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Abstract: Proposed mathematical and software analysis of reactor experiments allowed interpretation of the experimental results of a tritium release study. Tritium was continuously generated by the reaction of lithium-6 with thermal neutrons for various thermal conditions of lithium metatitanate (Li2TiO3). The main gas release parameters were calculated in order to assess the potential use of lithium metatitanate in tritium breeders. These parameters were: gas release rate, tritium retention, retention time, activation energy for thermal desorption as HT, activation energy for volume diffusion as Т+, and the corresponding pre-exponential (frequency) indexes. [Copyright &y& Elsevier]

Thermal behavior of talc samples (from locality Puebla de Lillo, Spain) were characterized by emanation thermal analysis (ETA), DTA and TG. The ETA, based on the measurement of radon release rate from samples, revealed a closing up of surface micro-cracks and annealing of microstructure irregularities of the talc samples on heating in the range 200–500°C. For ground talc sample a crystallization of non-crystalline phase formed by grinding, into orthorhombic enstatite was characterized as a decrease of radon mobility in the range 785–825°C and by a DTA exothermal effect with the maximum at 830°C. ETA results characterized the microstructure development of the talc samples on heating and served to evaluate their radon mobility and transport properties on heating and cooling. Transport properties of the talc samples were evaluated by using ETA experimental data measured during heating to 600 and 1300°C, respectively, and subsequent cooling to room temperature. [ABSTRACT FROM AUTHOR]

A hybridoma (FMC4) has been derived which secretes antibody showing selective reaction with human B lymphocytes. monocytes and some null lymphocytes. Few, if any, T lymphocytes in normal blood are stained, although stimulation of lymphocytes with PHA leads to an increase in the proportion of cells reacting with the hybridoma antibody. The antibody reacts with B and null lymphoblastoid cell lines but not with T cell lines. B chronic lymphocytic leukaemia (CLL) cells but not T-CLLs are stained and null-type acute lymphoblastic leukaemia (ALL) cells but not T-type ALL also react. Normal blood myeloid cells do not react with FMC4 supernatant whilst some myeloid leukaemias do. The expression of the antigen reacting with FMC4 supernatant suggests that FMC4 may secrete an antibody against the human equivalent of the la antigen. [ABSTRACT FROM AUTHOR]

A hybridoma has been isolated from the products of fusion of a myeloma cell line with spleen cells from mice immunized with a human B cell line. After cloning, the hybridoma secretes antibody with the following properties: (i) Human B-lymphohlastoid cell lines react with the antibody while T and null cell lines do not. (ii) The antibody reacts with the majority of leucocytes in the blood of patients with CLL, but with a minority of cells in the blood of patients with A ML or ALL of the null or T type, (iii) The antibody reacts with 9-21% of mononuclear cells in normal peripheral blood. The reacting cells are not T cells and overlap extensively with cells identified as B cells by other markers. The antigen identified by this antibody appears to be distinct from known B cell markers, and is put forward as a new B cell marker with diagnostic potential. [ABSTRACT FROM AUTHOR]

It is well documented that the proliferative capacity of T cells declines with advancing age. There are, however, conflicting data as to the role of the accessory cell and whether or not this loss in responsiveness extends to all T-cell stimuli and to all T cells. We report here on the capacity of subpopulations of peripheral blood CD4+ T cells from the healthy aged to proliferate in response to anti-CD2 receptor-induced activation in the complete absence of accessory cells by using various exogenous cofactors as second signals. These costimulatory factors included phorbol 12-myristate 13-acetate (PMA), interleukin (IL)-1, IL-2, IL-6 and IL-7 and the monoclonal antibodies, anti-CD28 and anti-CD44. Under these conditions, the proliferative responsiveness of CD4+CD45RO+ T cells from the aged was found to be comparable to young control cells for all stimuli tested, except anti-CD2 plus IL-7. This suggests that signal transduction pathways involving CD2, except IL-7-mediated events, are essentially intact in 'old' memory CD4+ T cells. On the other hand, several cofactors, namely IL-2, IL-6, IL-7 and to a lesser extent IL-1β and PMA, failed to support adequately CD2-induced activation in 'old' CD4+CD45RA+ T cells suggesting severe and multiple signalling deficiencies in this subset. [ABSTRACT FROM AUTHOR]

Triggering of the T-cell receptor by anti-CD3 monoclonal antibodies (mAb), for example OKT3, induces accessory cell (AC)-dependent interleukin-2 (IL-2) and IL-2 receptor synthesis, and ultimately, T-celI proliferation. We report on the ability of a HLA-class I specific monomorphic mAb, namely FMC16, to inhibit OKT3-driven T-cell mitogenesis. FMC16 was apparently selective for OKT3 because it did not block Concanavalin A (Con A) or mAb Leu-4 induced proliferation. Moreover, this effect was not due to non-specific toxicity nor interference with OKT3 binding. Kinetic analysis showed that FMC16 was inhibitory when added up to 24 hr after initiation of culture. FMC16 drastically reduced both IL-2 production and IL-2 receptor expression, but did not interfere with IL-2 responsiveness. The inhibitory effects were not altered by the addition of exogenous IL-2 if FMC16 was present at the beginning of culture; however, 11-2 did restore proliferation if FMCI6 was not added until 3 to 6 hr after initiation of culture. This coincided exactly with an IL-2 mediated increase in the level of TAC-positive cells. Furthermore, T-cell activation triggered by the synergistic action of OKT3 and a phorbol ester (TM) in the absence of AC was also blocked by FMC16, suggesting that inhibition was not AC-dependent. Taken together, these results indicate that FMC16 interferes with early signals leading to IL-2 production and IL-2 receptor expression and suggest that HLA-class I determinants play an early role in T-cell activation. [ABSTRACT FROM AUTHOR]

Cell types in a human experimental gingivitis model were analyzed sequentially on days 0, 4, 8, and 21 of a no oral hygiene period. The cells were characterized using enzyme and surface antigen markers. In all but two of the day 0 specimens a small inflammatory infiltrate was localized immediately beneath the junctional epithelium. These, essentially lymphocytic lesions, consisted of over 70% T-cells as suggested by the phenotype T-enzyme +ve/T-cell surface antigen +ve/B-cell surface antigen -ve/HLA-DR-ve/B-cell subset antigen -ve. At days 4,8, and 21, although the size of the infiltrate increased, its essential nature did not change. At all times the majority of lymphocytes (over 70%) had the characteristic T-cell phenotype. These results show that in the developing gingival lesion in humans a T-cell dominated lesion occurs and persists at least for the 3 week experimental period used in the present study. [ABSTRACT FROM AUTHOR]

Monoclonal antibodies made against lymphocyte differentiation antigens were used to characterize phenotypically the lymphoid cell subpopulations in sections of human lymphoid tissue and inflamed gingival tissue associated with the deciduous dentition in children. Four monoclonal antibodies designated FMC 1, FMC 4, FMC 7, and UCHT1 were used. These antibodies are specific for B-cells, p28,33 (Ia-like) antigen, a B-cell subset, and peripheral T-cells respectively. FMC 1 and FMC 4 positive cells (B-cells) were found mainly in the secondary follicles while UCHT1 positive cells (F-cells) were found in the parafolIicular areas of human tonsils. Cells in some, but not all, secondary follicles in the tonsils were FMC 7 positive. In the gingival tissue only 12.6 % of the infiltrating cells were FMC 1 positive, 12.2 % were FMC 4 positive, and 42 % FMC 7 positive. On the other hand over 75 % of cells appeared to be UCHTI positive. These results indicate that the majority of inflammatory cells in gingivitis associated with the deciduous dentition in children have the phenotype B-cell antigen-/p28,33 (Ia- like) antigein-/B-cell subset antigen- and possibly T-cell antigen. Such a phenotype is, at least by exclusion, suggestive of T-cells and as such confirms earlier studies using T-cell enzyme markers. [ABSTRACT FROM AUTHOR]

Vascular damage, initiated by host inflammatory cells, is a component of the pathophysiology of many acute and chronic inflammatory disorders. Neutrophil-mediated tissue damage is mediated primarily hyproteinases, particularly elastase and cathepsin G. In this study we have identified endothelial binding of two key serine proteinase inhibitors (serpins), α1-antitrypsin, the inhibitor of elastase, and α1-antichymotrypsin, the inhibitor of cathepsin G. These serpins are shed from the endothelium into the supernatant when neutrophils adherent to the endothelium are activated. Endothelium activated by lipopolysaccharide (LPS) augments this process, Serpin-proteinase complexes activate neutrophils and induce further cytokine release, thereby amplifying inflammatory processes. Strategies aimed at preventing endothelial serpin depletion may help minimize vascular damage during inflammation. [ABSTRACT FROM AUTHOR]