet receptor.

Adenosine Diphosphate↗
PubMed1988

Determination of neutral haemoglobin variants by immobilized pH gradient, reversed-phase high-performance liquid chromatography and fast-atom bombardment mass spectrometry: the case of a Hb Torino alpha 43 (CE1) Phe----Val.

A neutral haemoglobin variant was identified by the combined use of different analytical methods. Isoelectric focusing on immobilized pH gradients (under denaturing conditions) allowed to detect and alpha chain variant. HPLC of tryptic digest showed that its amino-acid variation resided on T alpha 6 peptide (position 41-56). In the fast-atom bombardment (FAB) positive mass spectrum of the tryptic digest, the protonated molecular ion of the T alpha 6 peptide occurred 48 mass units lower than the normal T alpha 6 fragment, corresponding to a Phe----Val substitution. To a partial sequence determination (aminopeptidase digestion of the T alpha 6 peptide, followed by amino acid determination and FAB-MS analysis of the digestion-generated mixture) the substitution appeared to be on Phe43 (CE1). This variant is already known as Hb Torino. The procedure here described proved to be fast and simple, and feasible whenever neutral variants are supposed to occur.

Child, Preschool↗
PubMed1988

Increased platelet-fibrinogen affinity in patients with myeloproliferative disorders.

Patients with myeloproliferative disorders (MPD) are known to have some abnormalities of platelet glycoproteins (Gp). Quantitative changes of the Gp Ib, IIb-IIIa, and/or their glucidic content have been reported. Since the Gp IIb-IIIa complex plays a major role in fibrinogen binding by activated platelets, we measured the platelet fibrinogen affinity in nine patients with polycythemia vera (PV) and one subject with chronic myeloid leukemia (CML) by the aggregometric method of Marguerie. In all patients the Kd of the platelet fibrinogen reaction was significantly decreased as compared to controls, with evidence in two cases with PV of a heterogeneity of platelet-fibrinogen receptor sites. The measurement of 125I-labeled fibrinogen-platelet binding, performed in seven patients (five PV and two CML), showed receptor populations with increased (Kd1 = 0.58 + 0.3 X 10(7) mol/L) and normal affinity (Kd2 = 5.12 + 3.1 X 10(7) mol/L). These results demonstrate a heterogeneity of platelet-fibrinogen receptors in these patients and may explain the thrombotic diathesis of MPD subjects.

Adult↗
PubMed1986

T lymphocyte subsets and platelet-associated IgG in idiopathic thrombocytopenic purpura: effect of splenectomy.

The modifications of cell-mediated immunity in idiopathic thrombocytopenic purpura (ITP) were investigated using the technique of Moretta et al. [J. exp. Med. 151: 969-974, 1980] to study T lymphocyte subsets in 35 ITP subjects at various clinical stages. In all these patients, platelet-associated IgG (PAIgG) were measured by a complement lysis inhibition technique. Untreated ITP patients did not show significant modifications of T lymphocyte subsets. Patients with thrombocytopenia not responsive to corticoids or splenectomy and increased PAIgG levels showed significant reduction of Fc-gamma-bearing T lymphocytes (T-gamma). Patients 'cured' by splenectomy (12 out of 17) showed a normal PAIgG level, a marked increase of T-gamma cells and a reduction of T-mu cells; patients 'not cured' by splenectomy showed an increased PAIgG level and a reduction of T-gamma cells. An increase of PAIgG levels and a reduction of T-gamma cells were found in 2 splenectomized patients after relapse. An association between chronic nonresponsive ITP and decrease of T-gamma cells was established.

Adolescent↗
PubMed1985

Biological activity of platelet activating factor-amidophosphonate (PAF-AP), a novel phosphonolipid selective inhibitor of platelet activating factor (PAF).

A novel amidophosphonate analog of Platelet Activating Factor (PAF), trimethyl (3-phosphonopropyl) ammonium hydroxide (R)-mono[2-acetamido-3-(hexadecyloxy)propyl] ester (PAF-AP), was synthesized. A potent inhibitor of aggregation induced by Platelet Activating Factor, arachidonic acid, Ca2+-ionophore, ADP, and thrombin, PAF-AP had no or very little effect on aggregation induced by epinephrine and collagen. Inhibition of phospholipase A2 and C2 activity was suggested from suppression of release of [14C]-arachidonic acid from pre-labeled platelet glycerophospholipids.

Adenosine Diphosphate↗
PubMed1984

Platelet activation in patients with benign and malignant ovarian diseases.

Plasma concentration of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) were measured by radioimmunoassay in 45 patients with benign and malignant ovarian diseases. All patients with ovarian carcinoma showed increased beta-TG and PF4 levels. Among benign ovarian diseases the patients with serous cystadenoma more frequently showed signs of platelet activation, whereas those with endometriotic cyst and mucinous cystadenoma generally had normal beta-TG and PF4 values. These results indicate that an increased platelet activation is consistently associated with malignant tumors of the ovary, whereas benign tumors show a different capacity to induce platelet activation.

Adult↗
PubMed1984

Modification of platelet function and arachidonic acid metabolism by bioflavonoids. Structure-activity relations.

The mechanism of the antiaggregating activity of flavonoids was studied in vitro. The activity of fifteen different compounds was tested on platelet aggregation and arachidonic acid metabolism. The effect of flavonoids on platelet adenosine 3',5'-cyclic monophosphate (cyclic AMP) levels under basal conditions, as well as after stimulation by prostacyclin (PGI2), was also measured. The glycons of flavonoids in general and the flavanone derivatives that we tested did not affect platelet function. On the other hand, flavone, chrysin , apigenin and phloretin inhibited platelet aggregation by depressing the cyclooxygenase pathway. In addition, flavone, chrysin and apigenin reduced the platelet cyclic AMP response to PGI2. This effect was probably mediated by an inhibition of adenylate cyclase. Myricetin and quercetin, however, increased the PGI2-stimulated rise of platelet cyclic AMP. Both of these flavonoids inhibited primarily lipoxygenase activity. Modification of platelet cyclic AMP metabolism through inhibition of phosphodiesterase activity was found to be the probable mechanism of their antiaggregating effect.

Arachidonic Acid↗
PubMed1984

Inhibition in vitro of platelet aggregation and arachidonic acid metabolism by flavone.

The effects of flavone on platelet aggregation and arachidonic acid (AA) metabolism were tested in vitro. When incubated at a concentration of 50 microM, flavone completely suppressed platelet aggregation induced by 150 microM AA in thirty-six out of forty-three subjects tested. A lower concentration (10 microM) was effective in about 50% of the donors. Flavone also inhibited the second wave of aggregation induced by epinephrine and ADP. Platelet thromboxane formation, estimated both by radioimmunoassay measurements and by studies of 14C-labeled AA metabolism, was depressed by flavone. Flavone-treated platelets preferentially utilized [14C]AA for the lipoxygenase pathway while cyclo-oxygenase activity was depressed. Adenosine 3':5'-cyclic monophosphate (cAMP) was measured in flavone-treated and control platelets. While their baseline levels were similar, flavone-treated platelets showed a lower stimulation of cAMP induced by prostacyclin (PGI2) than did controls. Phosphodiesterase activity was not affected by flavone as judged from the decay rates of PGI2-stimulated cAMP levels. From these findings we conclude that the antiaggregating activity of flavone is not a consequence of changes in platelet cAMP but is due to inhibition of cyclo-oxygenase.

Arachidonic Acid↗
PubMed1984

Ethanol raises prostacyclin in vivo and in vitro.

Moderate doses of ethanol were shown to induce a significant rise in prostacyclin (PGI2) concentration in cultures of endothelial cells derived from umbilical veins. Administration of 32 g of ethanol to six volunteers elevated plasma levels of PGI2 in parallel with those of blood alcohol. Although not specific for ethanol, this alcohol induced the largest change in PGI2. Withdrawal of the stimulant alcohol caused prompt reduction of the elevated prostacyclin to baseline values. The activity of ethanol appears to be due to a direct stimulation of cyclooxygenase. The release of [14C]arachidonic acid from prelabeled endothelial cells was decreased by ethanol. PGE2 production was also enhanced by exposure of endothelial cells to ethanol. The physiologic significance of these alcohol-induced changes in PGI2 levels remains to be established.

Adult↗
PubMed1983

Effect of eicosatetraenyl (3-aminopropyl) phosphonate (URI-73A) on platelet aggregation and arachidonic acid metabolism.

Eicosatetraenyl (3-aminopropyl) phosphonate (URI-73A), an experimental anti-hypertensive drug, when tested in vitro, inhibits platelet aggregation especially that induced by arachidonic acid (AA) and to a lesser degree by epinephrine. Preincubation of human platelets with this compound in the majority of individuals resulted in a dose-dependent inhibition of the platelet response to AA, mostly in the form of a delay and a reduction of maximal aggregation. Platelets from two smaller groups of donors either exhibited full aggregation or no aggregation. Both the prelabel and pulse label techniques used to study arachidonic acid metabolism yielded complementary results. Production of thromboxane and hydroxy fatty acids was reduced in thrombin-aggregated washed platelets preincubated with URI-73A. In addition, the release of AA from phospholipids was inhibited. Its complex effects on human platelets suggest that URI-73A may, as an AA analog, depress cyclooxygenase and lipoxygenase, and as a phospholipid analog inhibit phospholipase activity.

Adenosine Diphosphate↗
PubMed1983

[Beta-thromboglobulin and platelet regeneration time in children with mitral valve prolapse].

We studied 12 children with echocardiographic evidence of mitral valve prolapse (MVP) in order to demonstrate platelet activation or consumption as risk for thromboembolism. Therefore, with a standard radioimmunoassay, we measured the plasma levels of Beta-thromboglobulin (BTG), a platelet-specific protein released during platelet release reaction. Platelet turn-over was evaluated by measuring the Platelet Regeneration Time (PRT) with a non-radioisotopic method. Blood samples for BTG assay were collected at rest and after exercise. BTG plasma levels obtained in children with MVP were significantly higher than in normal subjects (p less than 0.01), both at rest and after exercise. We found no difference in either group between BTG level at rest and after exercise. The TRP was within the normal range in all patients except 2, in whom TRP was slightly shorter. Increased BTG levels and normal TRP suggest that in our patients platelet activation, but not consumption, was increased. In children with MVP, periodic controls of platelet activation may be useful to detect an increased risk of thromboembolism.

Adolescent↗
PubMed1982

Beta-thromboglobulin in patients with acute and chronic coronary artery disease.

Beta-thromboglobulin (beta TG) plasma levels were measured by radioimmunoassay in 14 patients with acute myocardial infarction (MI), in 13 with myocardial ischemia and recurrent episodes of angina and in 14 subjects with a past history of MI. Increased beta TG plasma values were observed in patients with acute MI and with myocardial ischemia whereas subjects with a past history of MI showed results not significantly different from normal subjects. Daily measurements in acute MI showed in five cases a second peak of beta TG values which suggests the occurrence of a deep vein thrombosis. The increased platelet consumption in MI was not related with the extent of the necrosis. We suggest, therefore, that platelet activation is associated with myocardial ischemia rather than necrosis.

Adult↗
PubMed1981

Megathrombocytes, platelet regeneration time and platelet associated IgG in idiopathic thrombocytopenic purpura and in thrombocytopenia associated with chronic liver disease.

Percentage of megathrombocytes, platelet regeneration time (PRT) and platelet-Associated IgG (Pl-A-IgG) were investigated in 12 patients with clinical features consistent with idiopathic thrombocytopenic purpura and in 11 patients with thrombocytopenia associated with chronic liver disease. Bone marrow smears were also examined and megakaryocytes classified into stages I-III according to the current principle. Of 12 patients with idiopathic thrombocytopenic purpura the percentage of megathrombocytes was increased in 9, PRT reduced in 10, and Pl-A-IgG increased in 8 patients. A statistically significant correlation was found between the percentage of megathrombocytes and the level of Pl-A-IgG. A slight correlation was also found between PRT and the percentage of megathrombocytes, while a significant correlation was found between megakaryocytes in stage I and the percentage of megathrombocytes, suggesting that growth of megakaryocytes probably contributes to platelet heterogeneity. In patients with thrombocytopenia and chronic liver disease, the percentage of megathrombocytes was in the normal range. A moderately increased level of Pl-A-IgG was found only in patients with active chronic hepatitis, PRT was reduced only in a few patients, while most of them also showed an increase of Pl-A-IgG.

Blood Platelets↗