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Biomedical subjects

L Peruzzi

Publications and source records attributed to L Peruzzi.

At least 37 records · Page 2Linked to original sources
PubMed1995

Macromolecular IgA and abnormal IgA reactivity in sera from children with IgA nephropathy. Italian Collaborative Paediatric IgA Nephropathy Study.

This multicenter study investigated the characteristics of circulating IgA molecules in 77 children: 42 had primary IgA nephropathy (IgAN), 20 were non-IgA glomerulonephritides (CGN) and 15 had urological problems (U). Fifteen assays were employed including the detection of macromolecular IgA [IgA immune complexes (IgAIC) by the conglutinin (K) assay, heavy molecular weight IgA in 2.5% polyethylene glycol (PEG), mixed IgA/IgGIC (Jacalin assay), IgA-Fibronectin (IgA-F) aggregates]IgA antibodies to alimentary antigens (gliadin, glycgli, glutein, ovalbumin, bovine serum albumin) and IgA binding to mesangial antigens (fibronectin, laminin, type IV collagen) or polycations (poly-L-lysine). Total IgA and IgA reacting with jacalin, supposed to bear an altered galactosylation, were measured as well. Mean levels of each kind of macromolecular IgA were significantly increased in children with IgAN in comparison to U disease (K-IgAIC p < 0.05, PEG-IgAIC p < 0.01, IgA/IgGIC p < 0.004, IgA-F aggregates p < 0.0003). However, IgA-F were the only macromolecular IgA significantly higher in IgAN than in CGN (p < 0.0005). IgA-F aggregates did not correlate with any urinary sign of activity, while K-IgAIC data were significantly related with microscopic hematuria (p < 0.05) and past history of gross hematuria (p < 0.02). Children with IgAN had mean levels of IgA reacting with the lectinic fractions of gliadin significantly higher than CGN (p < 0.01) and U groups (p < 0.003). IgAN displayed an enhanced production of IgA reacting with mesangial matrix components vs CGN (p < 0.03) and U (p < 0.0003) groups and showed altered interactions with positively charged molecules (poly-L-Lysine, p < 0.01) and carbohydrate residues (jacalin p < 0.05). In IgAN there is an increased circulation of altered IgA favouring the formation of macromolecular IgA, including true IgAIC or IgA aggregated by carbohydrate interactions. The affinity for the mesangial matrix glycoproteins and for the mesangial area electrical charge might further enhance the trapping and deposition of the immune material containing IgA. IgA-F aggregates seem to be a marker of this event, while complement binding molecules in IgAIC correspond to the hematuric manifestation of the nephritogenic process.

Adolescent↗
PubMed1994

Functional consequences of the binding of gliadin to cultured rat mesangial cells: bridging immunoglobulin A to cells and modulation of eicosanoid synthesis and altered cytokine production.

Oral immunization with gliadin (GLI) can induce immunoglobulin A mesangial deposits (IgA nephropathy [IgAN]) in mice. A role for GLI in human IgAN has been inferred from an association with celiac disease, increased serum anti-GLI IgA in patients with IgAN, and benefit from a gluten-free diet observed in some IgAN patients. These effects might be due to the antigenic or lectinic properties of GLI. The aim of our study was to investigate whether GLI binding to glycosylated residues (ie, lectinic activity) favors binding of GLI to cultured rat mesangial cells, bridging IgA macromolecules. We also sought to determine whether GLI binding alters mesangial cell function. Gliadin binds to rat mesangial cells in the third and fourth passages, as determined by immunofluorescence. Gliadin binding is inhibited by co-incubation with 1 mol/L N-acetyl-D-glucosamine and 1 mol/L alpha-D-mannose, sugars competitive for this lectinic bond. Quantification by biotinylated GLI revealed a significant dose-dependent binding of GLI (P < 0.001) inhibited by N-acetyl-D-glucosamine (P < 0.05). Some saccharolytic enzymes, like invertase, modify the cell surface to decrease GLI binding (P < 0.02). In addition, GLI promoted the binding of purified mouse polymeric IgA to mesangial cells. The binding of GLI to mesangial cells modulates arachidonic acid metabolism by cultured mesangial cells, significantly inhibiting prostaglandin E2 production (P < 0.02), increasing synthesis of thromboxane B2 (P < 0.01) and tumor necrosis factor (P < 0.001), but not interleukin-1 beta. These responses were abrogated by co-incubation with N-acetyl-D-glucosamine and/or pretreatment with invertase. Non-immune binding of an environmental alimentary lectin, GLI, to mesangial cells in culture might favor the binding of IgA and IgAIC to mesangial cells, enhancing both IgA mesangial trapping and in situ IgA deposit formation. This could occur via GLI-specific antibodies or by virtue of the binding of nonspecific IgA on a lectinic basis, or both. Moreover, related changes in eicosanoid synthesis might stimulate mesangial cell growth and mesangial matrix production, together with mesangial cell contraction, contributing to the pathogenesis of IgAN.

Animals↗
PubMed1994

[Optimization of the treatment of idiopathic nephrotic syndrome in children].

From 1981 to 1992, 81 children affected by idiopathic nephrotic syndrome were treated in our Division. The majority were males (74%), with mean age at diagnosis of 4.8 (0-14)) years. They had a mean follow-up of 5.7 (0.5-11) years. The renal function at diagnosis was normal in all cases, proteinuria was selective in 86.4% of the cases. 28 children with somehow atypical behaviour underwent renal biopsy. In this negatively selected group the more frequent histologic forms were focal segmental glomerular sclerosis (33.5%), minimal change disease (37.4%), IgM mesangial glomerulonephritis (16.6%), membranous nephropathy (12.5%). First choice drug was in all cases prednisone. In the last years the trend for steroid therapy was to adopt long protocols (16 weeks), with a total dose of 105-133 mg/kg per therapeutic cycle. About 90% of children had a favourable response to steroids, but half of them were frequent relapser. In these cases the long term stable remission was obtained with steroids alone in 10.8% of the cases, with the association of cyclophosphamide in 62%. In a minor fraction and in the steroid resistant (13.6% of the total cases) levamisol and cyclosporin were also adopted. 2.4% of the cases progressed to end stage chronic renal failure. Most of the steroid sensitive children were in remission after 3-4 years of disease, only 6% relapsed more than 5 years after diagnosis.

Adolescent↗
PubMed1994

[IgA serology in idiopathic IgA deposit nephropathy in children].

It is generally thought that in primary IgA nephropathy (IgAN) an altered immune response favours high levels of serum IgA directed against environmental or mesangial antigens (Ag) leading to circulating IgA containing immune complexes (IgAIC). The aim of this multicenter collaborative study was to evaluate some of the IgA immunologic abnormalities in children with IgAN. We investigated 42 children with biopsy-proved IgAN, 21 children with non-IgA glomerulonephritides (CD) and 15 with previous urologic disorders without any evidence of immunologic disease (U). The following methods were used: detection of macromolecular IgA (IgAIC by the conglutinin solid-phase assay, heavy MW IgA measured in 2.5% polyethylene glycol precipitate, IgA-fibronectin aggregates, mixed IgA-IgGIC); serum levels of IgA to alimentary Ags (gliadin, glyc-gli, ovalbumin, bovine serum albumin) and mesangial Ags (fibronectin, laminin, type IV collagen) and reactivity of IgA with the lectin jacalin. In children affected with IgAN serum levels of macromolecular IgA were significantly higher in comparison to U group (p < 0.05-p < 0.0005). IgA-fibronectin aggregates only were significantly higher also than CD group (p < 0.0005). Mean levels of antigliadin IgA were significantly higher in IgAN than in controls (CD p < 0.01 and U p < 0.03) and similar data were found for IgA to mesangial matrix (laminin and fibronectin), which were significantly greater in IgAN than in CD and U (p < 0.01-p < 0.0002). Serum IgA in children with IgAN showed a greater affinity for both polycations and glycosylated molecules. Children affected by IgAN present abnormalities in serum IgA similar to those observed in adults with the same disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Angiotensin II local hyperreactivity in the progression of IgA nephropathy.

Immunologic and hemodynamic factors are likely to work in synergism in the progression of immunoglobulin A nephropathy (IgAN) toward sclerosis. The local activation of the renin-angiotensin system may be one the most relevant mechanisms. We investigated the hemodynamic effects of the acute administration of angiotensin-converting enzyme inhibitor (ACEI) (captopril 50 mg). The glomerular filtration rate (GFR) and the effective renal plasma flow (ERPF) were measured by 51Cr-EDTA and 125I hippurate clearances. The correspondent filtration fractions (FFs) in basal conditions and after administration of ACEI were calculated, then the changes in FF (delta FF and % delta FF) were determined. We studied 27 IgAN patients. Eighteen patients had normal renal function (GFR, 112 +/- 19 mL/min/1.73 m2) and nine had moderate renal impairment (GFR, 54 +/- 13 mL/min/1.73 m2). Sixteen patients had proteinuria > or = 0.5 g/d. In addition, 12 glomerulonephritis control cases and eight healthy subjects were investigated. After the administration of ACEI in healthy subjects we observed slight modifications in the GFR, a significant increase in the ERPF (P < 0.005), and a significant decrease in FF (P < 0.04). Similarly, in IgAN patients with normal renal function the GFR increased slightly, the ERPF increased significantly (P < 0.01), and there was a decrease in FF (P < 0.01). The delta FF and % delta FF values were not significantly different from those found in the controls. In patients with initial renal failure GFR remained unchanged, ERPF increased significantly (P < 0.005), and FF significantly decreased (P < 0.004). However, the changes in delta FF and % delta FF were significantly greater than those found in healthy controls (P < 0.01) and in IgAN patients with normal renal function (P < 0.001). IgAN patients with proteinuria levels > or = 0.5 g/d showed greater changes in delta FF and % delta FF after the administration of ACEI than patients with proteinuria levels lower than 0.5 g/d (P < 0.003 and P < 0.04, respectively) or proteinuric control cases (P < 0.05 and P < 0.01, respectively). This different response in proteinuric and nonproteinuric patients was evident even when the analysis was limited to the subgroup of IgAN patients with normal renal function. The decrease in FF consequent to an increase in the ERPF after the administration of ACEI suggests a local hyperactivity of the renin-angiotensin system in some cases of IgAN.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1993

Glomerular permselectivity to macromolecules in reflux nephropathy: microalbuminuria during acute hyperfiltration due to aminoacid infusion.

Reflux nephropathy is an important cause of chronic renal failure in children. After the parenchymal scar, the progression is thought to be mediated by glomerular hypertension in remnant nephrons resulting in modifications in permselectivity to macromolecules. Proteinuria correlates with a progressive course. The glomerular permselectivity to macromolecules in basal conditions and after acute hemodynamic stress was investigated in 28 children whose bilateral vesico-ureteric reflux (VUR) had been previously surgically corrected (meanly 5.6 years before) and with normal creatinine clearance (CrCl). Bilateral renal scarring (0 to 8 scale for both kidneys) was 4.3 +/- 1.6. Albuminuria (UAE) was evaluated in basal conditions and under acute hyperfiltration induced by amino acid (Aa) infusion. After isotonic saline at 310 ml/hour/1.73 m2, 6 mg/kg/min of Aa were infused for 2 hrs. UAE was significantly higher than controls in basal conditions (p < 0.01), and further increased after Aa infusion (p < 0.02). Microalbuminuria was detectable in 53.5% of the children in basal conditions and in 64.3% after Aa. Also urinary beta 2 microglobulin significantly increased at the end of the test (p < 0.001). CrCl significantly increased at the first hour (p < 0.05). Children with severe renal parenchymal scarring had greater UAE (p < 0.01) and beta 2M (p < 0.02) values after provocative test than those with mild renal damage. In 8 children GFR and ERPF were measured by means of inulin and p-hippurate clearance respectively. The variations in UAE during Aa infusion were significantly correlated with GFR dynamics (p < 0.05) while they were not influenced by ERPF modifications.(ABSTRACT TRUNCATED AT 250 WORDS)

Albuminuria↗
PubMed1993

Cytokine mRNA expression by cultured rat mesangial cells after contact with environmental lectins.

We previously demonstrated that gliadin, a lectinic component of gluten, induces IgA mesangial deposits in orally immunized mice, binds in vitro polymeric IgA and cultured rat mesangial cells modulating their arachidonic acid metabolism. We investigated the effects of gliadin and other environmental lectins on some mesangial cell functions, including synthesis and release of cytokines and lipid mediators. Several lectins, particularly gliadin, affected the mRNA expression of c-myc and c-fos, two proto-oncogenes involved in the transcriptional enhancement of the gene cascade, which are markers of cell growth, differentiation and mitosis. Lectins modulated the ability of cultured rat mesangial cells to express mRNA for cytokines involved in the inflammation and in the regulation of the immune response. TNF-alpha and IL-6 mRNA transcription were enhanced by gliadin and other lectins, and TNF release was variably increased. Conversely, IL-1 production was less affected or slightly depressed. PAF production was not detectable while PGE2 was generally reduced and TXB2 enhanced. Gliadin was one of the lectins most active on the mesangial cells, and its effects were reversed by the addition of N-Acetylglucosamine, a sugar specific for some lectinic bindings, suggesting a carbohydrate interaction. The effects of the various lectins were distinct and only partially convergent, ruling out an aspecific mesangial cell activation. These data suggest that lectins might interfere with mesangial cell functions and modify the mesangial cell homeostasis.

Animals↗
PubMed1992

[Anesthesia and central nervous system in carotid surgery].

The Authors, in the debate concerning the most appropriate anesthesiologic treatment in thromboendarterectomy surgery, relate their experience using three different types of general anaesthesia under electroencephalographic monitoring. The results are commented correlating data with some physiopathologic considerations. Carotid surgery, in particular the operation of thromboendarterectomy (TEA), during the last few years has assumed features and frequency typical of a routine procedure. Nevertheless, if from a surgical point of view the criteria of choice of the patients and the surgical techniques have been well standardized, in the anesthesiologic field the discussion between the supporters of the locoregional anaesthesia on one side and of the general anaesthesia on the other side is still open. By this report we mean to bring a contribution to the debate correlating our anesthesiologic files with some physiopathologic notations on the theme.

Aged↗
PubMed1990

CD38 molecule: structural and biochemical analysis on human T lymphocytes, thymocytes, and plasma cells.

The structure of the CD38 molecule has been evaluated by one- and two-dimensional gel analysis and by enzymatic digestions. The source of the Ag was mainly membrane preparations obtained from MLC cells, from normal thymocytes, and from the plasmocytoma line LP-1. Membranes were solubilized in NP-40 and the extracts fractionated by immunoaffinity chromatography [using a specific anti-CD38 antibody (A10 mAb) covalently linked to Sepharose protein A]. The purified Ag migrated as a single chain of Mr = 45,000 not associated with beta 2-microglobulin. Two-dimensional IEF gel electrophoresis revealed five spots (isoelectric point (pI) range: 6.5 to 6.9). After neuraminidase treatment, the mobility of the five polypeptides shifted to a more basic pI. Endoglycosidase-H treatment reduced the Mr of CD38 by 20%, revealing a broader band centered at Mr = 36,000. Treatment of CD38 molecule with V8 Staphylococcus aureus protease yielded a single dominant band at Mr = 38,000 which was still reactive with A10 mAb. The CD38 molecular was trypsin-resistant in both denatured or native conditions. These results clearly show the glycoprotein nature of CD38 molecule, which includes 2 to 4 N-linked oligosaccharide chains containing sialic acid residues. Furthermore, the present data indicate that the CD38 molecule does not display an apparent biochemical polymorphism among the different CD38+ cells or lines.

ADP-ribosyl Cyclase↗
PubMed1990

Characterization by monoclonal antibody of a highly conserved antigenic determinant expressed on human platelet membranes and intermediate filament type III.

The murine monoclonal antibody (MoAb) CB21, raised after immunization with sonicated extracts of human platelets, has been shown to react with a line-restricted surface molecule and also a cytoplasmic structure displaying no restriction in terms of lineage and species. The surface structure recognized by the CB21 MoAb is exclusively expressed on the surface membrane of human platelets, being undetectable on other cells or lines so far tested. After permeabilization, the majority of the cells and lines tested with the CB21 MoAb displayed strong cytoplasmic reactivity with a constant typical filamentous distribution. Biochemical and morphological analyses showed that the cytoplasmic counterpart recognized by the CB21 MoAb is the intermediate filament type III.

Animals↗
PubMed1989

Microplate selection technique (MPST). A new method for selecting mouse transfectants expressing human gene products.

This paper examines the analytical power of fluorescence activated cell sorting and immunorosetting technique as compared with the newly devised microplate selection technique in identifying transfected murine L cells expressing human surface molecules. The microplate selection technique relies on the mechanical transfer of transfected cells to a terasaki microplate, where an indirect immunofluorescence assay is carried out. It is a simple procedure not requiring costly equipment and with a detection capacity equivalent to that of the fluorescence activated cell sorter. The microplate selection technique proved to be sensitive enough to detect all the transfectants produced during the present study.

Animals↗
PubMed1989

Identification of a new epitope of the 4F2/44D7 molecular complex present on sarcolemma and isolated cardiac fibers.

The murine monoclonal antibody (mAb) CB43, raised against the K-562 erythroleukemia line, reacts with monocytes, tissue macrophages, thymocytes and with all the human lines tested but not with resting lymphocytes, large granular lymphocytes, granulocytes and erythrocytes. However, activated lymphocytes and natural killer cells express the CB43 antigen. Embryonic and fetal fibroblasts are positive, while adult fibroblasts are negative. Proximal convoluted tubules in kidney, epithelial cells in esophagus and breast, and sarcolemma in skeletal muscle are reactive with mAb CB43. This antibody can also bind to isolated guinea pig cardiac myocytes, and, furthermore, can induce a transient inotropic effect on isolated atria. The reactivity with different cell and tissue types and the functional effects of the CB43 mAb were reminiscent of the 4F2/44D7 antibodies, shown previously to block Na+/Ca2+ exchange in heart and skeletal muscle. Co-immunoprecipitation studies with CB43 and 44D7 mAb, using radiolabeled Daudi cells, revealed co-migration of polypeptides of 87 and 38 kDa. However, the epitope recognized by CB43 is not present on the human heavy chain which bears the 44D7/4F2 epitope as demonstrated by the lack of reactivity of CB43 mAb with mouse L cells transfected with the 4F2 heavy chain gene. Thus, CB43 represents a newly described epitope present on the human light chain or dependent on the conformation of the human dimer.

Adult↗
PubMed1989

Generation and selection of monoclonal antibodies identifying surface molecules discriminating between fetal and adult fibroblasts.

The present report describes the reactivity of two murine monoclonal antibodies, i.e., CB11 and CB43, the first obtained by using embryonic material as immunizer and the second elicited against a human cell line. These reagents recognize two distinct molecules marking a peculiar differentiation stage on fetal/embryonic fibroblasts. The first structure is a single chain of 14.5 kd, the second one a heterodimer of 40-80 kd. Even if these reagents are not strictly fibroblast restricted, translineage expression does not diminish the medical relevance of the reagents; in fact, they may have application in prenatal diagnostics and amniocentesis testing, in which it is necessary to discriminate between fetal and maternal cells.

Adult↗
PubMedDate not supplied

Growth hormone secretion in Prader-Willi syndrome.

Prader-Willi Syndrome (PWS) is a multisystem defect characterized by obesity, hypogenitalism and short stature for genetic background. Low GH serum levels have been found in patients with PWS and were related to a hypothalamic-pituitary dysfunction. We studied spontaneous nocturnal GH secretion and GH-response to provocative tests in five patients affected by PWS. We observed in three of them (Group A) abnormally low GH and IGF-1 serum levels. In the other two patients (Group B) GH secretion and IGF-1 serum levels were normal. In all patients no thyroid dysfunction was observed. These data might suggest the presence of two different subgroups of patients affected by PWS, from an endocrinological point of view. An abnormally low GH secretion would be evident only in a subgroup of patients, which appears to be normal in the remaining patients. This casistic is small in number, but if our data will be confirmed by more extensive studies it may be possible to identify a specific population of PWS patients who could benefit from recombinant GH-therapy.

Adolescent↗