4 research outputs found
Pair of accelerated black holes in a de Sitter background: the dS C-metric
Following the work of Kinnersley and Walker for flat spacetimes, we have
analyzed the anti-de Sitter C-metric in a previous paper. In the de Sitter
case, Podolsky and Griffiths have established that the de Sitter C-metric (dS
C-metric) found by Plebanski and Demianski describes a pair of accelerated
black holes in the dS background with the acceleration being provided (in
addition to the cosmological constant) by a strut that pushes away the two
black holes or, alternatively, by a string that pulls them. We extend their
analysis mainly in four directions. First, we draw the Carter-Penrose diagrams
of the massless uncharged dS C-metric, of the massive uncharged dS C-metric and
of the massive charged dS C-metric. These diagrams allow us to clearly identify
the presence of two dS black holes and to conclude that they cannot interact
gravitationally. Second, we revisit the embedding of the dS C-metric in the 5D
Minkowski spacetime and we represent the motion of the dS C-metric origin in
the dS 4-hyperboloid as well as the localization of the strut. Third, we
comment on the physical properties of the strut that connects the two black
holes. Finally, we find the range of parameters that correspond to non-extreme
black holes, extreme black holes, and naked particles.Comment: 11 pages, 11 figures (RevTeX4). Published version: references adde
Immunological basis of septal fibrosis of the liver in Capillaria hepatica-infected rats
Immunological basis of septal fibrosis of the liver in Capillaria hepatica-infected rats
Rats infected with the helminth Capillaria hepatica regularly develop septal fibrosis of the liver similar to that induced by repeated ip injections of pig serum. Fibrosis starts when the focal parasitic lesions begin to show signs of resorption, thus suggesting an immunologically mediated pathogenesis of this fibrosis. To explore this possibility, the development of C. hepatica-related hepatic fibrosis was observed in rats exposed to worm antigens from the first neonatal day onward. Wistar rats (150 g) were either injected ip with an extract of C. hepatica eggs (protein concentration: 1 mg/ml) or received immature eggs by gavage from the first neonatal day until adult life and were then infected with 500 embryonated eggs. Changes were monitored on the basis of serum levels of anti-worm antibodies and hepatic histopathology. Rats submitted to immunological oral tolerance markedly suppressed C. hepatica-related serum antibodies and septal fibrosis of the liver when infected with the helminth later on. Tolerance trials with ip injections of worm antigens gave essentially negative results. The partial suppression of septal fibrosis of the liver after the induction of immunological tolerance to C. hepatica antigens in rats indicates an immunological basis for the fibrosis and emphasizes the importance of immunological factors in the pathogenesis of hepatic fibrosis