[Post cards filing and x-rays; a handsome contribution to the history of radiology]. / Cartophile et radiations: une contribution appreciable a l'histoire de la radiologie.

Such a surprising collection points out that every step towards radiological improvement was fully illustrated by a lot of post cards showing public stance about progress into that speciality. From the onset, inquisitiveness of mind and believing to wonderful results due to unseen rays prevailed. Next, came into sight the usefulness of x-rays for diseased people and, during the 1914-1918 war a better chance to save wounded soldiers fated to surgery. Further back than W.W.II, everyone was full of admiration for the great success of radiology facing to tuberculosis, a real plague in those times! Since 1945, post cards displayed the amazing growth of x-rays apparatus. Then, at last, a part from rare outstanding pictures intended to promote modern radiological sets, it remains only few funny post cards about that theme; and no one with regard to recent discovery as Scanner or M.R.I.

Effects of a primary immune response to T-cell dependent antigen on serotonin metabolism in frontal cortex: in vivo microdialysis study in freely moving Fischer 344 rat.

Antigenic challenge is known to influence brain catecholamine turnover, e.g. hypothalamic norepinephrine activity, but little is known about effects on the activity of serotoninergic neurons, i.e. the release of the neurotransmitter at nerve terminals. In the present study, we first investigated the changes of central serotonin (5-HT) metabolism in Fischer 344 male rats at 2, 3, 4 and 5 days following i.v. immunization with sheep red blood cell (SRBC). Major decreases in 5-HT levels were evident in the hypothalamus (Hy) and cortex (Cx) at a time which corresponded to the late phase of the production of specific antibodies to SRBC measured with a plaque-forming cell assay (PFC). A pretreatment with an immunosuppressive drug, cyclosporin A (CsA; 12.5 mg/kg by gavage for 7 days) prevented the decreases in cortical 5-HT levels. Concomitantly, a 2-fold increase in the basal 5-HT release at frontocortical nerve terminals was observed by using in vivo microdialysis in awake rats on Day 3 following SRBC inoculation. This effect was totally suppressed by CsA. Our data suggest that the decrease in brain 5-HT levels that occurs after antigen administration may reflect a specific short-lasting CsA-dependent-release of 5-HT at frontocortical nerve terminals at a time (Day 3 or 4) when the splenic immune response is maximal.

Molecular mechanism of 7,12-dimethylbenz[a]anthracene-induced immunosuppression: evidence for action via the interleukin-2 pathway.

Previous studies in this laboratory have demonstrated that exposure of mice to the carcinogenic polycyclic aromatic hydrocarbon 7,12-dimethylbenz[a]anthracene results in suppression of both humoral and cell-mediated immunity. This suppression is unaccompanied by any significant alteration in splenic lymphocyte subpopulation composition, suggesting that the immune deficit was due to a modulation of lymphocyte function. Additional studies implicated the T helper lymphocyte as the probable target for 7,12-dimethylbenz[a]anthracene-induced immunosuppression, apparently through an inhibition of interleukin 2 production. The purpose of the present study was to examine the mechanism of 7,12-dimethylbenz[a]anthracene-induced T lymphocyte dysfunction at the molecular level and to determine the consequences of 7,12-dimethylbenz[a]anthracene exposure on the interleukin 2 pathway. In vitro exposure of Con A-activated splenocytes to 7,12-dimethylbenz[a]anthracene resulted in suppression of the mitogenic response, suppressed interleukin 2 production, and reduced the expression of the high affinity receptor for interleukin 2. In contrast, expression of the low affinity interleukin 2 receptor was not affected. In addition, interleukin 2-dependent lymphoblasts and long term cultured splenocytes exhibited a dose-dependent decrease in proliferation following in vitro exposure to 7,12-dimethylbenz[a]anthracene. These results suggest that 7,12-dimethylbenz[a]anthracene-induced immunosuppression may be mediated, at least in part, through the interleukin 2/interleukin 2 receptor pathway.

Suppression of murine cytotoxic T-lymphocyte induction following exposure to 7,12-dimethylbenz[A]anthracene: dysfunction of antigen recognition.

Exposure of murine lymphocytes to the carcinogenic polycyclic aromatic hydrocarbon 7,12-dimethylbenz[a]anthracene (DMBA) results in significant suppression of a variety of immunological parameters, including the induction of cytotoxic T-lymphocytes (CTL). This CTL suppression may be reversed in vitro by the addition of exogenous cellular activation products, including IL-2. The current study demonstrated that DMBA-induced CTL suppression occurs throughout the induction process, with the most pronounced effect occurring within 24-48 h of initiation. IL-2-mediated restoration of suppression is effective only within this critical window. These findings suggest an effect by DMBA on both the T-helper (Th) and CTL-precursor (CTLp) subsets. Alloantigen-specific CTL generated from murine thymocytes in the presence of DMBA and Th-derived factors (thus circumventing the Th) displayed an almost identical degree of CTL suppression to that of splenocytes, indicating a direct effect of DMBA on the CTLp. Antigen nonspecific, polyclonal CTL activation by the lectin leucoagglutinin or by IL-2 (LAK cells) was unaffected by chemical exposure, indicating that DMBA preferentially affects antigen-specific activation rather than the cytolytic process itself. Conversely, polyclonal CTL induced with monoclonal antibodies directed against the T-cell receptor-associated subunit CD3, in the presence of conditioned medium, was suppressed in a manner similar to antigen-mediated CTL. The CD3 receptor subunit acts as a transmembrane activation signal following binding of antigen to the specific receptor, further implicating dysfunction of antigen recognition or signal processing following DMBA exposure. This was confirmed by the observation that DMBA exposure prevents the anamnestic response of CTL memory cells following re-exposure to eliciting tumor antigen.(ABSTRACT TRUNCATED AT 250 WORDS)

Suppression of cytolytic function in murine lymphocytes exposed to 1,4-bis[(2-aminoethyl)amino]-5,8-dihydroxy-9,10-anthracenedione dihydrochloride (AEAD): inhibition of proliferation by cytotoxic T-lymphocyte precursors.

Previous reports have shown that exposure of murine splenic lymphocytes to the substituted anthraquinone 1,4-bis[(2-aminoethyl)amino]-5,8-dihydroxy-9,10-anthracenedione dihydrochloride (AEAD) results in a persistent, strong immunosuppression which is limited to induction of cytotoxic T-lymphocytes (CTL). In the present study the cellular mechanism of this specificity was examined in detail. Proliferation of T-lymphocytes is inhibited by in vitro exposure to AEAD, with suggestive evidence that this inhibition may be selective for the CTL precursor cells. Activation and differentiation of CTL precursors into functional CTL, as well as the function of T-helper lymphocytes, was unaffected by AEAD exposure. Rather, the committed CTL precursor cells are prevented from clonal proliferation, resulting in a much smaller population of antigen-induced CTL effectors. Finally, it was shown that AEAD is unable to prevent the anamnestic response of CTL memory cells to eliciting antigen. Taken together these data provide strong evidence that AEAD-induced CTL suppression results from its antiproliferative effect, directed primarily toward the CTL precursor subpopulation. This effect is manifested as decreased CTL function due to lower absolute number of specific CTL, since AEAD has no significant direct effect on expression of either specific or polyclonal cytolysis by T-lymphocytes.