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Biomedical subjects

E Maggi

Publications and source records attributed to E Maggi.

At least 91 records · Page 5Linked to original sources
PubMed1996

[The procedures and results of a quality control program in mammography carried out on a regional basis].

In 1990 the region of Tuscany instituted a quality control program for mammography, in order to check the working conditions of mammography centers in the region, to investigate the feasibility of applying some working standards in line with European recommendations, and to promote the training of personnel. The program involves the following: a test of newly acquired mammographic equipment to establish that it meets the required standards; an annual test of generators, X-ray beams, grid, AEC, screen-film system, film processing, dose and image quality; daily test (phantom radiography and film sensitometry) performed by the personnel of each mammographic Unit; and a sustained advisory service for the technical problems occurring between checks. Thirty-nine of 57 centers participated on a voluntary basis, and 135 checks were performed annually. The results of the program show a performance below the recommended standard in relation to AEC, film sensitometry and the adequacy of lights in dark rooms in 40%, 50% and 63%, respectively, of the centers. Entrance exposure was over 1500 mR, with a maximum value of 3450 mR, in 6 cases in the first round. 5 cases in second, and only 1 case in the third. In general, the results are slightly improving, but mammography optimization is still a long way off. It is necessary to carry out suitable programs for quality control in mammography on a regional basis and to establish precise guidelines for individual mammographic Units to follow in order to meet the European standards.

Breast↗
PubMed1996

Carotid intima-media thickening and in vivo LDL oxidation in patients with essential hypertension.

Low density lipoproteins (LDL) from hypertensive patients are more prone to in vitro oxidation and undergo a more pronounced oxidation in vivo. Due to the pro-atherogenic activity of oxidatively modified LDL, the correlation between the carotid intima-media thickening (IMT) and the markers of in vivo LDL oxidation was investigated in hypertensive patients. A cross-sectional study on 101 normocholesterolemic patients with newly diagnosed and untreated essential hypertension was performed. The occurrence of in vivo LDL oxidation was evaluated by measuring the titers of autoantibodies against Cu(2+)-oxidised LDL (oxLDL) and malondialdehyde-derivatised LDL (MDA-LDL). The extent and degree of atherosclerosis and the IMT were measured by means of carotid and femoral ultrasonography with a duplex scanner equipped with a high resolution probe. We did not find significant correlations between in vivo LDL oxidation parameters and the extent of atherosclerotic lesion in the entire group of hypertensive patients. However, a significant direct correlation was detected between the carotid IMT and the titer of autoantibodies against both oxLDL and MDA-LDL in hypertensive patients without advanced atherosclerotic plaques. The results obtained support the hypothesis that enhanced LDL oxidation may be one of the pathophysiological events related to the formation and progression of early atherosclerotic lesions (IMT) in carotid arteries of hypertensive patients.

Adult↗
PubMed1995

[Oxidation of low-density lipoproteins. Correlation between reduced resistance in vitro and increased oxidation in vivo].

OBJECTIVES: The oxidation of low-density lipoproteins has been recently proposed as one of the critical factors in promoting atherogenesis. This process results from the balance between the prooxidant stimuli and the endogenous antioxidants present in LDL and strictly depends on the concentration of oxidizable substrates, namely unsaturated fatty acids. METHODS: Twelve male hypertriglyceridaemic patients were investigated before and after oral supplementation with omega-3 polyunsaturated fatty acids (PUFA) and compared with eighteen untreated healthy matched control subjects. The plasma lipid profile was measured in all patients. LDL oxidation was evaluated as both the susceptibility to in vitro oxidation and the presence of plasma anti-oxidized LDL antibodies (as a marker for in vivo oxidation). RESULTS: Omega-3-fatty acid supplementation caused a significant reduction in plasma triglyceride level (267 +/- 38 vs 375 +/- 33 mg/dl, p < 0.01) and decreased the resistance of LDL to oxidation as revealed by an early and accelerated generation of conjugated dienes following exposure to CuSO4 (105.3 +/- 7 vs 133 +/- 9.3 min, p < 0.01). Moreover, the concentration of the antioxidant vitamin E in LDL was slightly but significantly decreased at the end of the treatment (2.59 +/- 0.19 vs 2.89 +/- 0.17 nmol/mg LDL, p < 0.05), but its efficiency in preventing LDL oxidation was unaltered. Furthermore, a marked increase of the plasma anti-oxidised LDL antibody titre was found in nearly all patients at the end of the treatment (2.08 +/- 0.48 vs 1.37 +/- 0.2 anti-oxidised/anti-native LDL antibody ratio, p < 0.001). CONCLUSION: These results indicate that PUFA supplementation decreases the resistance of LDL to in vitro oxidation and that this decreased resistance is accompanied by an enhanced LDL oxidation in vivo.

Adult↗
PubMed1995

Polyinosinic acid: polycytidylic acid promotes T helper type 1-specific immune responses by stimulating macrophage production of interferon-alpha and interleukin-12.

The effects exerted on the development in vitro of Dermatophagoides pteronyssinus group I (Der p I)-specific T cell lines and T cell clones by addition of polyinosinic acid: polycytidylic acid (poly I:C) in lymphocyte bulk culture were examined. Der p I-specific T cell lines generated in presence of poly I:C exhibited reduced ability to produce interleukin (IL)-4 and IL-5 and developed into Der p I-specific CD4+ T cell clones showing a T helper (Th) type 0 or Th1, instead of Th0/Th2 cytokine profile. This effect was prevented by addition to lymphocyte bulk cultures of a mixture of antibodies specific for interferon (IFN)-alpha and IL-12, whereas the addition of anti-IFN-alpha or anti-IL-12 antibody alone was uneffective. Poly I:C also showed the ability to stimulate the production of noticeable amounts of both IFN-alpha and IL-12 by human monocytes. Taken together, these data suggest that poly I:C is a Th1-inducing agent whose activity is mediated by its ability to stimulate the production of IFN-alpha and IL-12 by monocytes.

Cells, Cultured↗
PubMed1995

CD30 ligation induces nuclear factor-kappa B activation in human T cell lines.

CD30 is a recently described member of the tumor necrosis factor/nerve growth factor receptor superfamily. In this report, we show that following incubation of L540 cells (Hodgkin's disease-derived, T cell-like, CD30+ cells) with the agonistic anti-CD30 monoclonal antibodies (mAb) M44 and M67, two nuclear factor (NF)-kappa B DNA binding activities were induced in nuclear extracts, as determined in gel retardation assays. The effect of the mAb towards NF-kappa B activation was rapid, as it occurred within 20 min, and was sustained for up to 6 h. By comparison, an isotype-matched antibody had no effect on NF-kappa B activation. Moreover, in human T helper (Th) clones functionally characterized as being of the type 0, type 1 and type 2 (28%, < 1% und 93% CD30+, respectively), the extent of CD30-mediated NF-kappa B activation correlated with the proportion of CD30+ cells. In all cell lines investigated, the NF-kappa B complexes induced following CD30 engagement were shown to contain p50 NF-kappa B1, p65 RelA, and possibly other transcription factors. Collectively, our results demonstrate that nuclear translocation and activation of NF-kappa B rank among the short-term cellular responses elicited following CD30 ligation.

Antibodies, Monoclonal↗
PubMed1995

CD30 and type 2 T helper (Th2) responses.

CD30 is one of the members of the tumor necrosis factor receptor superfamily, originally described as a marker of Reed-Sternberg and Hodgkin's cells in Hodgkin's lymphoma. CD30 appears to be preferentially expressed on, and its soluble form (sCD30) released by, CD4+ and CD8+ T cell clones capable of producing T helper 2 (Th2)-type cytokines. In noneoplastic conditions, CD30+ T cells are barely detectable in vivo; however, a few allergen-specific CD4+CD30+ T cells inducible to the production of Th2-type cytokines could be sorted out from the circulation of allergic subjects after allergen exposure. Moreover, high numbers of CD30+ T cells were found in the lymph node of a patient suffering from Omenn's syndrome, a rare congenital Th2-mediated immunodeficiency disorder. More importantly, high serum levels of sCD30 were observed in some conditions in which a pathogenetic role for Th2 cells has been suggested, such as Omenn's syndrome, atopy, systemic lupus erythematosus, and after infection with measles virus or human immunodeficiency virus. Thus, detection of CD30+ T cells and/or of increased levels of sCD30 may reflect the presence of immune responses or immune alterations characterized by the prevalent activation of Th2-like cells.

HIV Infections↗
PubMed1995

CD30, Th2 cytokines and HIV infection: a complex and fascinating link.

CD30 is a member of the tumor necrosis factor (TNF)/nerve growth factor (NGF) receptor superfamily, and was originally described as a marker of Hodgkin's and Reed-Sternberg cells in Hodgkin's lymphoma. CD30 is preferentially expressed on CD4+ and CD8+ T-cell clones that produce T helper 2 (Th2)-type cytokines, and is also released in a soluble form by these cells. Elevated serum levels of soluble (s)CD30 have been found in some conditions in which a pathogenic role for Th2 cells has been suggested, such as atopy, Omenn's syndrome, systemic lupus erythematosus, as well as following infection with measles virus or human immuno-deficiency virus (HIV). Here, Gianfranco Del Prete and colleagues suggest a complex and fascinating link between the expression and release of CD30, and the immunopathogenesis of HIV infection.

Cytokines↗
PubMed1995

Activation of HIV expression by CD30 triggering in CD4+ T cells from HIV-infected individuals.

CD30 is a member of the tumor necrosis factor receptor superfamily, preferentially expressed by T cells producing type 2 helper (Th2) cytokines, whose ligand (CD30L) has been identified on B cells, activated macrophages, and a subset of activated T cells. We show here that cross-linking CD30 with an agonistic CD30-specific monoclonal antibody, as well as with CD30L+ CD8+ T cell clones or CD30L+ B cells, enhanced HIV replication in CD4+ T cells from HIV-infected individuals, and such a potentiating effect was inhibited by anti-CD30L antibody. The anti-CD30L antibody also exerted a suppressive effect on spontaneous HIV replication occurring in lymph node cells from an HIV-sero-positive patient, showing CD30L expression by both B and CD8+ T lymphocytes. Thus, CD30 triggering by CD30L-expressing cells may plan an important role in the activation of HIV expression from latently infected CD4+ T cells.

B-Lymphocytes↗
PubMed1995

Isolation and characterization of allergen-binding cells from normal and allergic donors.

BACKGROUND: Flow cytometry of the immune system so far has been limited to the analysis of subpopulations according to lineage markers. The cells involved in a particular immune response could not be assayed due to their low frequency. Here we show the potential of antigen-specific high gradient magnetic cell sorting to enrich cells for visualisation in multiparameter cytometry, functional studies and immortalization. OBJECTIVES: The aim of this study was the development of an efficient technology for staining and isolation of antigen-binding cells from human peripheral blood. In particular, allergen-specific cells from normal and allergic donors should be analysed and compared to develop a cellular diagnosis of allergy. STUDY DESIGN: The rare antigen-specific cells were sorted by high-gradient magnetic cell sorting with MACS. Haptenized phospholipase A2 (PLA2), the major allergen of bee venom, or haptenized ParoI, the major allergenic component of Parietaria officinalis, were used as antigens. The cells from normal and allergic donors, binding to the allergen were characterized phenotypically by immuno-fluorescence. Allergen-specific B-cells were immortalized by EBV transformation. RESULTS AND CONCLUSION: Allergen-specific cells can be enriched from blood of both allergic and normal donors to purities of up to 75%, by high gradient magnetic cell sorting. The specificity of labelling with allergen was confirmed by establishing allergen-specific EBV-transformed B-cell lines from the sorted cells. Clear differences exist in the cellular composition of allergen-binding cells from normal compared to allergic donors. In normal donors the allergen-binding cells are B-cells expressing CD19 and CD21. In allergic donors, in addition to allergen-binding B-cells, occurring in about equal absolute numbers as in normal donors, basophilic granulocytes are labeled by allergen. These cells express CD38, CD9 and CD25 on their surface, and stain for IgE.

Allergens↗
PubMed1995

No relationship between skin-infiltrating TH2-like cells and allergen-specific IgE response in atopic dermatitis.

More than 500 CD4+ T-cell clones (TCCs) derived from the skin of eight patients with atopic dermatitis (AD), two patients with nonatopic dermatologic disorders, two patients with allergic rhinitis, and one healthy nonatopic donor were analyzed for both their pattern of cytokine production and their antigen specificity. The proportions of TCCs from patients with AD producing interleukin-4 in response to stimulation with phorbol 12-myristate 13-acetate plus anti-CD3 antibody were higher, whereas the proportions of interferon-gamma--producing TCCs were lower than those of control subjects. In two patients with AD, the majority of TCCs had a TH2/TH0-like phenotype, whereas in six patients with AD a TH1/TH0-like phenotype was prevalent. TCCs with a TH2/TH0-like phenotype were also isolated from the healthy skin of two patients with allergic rhinitis and one nonatopic donor. In contrast, no TH2-like TCCs were derived from the skin of the two patients with dermatologic disorders of nonallergic origin. No unambiguous correlations was found between the proportions of TCCs producing interleukin-4 or interferon-gamma (or of TCCs with TH2- or TH1-like profile) and the level of total serum IgE, suggesting that CD4+ T cells infiltrating the atopic skin do not play a major role in the production of serum IgE antibodies. When TCCs from five patients with AD were examined for their specificity, the proportions of allergen-specific (Dermatophagoides pteronyssinus and Lol p 1) clones were consistently 6% or lower even in patients with high titers of ryegrassor D. pteronyssinus-specific IgE antibodies. Because similar percentages of allergen-specific TCCs were found in skin from two healthy control subjects, the role of aeroallergens in favoring and maintaining skin lesions in patients with AD remains unclear.

Adolescent↗
PubMed1995

Autoantibodies against oxidatively modified low-density lipoproteins in NIDDM.

Diabetes is an independent risk factor in the development of atherosclerosis, although the pathophysiological processes underlying this association are poorly understood. The oxidation of low-density lipoprotein (LDL) is considered a key event in the development and progression of atherosclerosis because it generates molecular epitopes that are more atherogenic than parent LDL. A total of 138 patients suffering from non-insulin-dependent diabetes mellitus (NIDDM) and 80 matched control subjects were investigated. LDL oxidation was evaluated as the presence of autoantibodies against oxidatively modified LDL, since they mirror the in vivo occurrence of oxidative processes. NIDDM patients had an antibody ratio (calculated as the ratio of antibodies against modified versus native LDL) significantly higher than control subjects for Cu(2+)-oxidized LDL (1.88 +/- 0.6 vs. 1.05 +/- 0.3, P < 0.01, for IgG), malondialdehyde-modified LDL (2.54 +/- 0.73 vs. 2.04 +/- 0.11, P < 0.01, for IgG and 3.96 +/- 1.51 vs. 2.90 +/- 0.15, P < 0.01, for IgM), and malondialdehyde-modified human serum albumin (1.79 +/- 0.54 vs. 1.46 +/- 0.1, P < 0.05 for IgG). The possible role played by glycation in sensitizing LDL to oxidation was investigated by measuring autoantibodies against both glycated LDL (glycLDL) and glycoxydated LDL (glycoxLDL). NIDDM patients had an antibody ratio significantly higher than control subjects for anti-glycLDL and anti-glycoxLDL IgG (1.79 +/- 0.38 vs. 1.12 +/- 0.23, P < 0.01 and 2.55 +/- 1.03 vs. 1.39 +/- 0.44, P < 0.01, respectively) but not anti-glycLDL and anti-glycox-LDL IgM.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1995

Presence of autoantibodies against oxidatively modified low-density lipoprotein in essential hypertension: a biochemical signature of an enhanced in vivo low-density lipoprotein oxidation.

OBJECTIVE: We have previously reported that low-density lipoproteins (LDL) isolated from patients with essential hypertension are more susceptible to in vitro oxidation than lipoproteins isolated from normotensive control subjects. In the present study we investigated the occurrence of in vivo LDL oxidation in hypertensive patients. DESIGN: The presence of antioxidatively modified LDL autoantibodies was taken as a suitable index of in vivo LDL oxidation because, after oxidative modifications, LDL express antigenic epitopes that elicit an immune response. The antibody titres were measured in plasma from untreated patients with newly diagnosed essential hypertension. METHODS: An enzyme-linked immunosorbent assay method was employed, using native LDL, Cu(2+)-oxidized LDL and malondialdehyde-derivatized LDL (MDA-LDL) as antigens. Human serum albumin and MDA human serum albumin were also used to monitor cross-reactivity with other oxidized molecules. The antibody titre was expressed as the ratio between anti-modified and anti-native antigen absolute values. RESULTS: The patients with essential hypertension had an antibody ratio significantly higher than control subjects with respect to anti-Cu(2+)-oxidized LDL immunoglobulins G and M, and with respect to anti-MDA-LDL immunoglobulins G and M. A significant positive correlation was found between anti-MDA-LDL and anti-Cu(2+)-oxidized LDL antibody titres. The anti-MDA human serum albumin antibody titre was not different in the two groups of patients. An inverse correlation was detected between the anti-MDA-LDL immunoglobulin M titre and the age of the patients. CONCLUSIONS: The results obtained are consistent with the view that, during the early phases of hypertension development, LDL undergo in vivo oxidation that is mirrored by the generation of autoantibodies against epitopes of oxidized LDL. The oxidation process appears specific for LDL and might be relevant both for the progression of hypertension and for the development of the atherosclerosis that often complicates hypertension itself.

Antibody Specificity↗
PubMed1994

CD30 expression by CD8+ T cells producing type 2 helper cytokines. Evidence for large numbers of CD8+CD30+ T cell clones in human immunodeficiency virus infection.

A large panel of CD8+ T cell clones generated from peripheral blood lymphocytes (PBL) of healthy donors or human immunodeficiency virus (HIV)-infected individuals were assessed for both cytokine secretion profile and CD30 expression and release. The great majority of CD8+ T cell clones generated from healthy individuals showed the ability to produce interferon gamma (IFN-gamma), but not interleukin 4 (IL-4), and none of them either expressed membrane CD30 or released substantial amounts of soluble CD30 (sCD30) in their supernatant. In contrast, high numbers of CD8+ T cell clones generated from HIV-infected individuals, which produced IL-4 (and IL-5) in addition to IFN-gamma or IL-4 (and IL-5) alone, expressed membrane CD30 and released detectable amounts of sCD30 in their supernatants. Indeed, CD30 expression appeared to be positively correlated with the ability of CD8+ T cell clones to produce IL-4 and IL-5 and inversely correlated with their ability to produce IFN-gamma, whereas no correlation between CD30 expression and production of IL-10 was observed. These data suggest that CD30 is a marker for CD8+ T cells that have switched to the production of type 2 helper cytokines.

Acquired Immunodeficiency Syndrome↗
PubMed1994

Th2-like CD8+ T cells showing B cell helper function and reduced cytolytic activity in human immunodeficiency virus type 1 infection.

We analyzed at clonal level the functional profile of circulating or skin-infiltrating T lymphocytes from two individuals infected with the human immunodeficiency virus type 1 (HIV-1), suffering from a Job's-like syndrome (eczematous dermatitis, recurrent skin and sinopulmonary infections, and hypergammaglobulinemia E) and showing virtually no circulating CD4+ T cells. Most of the CD3+ T cell clones generated from both patients were CD4- CD8+ TCR alpha beta +. The others were CD4- CD8- TCR alpha beta + which exhibited reduced mRNA expression for the CD8 molecule or no mRNA expression for either CD4 or CD8 molecules. The great majority of both CD4- CD8+ and CD4- CD8- did not produce interferon (IFN) gamma and exhibited reduced cytolytic activity. Rather, most of them produced large amounts of both interleukin (IL) 4 and IL-5 and provided B cell helper function for IgE synthesis. These data suggest that a switch of cytolytic CD8+ T cells showing a Th1-like cytokine secretion profile to cells that make Th2-type cytokines, exhibit reduced cytolytic potential, and provide B cell helper function can occur in the course of HIV-1 infection. These cells may contribute to the reduced defense against viral infections and intracellular parasites and account for the elevated IgE serum levels, eosinophilia, and the allergic-like clinical manifestations seen in a proportion of HIV-1-infected individuals.

B-Lymphocytes↗