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Biomedical subjects

A Mazzone

Publications and source records attributed to A Mazzone.

At least 37 records · Page 2Linked to original sources
PubMed1999

The effects of iloprost infusion on microcirculation is independent of nitric oxide metabolites and endothelin-1 in chronic peripheral ischaemia.

BACKGROUND: Endothelial vascular tone modulators are thought to be involved in aetiopathogenesis of systemic sclerosis (SS) and of peripheral artery occlusive disease (PAOD). Iloprost, a prostacyclin (PGI2) analogue, induces clinical benefit in patients suffering from peripheral ischaemia. This study was performed to investigate the effect of this drug on endothelial function in vivo to elucidate the role of vascular tone modulators. METHODS: Fourteen PAOD and 15 SS patients were treated for 24 and 10 days respectively. On the first day, before and after therapy, nitric oxide metabolites (NO2-/NO3-) and endothelin-1 (ET-1) plasma concentrations were detected; moreover, the endothelium-dependent vasodilatation in response to artificial ischaemia was evaluated by means of an echo-Doppler device. RESULTS: The echo-Doppler evaluation showed that the percentage of arterial reactive dilatation was not modified by placebo or by iloprost, and that the increase in blood velocity flow lasted for a significant longer time after drug infusion (226.79 +/- 17.49 vs. 310.71 +/- 36.32 s; P > 0.04). NO2-/NO3- and ET-1 plasma concentration were higher in patients than in control subjects (P < 0.004). After 6 h of iloprost infusion, no significant modifications were detected. CONCLUSION: This study provides evidence that iloprost enhances the microvascular functional capacity and clinical benefit for patients. The effects of the drug seem to be independently or not directly correlated with its interactions with vascular tone modulators such as NO2-/NO3- or ET-1.

Adult↗
PubMed1999

Cloning, structural organization and chromosomal localization of the mouse aquaporin-8 water channel gene (Aqp8).

The gene encoding the mouse Aquaporin-8 water channel protein (Aqp8) was cloned and its genomic structure was defined. Aqp8 consists of six exons with boundaries at amino acids 1-4, 5-87, 88-129, 130-201, 202-246 and 247-261 which partially correspond to those of other known aquaporin genes. All splice sites conform to the GT-AG rule except the first one which is GT-GG. Primer extension and RNase protection analyses using mouse liver RNA demonstrated three initiation transcription sites located 385, 156 and 146 bp upstream from the translational start codon. No defined TATA box was found in the 5'-flanking region where numerous CAAT motifs and one GATA box were identified. Fluorescence in situ hybridization localized the Aqp8 locus to mouse chromosome 7F3. The 7F region is syntenic with human chromosomes 11, 16 and 10. These results (i) reveal marked structural distinction between the Aqp8 gene and the other known mammalian aquaporin genes, (ii) may now permit the molecular characterization of Aqp8 expression and (iii) represent a fundamental step for the construction of a target vector to generate transgenic Aqp8 knockout mice.

5' Untranslated Regions↗
PubMed1998

Peripheral benzodiazepine receptor expression on leukocytes and neutrophil function during anticonvulsant monotherapy.

Epileptic patients on long-term therapy with a single anticonvulsant showed enhanced expression of peripheral benzodiazepine receptors (pBZrs) on neutrophils, monocytes and lymphocytes. N-Formyl-methionyl-leucyl-phenylalanine-induced chemotaxis was significantly impaired in neutrophils from patients on carbamazepine (p < 0.01 vs. controls). Neutrophils from patients on phenytoin had enhanced phorbol myristate acetate-stimulated O-2 production (p < 0. 01 vs. controls) and neutrophils from patients on valproic acid had impaired phagocytosis frequency and Staphylococcus aureus lethality index (p < 0.01 vs. controls). Overexpression of pBZrs on leukocytes may reflect the clinical response to anticonvulsants and may play a role in the immunological effects of some of these drugs.

Adolescent↗
PubMed1998

[Canalith repositioning maneuver: proposal of a new therapy for benign paroxysmal positional vertigo of the posterior semicircular canal].

A new therapy is proposed for the treatment of Benign Paroxysmal Positional Vertigo (B.P.P.V.) of the Posterior Semicircular Canal (P.S.C.): the Canalith Repositioning Maneuver (C.R.M.). The need for a new maneuver to treat B.P.P.V. of the P.S.C. arises from the difficulties encountered in daily practice, under particular conditions (i.e. elderly, obese, traumatized patients and in the presence of rachis pain, etc.), to perform the most common rehabilitative techniques such as the Semont Maneuver and Epley's Canalith Repositioning Procedure (C.R.P.). The results achieved using this new technique on a group of 47 consecutive out-patients are presented and compared to those achieved using the Semont Maneuver in an analogous group of 23 patients. C.R.M. and the Semont Maneuver were performed once per treatment session and all patients were checked every 3 days until the symptoms of B.P.P.V. disappeared. Thereafter they were invited to return for check-up if signs of vertigo returned (follow-up 6-25 months). The two techniques proved equally effective: 87.5% of the cases were resolved with C.R.M., 82.6% with the Semont Maneuver. However, the C.R.M. provided other advantages as it resolved the problem immediately (i.e. in a single session) in 81% of the cases vs. 68.4% for the Semont Maneuver. In view of the Canalith theory, the action mechanism envisaged for all three maneuvers--C.R.M., the Semont Maneuver and the Epley C.R.P.--can be explained assuming that the canalith passes from the ampullar to the non ampullar branch of the (P.S.C.) passing finally through the Common Duct and into the Utricle. C.R.M. is a specific treatment for the B.P.P.V. of the P.S.C. and is simple to perform, well tolerated and quite effective. It is indicated in all cases of B.P.P.V. of the P.S.C. both as initial treatment and as alternative to other treatment methods which have proved ineffective or difficult to perform. Indeed, in therapy it is best to be quite skilled in more than one technique, availing oneself of a full range possibilities; in this way the cure can be tailored to the patient in each individual case and not vice versa.

Adolescent↗
PubMed1998

[beta-Interferon therapy of chronic hepatitis HCV+, 1b genotype].

Various papers reported that chronic viral hepatitis is the principal cause of chronic liver disease, as cirrhosis and hepatocarcinoma. Interferon is the only agent known to have a beneficial effect in chronic hepatitis. The response rate has been less than 10 percent in patients with genotype 1b, but in patients with genotype 2 or 3 it has been greater than 40 percent. Aim of our investigation was to study 10 patients suffering from chronic viral hepatitis HCV related, genotype 1b, non responder to interferon-alpha therapy. In these patients we administered beta-interferon at the dose of 6 million units, 3 times a week, for 3 months. A significant reduction of aminotransferase level was reported after 3 months of the start of the therapy. An higher level of beta-interferon plasma rate was found in 3 non responder patients. The interaction of beta-interferon with the immune system was demonstrated with an increase of CD8+ lymphocytes that correlated with decrease of HCVRNA. The treatment with beta-interferon have a beneficial effect in patients with chronic hepatitis HCV related, genotype 1b, no responder to interferon-alpha therapy.

Alanine Transaminase↗
PubMed1997

Expression of adhesion molecules and functional stimulation in human neutrophils: modulation by GM-CSF and role of the Bcr gene.

Although devoid of proliferative capacity, polymorphonuclear neutrophils (PMN) express receptors for haemopoietic growth factors and need growth factors for survival and functional stimulation. This study showed that in vitro treatment of human PMN with GM-CSF for up to 48 h increases cell surface expression of the beta 2-integrin molecules CD11b/CD18 and CD11c/CD18 and of the receptor for the chemotactic peptide fMLP. Such modifications are usually expression of PMN activation. PMN treated with GM-CSF also displayed increased phagocytosis of latex particles and enhanced oxidative burst and superoxide anion release. Since integrins mediate PMN adhesion to endothelium, homotypic adhesion, chemotaxis/phagocytosis and the triggering of respiratory burst, our results suggested that functional stimulation of PMN persisted following prolonged exposure of PMN to growth factors and that it was not a temporary phenomenon which lasted only for the first 12-24 h of treatment. We also used oligonucleotides antisense to the Bcr gene mRNA to inhibit expression of the gene and evaluate its function in PMN, following the recent observation that PMN from Bcr-null mutant mice produced increased amounts of reactive oxygen metabolites upon activation. The antisense oligonucleotides had no effect on the parameters investigated. This may indicate that increased production of O2 by neutrophils in which the Bcr gene is not expressed requires either that gene expression is absent in the earlier stages of myeloid differentiation/maturation, so that when inhibition occurs in the terminally differentiated neutrophils their functional status is no longer influenced, or that the residual low-level expression of the gene which may be present in the antisense-treated cells is sufficient to provide a normal response to stimulation.

Antibodies, Monoclonal↗
PubMed1997

Increased expression of CD11b/CD18 on phagocytes in ischaemic disease: a bridge between inflammation and coagulation.

The aim of this study was to assess the expression of CD11b/CD18 integrin adhesion molecules on the phagocytes of patients with ischaemic diseases, and to evaluate the concentration of soluble adhesion molecules that are released from endothelium (sICAM-1) and from phagocytes (sL-selectin). A total of 370 patients were enrolled: 120 with coronary artery disease (CAD); 50 with peripheral artery occlusive disease (PAOD); and 200 control subjects with no clinical manifestations of ischaemic disease. CD11b/CD18 integrin was detected by flow cytometry, whereas sL-selectin and sICAM-1 concentrations were detected using a sandwich-type immunoassay. CD11b/CD18 integrin expression was found to be higher in the patients with ischaemic disease than in the control subjects (P < 0.001). The PAOD patients had higher values of CD11b/CD18 integrin than the CAD ones (P < 0.01). The concentration of soluble adhesion molecules did not show any significant differences within the three groups (P = NS). The high expression of CD11b/CD18 integrin in ischaemic disease patients may depend on the increased, but probably stable, cytokine network that has been demonstrated to occur in chronic ischaemic diseases: the difference observed between PAOD and CAD patients could be the consequence of higher inflammatory activation probably resulting from the greater extent of the atherosclerotic process in PAOD, or of the more localized ischaemic area in CAD patients. CD11b/CD18 can therefore be considered a marker of chronic phagocyte activation during ischaemic disease. On the other hand, sICAM and sL-selectin concentrations were found to be within the normal range; they have recently been considered as a marker for acute ischaemic events and acute inflammatory process activation. Our results confirm that in uncomplicated atherosclerosis no acute inflammatory process activation should occur.

Blood Coagulation↗
PubMed1997

Carbamazepine affects neutrophil function through an action on peripheral benzodiazepine receptors.

The aims of this study were to assess the possible role of peripheral benzodiazepine receptors (pBZrs)1 in mediating the in vitro effects of carbamazepine (CBZ) on some neutrophil functions in healthy volunteers and to investigate neutrophil function and pBZr expression in patients with epilepsia on CBZ monotherapy for at least 1 year. In vitro CBZ (42-168 microM) concentration-dependently inhibited chemotaxis induced by N-formyl-methionyl-leucyl-phenylalanine (FMLP) or lipopolysaccharide (LPS)-activated human serum. CBZ did not affect random migration, phagocytosis index, phagocytosis frequency, NBT reduction frequency, C. albicans lethality index and resting superoxide production. The pBZr antagonist PK 11195 (1 microM, per se ineffective) reversed the inhibitory effect of CBZ on chemotaxis induced by endotoxin-activated serum or FMLP. The pBZr agonist Ro 5-4864 (10-100 microM) mimicked the effect of CBZ on chemotaxis induced by endotoxin-activated serum or FMLP and had no effect on the other parameters. Neutrophils from epileptic patients on chronic CBZ monotherapy had impaired FMLP- and serum-induced chemotaxis and enhanced expression of pBZrs on neutrophils. These data strongly suggest an involvement of pBZrs in mediating the in vitro effects of CBZ on chemotaxis; furthermore, impairment of the same neutrophil function parameters and overexpression of pBZrs in patients are consistent with the hypothesis of an in vivo interaction of CBZ with pBZrs.

Adolescent↗
PubMed1997

Meningeal carcinomatosis in patient with esophagus adenocarcinoma.

Meningeal carcinomatosis (MC) is an uncommon from of metastasis of solid tumors. We reported a clinical case of a woman with esophagus adenocarcinoma that a few months after surgical operation, presented episodes of vomiting, nausea, hypertension, mental change, unconsiousness; A contrast-enhanced CT of the brain revealed an "area of enhancement in the caudate nucleus" and cerebrospinal fluid cytologic studies evidenced the presence of carcinomatous cells. The clinical state of the patient deteriorated and she died a few days later. Autopsy confirmed meningeal carcinomatosis without parenchymal involvement.

Adenocarcinoma↗
PubMed1996

Expression of neutrophil and monocyte CD11B/CD18 adhesion molecules at different sites of the coronary tree in unstable angina pectoris.

To assess the site of leukocyte activation in unstable angina, the expression of neutrophil and monocyte CD11B/CD18 adhesion molecules in 26 patients was measured from blood samples taken from the coronary ostium, the coronary sinus, and the coronary artery just distal to the culprit lesion (postobstructive chamber). CD11B/CD18 adhesion molecules detected by direct immunofluorescence evaluated by flow cytometry were significantly higher in the coronary sinus blood than in both the coronary ostium and the postobstructive chamber blood, suggesting that leukocyte activation takes place at the microcirculatory interface with the injured myocardium, probably as the result of short but repeated episodes of myocardial ischemia.

Adult↗
PubMed1996

Iloprost effects on phagocytes in patients suffering from ischaemic diseases: in vivo evidence for down-regulation of alpha M beta 2 integrin.

This study has been designed to demonstrate the in vivo effects of iloprost therapy on expression of adhesion molecules on phagocytes. Sixty patients suffering from peripheral arterial occlusive disease (PAOD) and/or from skin ulcers due to secondary progressive systemic sclerosis (PSS) were enrolled in a double-blind controlled parallel study. Thirty patients (group I) underwent iloprost infusion and 30 patients (group II) were treated with aspirin. Clinical assessment and measurement of phagocyte activation in vivo, using quantitative flow cytometry, were performed on entry and after 6 h on the first day of therapy. After 3 months of therapy, complete healing of all cutaneous lesions was observed in 84% of the patients treated with iloprost compared with the control patients (P < 0.001). Neutrophils and monocytes of PAOD and PSS patients showed a significant decrease in the expression of the alpha M beta 2 integrin adhesion receptor after 6 h of iloprost infusion. Neutrophils and monocytes released a lower amount of anion superoxide (O2-) after 6 h of iloprost treatment. These data confirm other clinical observations but demonstrate that in vivo this drug modifies the expression of the alpha M beta 2 integrin of phagocytes that has a key role in leukocyte-endothelium interactions in cases of inflammation and thrombosis.

Adult↗
PubMed1996

Granulocyte dysplasia and dysfunction, and CD11/CD18 defects in myelodysplastic syndromes.

In myelodysplastic syndromes (MDS), dysplastic changes in neutrophils are a common feature reflecting the total degree of bone marrow dysplasia. Furthermore, granulocyte function is abnormal, so that a high risk of life-threatening infections has been documented. In this review we shall focus on the defects of both granulocytes and their CD11b/CD18 glycoprotein complex, which regulate granulocyte adherence, locomotion, diapedesis and migration into inflammatory sites, in patients suffering from primary MDS. The defective surface membrane glycoprotein expression of myelodysplastic phagocytes is not only a useful diagnostic tool, but also a powerful prognostic one, since MDS patients with such defects present both an increased susceptibility to infections and a decreased survival. Moreover, the administration of colony-stimulating factors is known to be able to elicit long-lasting improvement in neutrophil count, CD11b/CD18 expression and function, marrow myeloid maturation, and possibly to decrease bacterial infections in MDS patients.

CD11 Antigens↗
PubMed1996

[Job syndrome (hyper-IgE) and hypo-IgA. A rare association of immunodeficiencies].

Job' syndrome and IgA immunodeficiency are a rare dysfunction of the immune system. In this work, we reported a case of a young woman who had recurrent episodes of bacterial infections in the urinary tract and genital, generalized erythematous eczematous patches and stomatitis of oral mucosa and fever. During the hospitalization, laboratory data showed high immunoglobulin IgE and low IgA levels. The T-lymphocyte presented a reduction of CD8+ cells. Tests of granulocyte function have showed a global deficit in the in vitro and in vivo chemotaxis. The correlation between these two clinic conditions is not completely clarified but it is possible to hypothesize that CD8+ lymphocytes produce an inhibition factor of chemotaxis. Job' syndrome is characterized by a selective reduction of CD8+ cells subpopulation which have an immunoregulatory function on the production of IgE by plasmacells. In the ipoIgA, an intrinsic inability of B-IgA cells to proliferate and to differentiate produce a defect in the IgA production. In these two clinic disorders there is an effective dysfunction of immune system. It is possible to hypothesize that an effective defect of CD8+ cells and an immaturity of B-cells may coexist in our patient. That justifies an abnormal production of Ig and a defect in granulocyte chemotaxis.

Adult↗