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The engineered macro-pore foam provides a new way to study thermonuclear burn physics by utilizing capsules containing deuterated (D) foam and filling tritium (T) gas in the engineered macro-pores. The implosion of a thermonuclear capsule filled with an engineered macro-pore foam will be complex due to the interaction of a shock wave with the engineered macro-pores. It is our goal to quantify how substantially complex foam structures affect the shape of shock and bulk shock speed. A cylinder-shape shock tube experiment has been designed and performed at the Omega Laser Facility. In order to examine how a foam structure will affect shock propagation, we performed several tests varying (1) engineered macro-pore size, (2) average foam density, and (3) with/without neopentane (C5H12) gas. X-ray radiographic data indicate that shock speed through engineered macro-pore foams depends strongly on average foam density and less on pore size. Experimental shock propagation data helped guide two numerical simulation approaches: (1) a 2D simulation with homogenizing foams rather than explicitly simulating engineered macro-pores and (2) a 2D toroidal-pore approximation adopting a toroidal-tube geometry to model engineered macro-pores.

SUMMARY Using a flow cytometrie method, CD4+, CD8+, αβ TCR+ and TCR variable region gene product (TVRGP)-specific T cells were analysed in heallhy heterosexual males (HHeM). HIV-seronegative homosexual males (SNHM). asymptomatic seropositive homosexual males (ASPH) and homosexual males with AIDS who were either well (AIDS-A). or unwell in hospilal (AIDS-B). Total CD4+ and CD8+ T cell numbers were similar in HHeM and SNHM. CD4+ T cells were significantly reduced in ASPH relative to both HHeM and SNHM and in AIDS-A and AIDS-B relative to SNHM. TVRGP-specific T cells expressed as a percentage of TCR αβ+ cells showed no significant difference in HHeM. SNHM and AIDS-B. The proportion of αβ+ cells expressing the Vβ5·1, Vβ12 and Vα2 gene product (GP) was. however, significantly reduced in ASPH and AIDS-B relative to HHeM. SNHM and AIDS-A. Possible causes of TVRGP-specific T cell deletion arc discussed.

SUMMARYT cell antigen specificity is determined by the products of the genes which encode the variable regions of their receptors. Of the T cell receptor (TCR) variable region gene products examined, only Vβ6.7a TCR-positive lymphocytes were reduced in primary Sjogren’s syndrome patients with IgG 1 hypergammaglobulinaemia compared with an age-, sex- and HLA-matched control population. The levels of Vβ6.7a T cells were also significantly reduced when these patients were compared with an age- and sex-matched but HLA-unmatched control group and non-tissue typed normal people of both sexes. Since published studies show no such abnormality in rheumatoid arthritis, systemic lupus erythematosus or other autoimmune diseases, this abnormality may reflect a pathogenic process specific to primary Sjogren’s syndrome.

To evaluate the risk of childhood leukemia in relation to residential electric and magnetic field (EMF) exposures.A case control study based on 88 cases and 133 controls used different assessment methods to determine EMF exposure in the child's current residence. Cases comprised incident leukemias diagnosed at 0-14 years of age between 1985-1993 from a larger study in southern Ontario; population controls were individually matched to the cases by age and sex. Exposure was measured by a personal monitoring device worn by the child during usual activities at home, by point-in-time measurements in three rooms and according to wire code assigned to the child's residence.An association between magnetic field exposures as measured with the personal monitor and increased risk of leukemia was observed. The risk was more pronounced for those children diagnosed at less than 6 years of age and those with acute lymphoblastic leukemia. Risk estimates associated with magnetic fields tended to increase after adjusting for power consumption and potential confounders with significant odds ratios (OR) (OR: 4.5, 95% confidence interval (CI): 1.3-15.9) observed for exposuresor = 0.14 microTesla (microT). For the most part point-in-time measurements of magnetic fields were associated with non-significant elevations in risk which were generally compatible with previous research. Residential proximity to power lines having a high current configuration was not associated with increased risk of leukemia. Exposures to electric fields as measured by personal monitoring were associated with a decreased leukemia risk.The findings relating to magnetic field exposures directly measured by personal monitoring support an association with the risk of childhood leukemia. As exposure assessment is refined, the possible role of magnetic fields in the etiology of childhood leukemia becomes more evident.

OBJECTIVES: To evaluate the risk of having a child with a congenital anomaly in relation to occupational exposure to low level ionising radiation in the pre-conception period. METHODS: A case-control study based on the Canadian congenital anomalies registry used record linkage techniques to identify congenital anomalies among male and female workers in Canada9s largest electric company. Cases were defined as parents of a child with a congenital anomaly born between April 1979 and December 1986 who had a congenital anomaly diagnosed within the first year of life. Controls were an individually matched sample of parents of a liveborn child without an anomaly. Risk of congenital anomaly was assessed in relation to parental exposure to ionising radiation acquired through work within a nuclear generating station of an electric power company. Exposure was assessed according to employment, whether or not the worker was monitored for radiation exposure, and quantitative estimates of radiation dose. RESULTS: Employment within the electric power industry was not associated with an increased risk of congenital anomalies in the offspring of mothers or fathers. Risk estimates for workers monitored (those who are likely to be exposed to ionising radiation) were 1.75 (95% confidence interval (95% CI) 0.86 to 3.55) for mothers and 0.84 (95% CI 0.68 to 1.05) for fathers. Exposure for fathers before conception, defined cumulatively and for six months before conception, was not associated with increased risk of anomalies in their offspring. There were no significant increases in risk found between type of anomaly and any measure of exposure, although the statistical power in these groups was limited. The study had insufficient numbers to evaluate the effects of ionising radiation in mothers as only three mothers had recorded doses > 0 mSv. CONCLUSIONS: Overall, workers in a nuclear power industry, and specifically those exposed before conception to low levels of ionising radiation, do not appear to be at an increased risk of having a liveborn child with a congenital anomaly.

We have recently described a spontaneous murine model of autoimmune thyroid disease. The disorder was in part characterized by reduced thyroid epithelial cell-cell communication that was associated with abnormalities in three major connexins. To compare whether this finding was a common secondary occurrence in autoimmune thyroid disease, or unique to the spontaneous development in the MRL mice, we induced thyroiditis in Lewis rats. Immunization with thyroid extract and thyroglobulin resulted in extensive lymphocytic infiltration and increased expression of major histocompatibility gene complex (MHC) class II surface antigen in the diseased thyroid. Both experimental and control rat thyroid tissues produced gap junction proteins connexin 43, connexin 32, and connexin 26. The connexins in nondiseased tissue was located in the plasma membrane at points of cell-cell contact and labeled as discrete arrays of punctate fluorescence. The quantity of all three connexins were reduced in the diseased thyroid tissue. More importantly, the connexin proteins were not distributed as gap junctions at contacting cell interfaces. Both nondiseased and diseased thyroid tissue expressed messenger RNA (mRNA) for the three connexins, but the diseased tissue had reduced levels of mRNA for connexin 43 (45%), and to a lesser extent, connexin 26 (25%) and connexin 32 (20%). The reduced connexin mRNA, protein, and lack of assembled gap junctions measured in the diseased tissue were obtained under conditions where the infiltrating cells and their potent cytokine products were continuously present. To determine if this difference persisted when these inflammatory components were absent, primary cultures of thyroid cells from control and experimental rats were established and connexin localization experiments repeated. The diseased thyroid cells, like the diseased tissue, lacked plasma membrane associated connexin protein. The lack of gap junction assembly in the thyrocytes cultured from the diseased tissue was accompanied by a loss of functional coupling. Collectively, the data document that autoimmune diseased thyroid tissue from both the spontaneous mouse and induced rat models have reduced plasma membrane assembled gap junctions and deficient intercellular communication as determined by the inability to transfer lucifer yellow dye to contiguous cells. Nondiseased cultured thyrocyte monolayers and follicles transferred dye to second and third order neighboring cells in 80 and 95% of trials, respectively. In contrast, only 5-10% of the diseased thyrocytes transferred microinjected dye, and in these cases the transit was limited to primary contacting cells. Culturing removed inequities introduced by the infiltrating cells and their products. However, the established cultures of diseased thyroid cells retained their communication deficiency. This suggests that the loss of communication may be a common abnormality in autoimmune disease, and furthermore, this uncoupling could contribute to the loss of coordinated hormonal regulation (hypothyroidism) in the diseased thyroid gland in the absence of thyroid cell destruction.

SUMMARY Serum levels of the soluble form of the low-affinity receptor for IgE (FcERII, CD23) (sCD23) are elevated in autoimmune conditions associated with hypergammaglobulinaemia and B cell hyperactivity. Very high levels of sCD23 are found in patients with B-chronic lymphatic leukaemia (B-CLL) who are, however, frequently hypogammaglobulinaemic. We therefore compared the serum levels of sCD23 in healthy controls (n= 33) with three conditions associated with hypogammaglobulinaemia (HGG) and varying B cell numbers: X-linked agammaglobulinaemia (XLA, n= 12), common variable immunodeficiency (CVI, n= 20) and B-chronic lymphatic leukaemia (n= 33). Serum levels of sCD23 showed a significant correlation with the CD19+ B cell count in both normals and patients with CVI (r= 0 65, P < 0·0001). Amongst the different clinical groups, serum levels of sCD23 were increased in the order XLA < CVI < normals < CLL (medians 2·5, 7·7, 11·1 and 540, respectively; P < 0·001 for all comparisons except CVI versus normals P < 0·03 in a one-tailed test). In the CVI group, serum sCD23 was lowest amongst four patients with low B cell numbers. There was no overlap in sCD23 between patients with XLA and this subgroup of CVI patients. Serum sCD23 is, therefore, derived predominantly from B cells, and is significantly related to the peripheral blood B cell count.

A cohort mortality study was undertaken of forestry workers at a public electrical utility who had worked for six months or more during 1950-82 and who were routinely exposed to herbicides including phenoxy acids. A total of 1222 men with 25 274 years at risk experienced 80 deaths. Ascertainment of vital state at the end of follow up was 95.5%. The male population of the province (Ontario) was used as the reference group. Overall, no excess mortality was found in this cohort relative to the reference population. A statistically significant increase in deaths occurred, however, due to suicide (SMR = 210, 95% confidence interval, 95% CI 105-376) for the cohort as a whole. No deaths were seen due to cancers such as soft tissue sarcoma and non-Hodgkin's lymphoma that have been cited by other authors as being associated with exposure to phenoxy acid herbicides. Although the cohort is not large, the absence of deaths due to these cancers is consistent with findings from other studies with sufficient numbers to allow examination of specific risks. The cohort is still young, however, and at the end of follow up most had not reached an age when increased incidence of cancer would normally be expected.