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D Orsini

Publications and source records attributed to D Orsini.

5 recordsLinked to original sources
PubMed2003

Short-term temporal variation in PM2.5 mass and chemical composition during the Atlanta Supersite Experiment, 1999.

Measurements in urban Atlanta of transient aerosol events in which PM2.5 mass concentrations rapidly rise and fall over a period of 3-6 hr are reported. The data are based on new measurement techniques demonstrated at the U.S. Environmental Protection Agency (EPA) Atlanta Supersite Experiment in August 1999. These independent instruments for aerosol chemical speciation of NO3-, SO4(2-), NH4+, and organic and elemental carbon (OC and EC), reconstructed the observed hourly dry PM2.5 mass to within 20% or better. Data from the experiment indicated that transient PM2.5 events were ubiquitous in Atlanta and were typically characterized by a sudden increase of EC (soot) and OC in the early morning or SO4(2-) in the late afternoon. The frequent temporal decoupling of these events provides insights into their origins, suggesting mobile sources in metro Atlanta as the main contributor to early morning PM2.5 and more regionally located point SO2 sources for afternoon PM2.5 events. The transient events may also have health implications. New data suggest that short-term PM2.5 exposures may lead to adverse health effects. Standard integrated filter-based techniques used in PM2.5 compliance monitoring networks and in most past PM2.5 epidemiologic studies collect samples over 24-hr periods and thus are unable to capture these transient events. Moreover, health-effects studies that focus on daily PM2.5 mass alone cannot evaluate the health implications of the unique and variable chemical properties of these episodes.

Aerosols↗
PubMed1993

Reactivity of human gamma delta T cells to staphylococcal enterotoxins: a restricted reaction pattern mediated by two distinct recognition pathways.

Staphylococcal enterotoxins (SEs) are known superantigens for T cells expressing the alpha beta T-cell receptor (TCR). They bind to MHC class II molecules on antigen-presenting cells and can subsequently trigger T-cell responses by binding to V beta-gene products. The reactivity of gamma delta T cells with enterotoxins is less well defined although both proliferative and cytotoxic responses have been described. In the present study we have tested the cytotoxic reactivity of a panel of 41 gamma delta T-cell clones against target cells coated with the enterotoxins SEA, SEB, SEC1, SEC2, SEC3, SED, SEE or TSST. Three reaction patterns were observed with the gamma delta T-cell clones: (1) clones that specifically lysed SEA-coated target cells only; (2) clones that specifically lysed SEE-coated target cells only, and (3) clones that specifically lysed SEA-coated target cells only in the presence of certain human sera. The presence of SEA-specific antibodies in such human sera could be demonstrated. Moreover, gamma delta T-cell clones of this third category expressed the IgG FcRIII (CD16) which indicates that these clones are capable of mediating antibody-dependent cellular cytotoxicity towards SEA-coated target cells. Thus, the cytotoxic response of gamma delta T cells to SEs is mediated by two distinct pathways: an antibody-independent and an antibody-dependent pathway. The antibody-independent reactivity of gamma delta T cells was directed to either SEA or SEE, whereas antibody-dependent reactivity was found only towards SEA. The capacity of gamma delta T-cell clones to respond to stimulation with SEs, combined with their high cytolytic capacity in vitro, suggests that these cells can be involved in SE-directed immune responses and efficiently kill SE-coated target cells in vivo.

Clone Cells↗
PubMed1991

Reduced nephrotoxicity and hepatoxicity in cyclosporin A therapy by enalapril and spironolactone in rats.

The aim of the study was to define a therapy to be combined with an immunosuppressive drug such as cyclosporin A, in order to partially reduce the nephrotoxic and hepatotoxic effects in the treated rats. Two drugs were considered: enalapril, which is an inhibitor of the angiotensin-converting enzyme, and spironolactone, which is an antagonist of aldosterone. These two drugs interrupt the renin-angiotensinogen-angiotensin chain after this has been activated by cyclosporin A, preventing peripheral vasoconstriction and more specifically the constriction of both glomerular arterioles and hepatic vessels from occurring, thus diminishing the cyclosporin A toxicity in both liver and kidney.

Animals↗