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Biomedical subjects

D Gennari

Publications and source records attributed to D Gennari.

9 recordsLinked to original sources

1D dynamic beam modulation: methods to counteract inertia effects.

Dynamic modulation can be affected by inaccuracies when the required acceleration is larger than the highest allowed by the mechanical characteristics of the whole apparatus. In this study, inertia effects have been investigated with regard to the single absorber 1D modulation, analysing primarily how the acceleration performed by the modulating system affects the realization of 'single absorber' fluence profiles and the type of correction which could be devised. The observed percentage deviations from desired modulation at the lowest fluence coordinate of single minimum fluence profiles, when no correction is applied, were almost negligible for 'easy' modulations of the incident fluence (i.e. slow gradients); deviations became increasingly relevant as the moving absorber executed steeper gradients (a 17.6% higher dose being delivered in the minimum position when a 0.2 modulation is required). By applying the proposed corrections, the single absorber performances were improved to a satisfactory level, with a maximum deviation from desired modulation in the minima within 1.6%.

Algorithms↗

Phenotypic profile and functional characteristics of human gamma and delta T cells during acute toxoplasmosis.

Gamma and delta (gamma delta) T-cell receptor lymphocytes are increased during acute toxoplasmosis. These cells are BB3+ CD45RO+ CD8-. Purified gamma delta T cells failed to proliferate in response to Toxoplasma gondii antigen (stimulation index, 1.4 +/- 0.6) but were responsive to phytohemagglutinin stimulation (stimulation index, 20.8 +/- 1.9). Natural-killer-like cytotoxicity was strongly acquired only after in vitro culture of purified gamma delta T cells with recombinant interleukin 2 (40% +/- 7% specific lysis). Our data show that gamma delta T-cell receptor T cells with a peculiar phenotype are increased during human acute T. gondii infection.

Acute Disease↗

A subset of gamma delta lymphocytes is increased during HIV-1 infection.

The gamma delta T cell receptor (TcR) lymphocytes constitute 3-10% of human peripheral blood lymphocytes. Only a very small fraction of these cells is recognized by the delta TCS1 monoclonal antibody, directed against the V delta 1 chain of the receptor. We describe the immunological, virological and clinical data of a small group of seropositive subjects having high levels of gamma delta TcR T cells in the peripheral blood. Our flow cytometric studies show that most of these cells belong to the delta TCS1+ (V delta 1+), CD8 +/- (dim staining) subset. Patients with high gamma delta TcR T cell numbers were not characterized by the presence of an acute (IgM positive) or reactivated (as defined by high IgG titres against early antigen or IgA titres against viral capsidic antigen) Epstein-Barr virus infection. Cytomegalovirus infection was excluded by serological assays, and other herpes viral infections were not found after clinical examination. HIV p24 antigenaemia was present in two out of 11 subjects. AIDS patients had very high percentages of gamma delta TcR T cells. Altogether these data show that the selective expansion of delta TCS1+ cells in HIV1 seropositive subjects is not related to some exogenous antigen stimulation, but may be related to peculiar pathologic processes involving the immune system.

Antigens, Differentiation, T-Lymphocyte↗

Phenotypic analysis of a CD2- CD3+ T cell receptor gamma delta lymphocyte subset.

We have identified, in a patient with atopic dermatitis, a consistent population of peripheral blood lymphocytes expressing a CD3+ gamma/delta TCR complex, while being unreactive with CD2. Further immunofluorescence studies showed that these cells almost completely co-express CD29 and CD45RA and have high membrane levels of CD11a compared to the alpha/beta TCR T cells. Neither a genetic influence nor an acute or reactivated herpesvirus infection were found to be related to the expanded gamma/delta T-cell subpopulation. Our data confirm the previous observations regarding the presence in the peripheral blood of an expanded gamma/delta TCR, CD2- subset and show that these cells have a peculiar phenotypic profile. The reasons for this expansion are, however, still unknown.

Adult↗

Gamma delta T cell receptor-bearing lymphocytes during Epstein-Barr virus infection.

Lymphocytes bearing gamma delta T cell receptors (TCR) constitute a minor subpopulation of human peripheral blood lymphocytes. Their role and function during microbial infections are largely unknown. In 10 patients with Epstein-Barr virus-induced infectious mononucleosis, the gamma delta TCR-expressing T cell population expanded during the acute phase. These cells were largely delta TCS1-, CD4-, and CD8- but expressed activation antigens such as human leukocyte antigen-DR and CD38. The convalescent phase of infectious mononucleosis was characterized by a relative persistence of gamma delta T cells. Together these data suggest a possible role of gamma delta T cells in the control of primary Epstein-Barr virus infection in humans.

Acute Disease↗

CD8 lymphocytes during Epstein Barr virus (EBV) infection: A CD29 positive population is expanded in acute infectious mononucleosis.

The expression of phenotypic markers on CD4 and CD8 lymphocytes during the acute and convalescent phases of Epstein Barr virus (EBV) induced infectious mononucleosis was examined by two colour flow cytometry. Activated CD8 cells constitute the major population increased during acute infectious mononucleosis; in this phase we observed a preferential expansion of the CD8 CD29+ compared to the CD8 CD45RA+ cells. Serum soluble CD8 levels were also raised during the acute phase and a correlation with CD8 CD38+ and CD8 CD29+ cell numbers was found. The convalescent phase of infectious mononucleosis was characterized by a progressive return of CD8 subset and of soluble CD8 to baseline normal values. These results demonstrate that acute EBV infection induces the expansion of a CD8 subset with peculiar surface antigenic profile.

Acute Disease↗