Hepatitis B and hepatocellular particles.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M Gerber.
Explore the source record for details and available documents.
The isolation and purification of the naked intranuclear particles of a human liver infected with hepatitis B virus is described. The particles had a diameter of 27-28 nm, were hexagonal, and showed the presence of capsomeres and spikes with lengths of 7-10 nm projecting from the surfaces. The particles formed cubic arrays with center-to-center distances of 40-42 nm. The overall particle symmetry was icosahedral. The ultraviolet absorption spectrum of the particles showed a peak at 264 nm with a shoulder at 280 nm. Endogenous DNA polymerase activity was not detected in fractions containing particles. DNA polymerase activity was present when activated DNA or d(A-T)(n) was used as exogenous template.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Statistically significant inhibition of the T-cell-mediated cytotoxic response was observed when mouse splenocytes were irradiated in vitro with 0.15 Gy prior to ConA and allogeneic stimulation. Restimulation in mixed lymphocyte culture demonstrated the same difference between irradiated and non-irradiated cultures as for the first stimulation. Adherent cell depletion of responder cells did not modify the inhibitory effect of 0.15 Gy on the cytotoxic response. The study of Lyt-6 markers on activation showed a decrease in the total number of activated cells (but not of the percentage) in cultures processed with irradiated cells. The data suggest that a T cell, involved in the generation of cytotoxic lymphocytes and present in the Lyt-2-depleted population, is the target of low-dose irradiation.
We conducted a cross-sectional epidemiological study to evaluate personal exposure to nitrogen dioxide and its effect on blood antioxidants. Personal exposure of 107 volunteers was assessed for 14 d with passive monitors. We excluded heavy smokers (> 10 cigarettes/d) from the study. Sociodemographic and environmental data, as well as beta-carotene intake, were recorded. We mainly attributed the mean nitrogen dioxide personal exposure (31.9 +/- 12.7 microg/m3 [0.017 ppm or 0.70 microM/m3]) (R2 = 0.75) to residence site in the city, time spent in urban traffic, and use of gas stoves. The correlation between nitrogen dioxide exposure and blood antioxidant concentration was weak; in addition, the correlation coefficients for men and women were inconsistent. Nonetheless, we found some evidence of an interaction between carotene intake and nitrogen dioxide exposure: a significantly lower plasma beta-carotene level was evident among subjects who consumed < or = 4.5 mg/jour of carotene and who were exposed to nitrogen dioxide levels that exceeded 40 microg/m3 (0.021 ppm or 0.87 microM/m3) of nitrogen dioxide.
Major carotenoids in plasma--especially beta-carotene--are affected by oxidative stress (e.g., tobacco smoking). Environmental ozone induced oxidative stress in experimental in vitro and in vivo studies, and it also increased the incidence of lung cancer in mice. We proposed to measure, after controlling for other determinants, the impact of personal ozone exposure on carotenoids levels in plasma. During the summer, we recruited 58 volunteer subjects who worked in a periurban zone. We asked each subject to wear a passive sample, which measured ozone exposure for 5 consecutive d. At the end of this period, we assessed plasma antioxidants. We observed a negative significant regression coefficient between alpha- or beta-carotene and ozone exposure (r = -.39, p < .01, and r = -.45, p = .02, respectively). In a subsample of 45 nonsmoker subjects, among whom carotene intake was lower than the median intake value (i.e., 6.6 mg/d) of the overall group, we noted that a relatively low exposure to ozone (> or = 50 microg/m3 x h or > or = 23.8 ppb) induced a significant decrease in plasma beta-carotene levels (i.e., 0.7 micromol/l to 0.4 micromol/l). This significant decrease suggested that a high dietary intake of fruit or vegetables can have a beneficial influence on the levels of plasma antioxidants generated in response to ozone exposure.
Several methods are presented for the purification of core particles of hepatitis B virus (HBV) from nuclei of infected human hepatocytes. No endogenous DNA polymerase activity was found in any of the preparations of core particles even when circular double and single stranded DNAs were used as exogenous templates. The DNA polymerase activity associated with serum HB Ag was not stimulated by circular DNAs. Sodium dodecyl sulfate (SDS) at concentrations of greater than or equal to 0.1% inhibited the DNA polymerase activity of serum HB Ag. Exogenous templates such as native and activated calf thymus and Micrococcus lysodeikticus DNAs did not stimulate the DNA polymerase of serum HB Ag even in the presence of low concentrations of SDS. It is suggested that the DNA polymerase associated the HB Ag is specific for its own DNA as template.
We investigated the mechanisms by which lipoxygenase (LO) inhibitors decrease interleukin-2 (IL-2) production in Jurkat cells. We demonstrate that the inhibition, linked to blockade of the [Ca2+]i rise involving T cell receptor (TCR) triggering, resulted from the action of these compounds on the signal transduction pathway, upstream from inositol triphosphate synthesis. IL2 secretion induced by phorbol 12-myristate 13-acetate (PMA) and the calcium ionophore A23187, which bypasses the breakdown of inositol phospholipids induced by the ligand-receptor interaction, was still suppressed by LO inhibitors which implies that these drugs also have an inhibitory effect on other target(s). None of the three protein kinase C (PKC)-dependent events investigated was affected in Jurkat cells stimulated in the presence of LO inhibitors. Furthermore, these compounds did not inhibit IL2 production in PMA-treated Jurkat cells cultured with vanadate, which mimics the tyrosine kinase activation pathway and induces IL2 secretion. This suggests that in addition to their effect on the phosphatidylinositol diphosphate pathway-dependent [Ca2+]i rise, LO inhibitors might affect the tyrosine kinase pathway in TCR-activated Jurkat cells, but probably not the PKC-dependent pathway. These results are consistent with a role for LO metabolite(s) in signal transduction pathways.
The effect of localized irradiation given as single dose on the immune response of tumour-bearing mice was evaluated using the CRT. The tumour system (MBL2 on C57BL/6 females) was regularly lethal, although presence of CTL was demonstrated 15 days after transplantation (50,000 cells in the left hind limb). This T-dependent, antigen-specific cytotoxic activity observed on day 15 in the non-irradiated tumour-bearing group was abolished in the irradiated group (but not in the sham-irradiated group) and their CTL were incapable to mount a secondary response in MLTC-CML. The scattering of the 1,600 rad-single dose was sufficient to provoke this inhibition.
Explore the source record for details and available documents.