86 research outputs found
Dynamism in the solar core
Recent results of a mixed shell model heated asymmetrically by transient
increases in nuclear burning indicate the transient generation of small hot
spots inside the Sun somewhere between 0.1 and 0.2 solar radii. These hot
bubbles are followed by a nonlinear differential equation system with finite
amplitude non-homologous perturbations which is solved in a solar model. Our
results show the possibility of a direct connection between the dynamic
phenomena of the solar core and the atmospheric activity. Namely, an initial
heating about DQ_0 ~ 10^{31}-10^{37} ergs can be enough for a bubble to reach
the outer convective zone. Our calculations show that a hot bubble can arrive
into subphotospheric regions with DQ_final ~ 10^{28} - 10^{34} ergs with a high
speed, up to 10 km s-1, approaching the local sound speed. We point out that
the developing sonic boom transforms the shock front into accelerated particle
beam injected upwards into the top of loop carried out by the hot bubble above
its forefront traveling from the solar interior. As a result, a new perspective
arises to explain flare energetics. We show that the particle beams generated
by energetic deep-origin hot bubbles in the subphotospheric layers have masses,
energies, and chemical compositions in the observed range of solar
chromospheric and coronal flares. It is shown how the emergence of a hot bubble
into subphotospheric regions offers a natural mechanism that can generate both
the eruption leading to the flare and the observed coronal magnetic topology
for reconnection. We show a list of long-standing problems of solar physics
that our model explains. We present some predictions for observations, some of
which are planned to be realized in the near future.Comment: 44 pages, 20 figure
Glucocortiocoid Treatment of MCMV Infected Newborn Mice Attenuates CNS Inflammation and Limits Deficits in Cerebellar Development
Infection of the developing fetus with human cytomegalovirus (HCMV) is a major cause of central nervous system disease in infants and children; however, mechanism(s) of disease associated with this intrauterine infection remain poorly understood. Utilizing a mouse model of HCMV infection of the developing CNS, we have shown that peripheral inoculation of newborn mice with murine CMV (MCMV) results in CNS infection and developmental abnormalities that recapitulate key features of the human infection. In this model, animals exhibit decreased granule neuron precursor cell (GNPC) proliferation and altered morphogenesis of the cerebellar cortex. Deficits in cerebellar cortical development are symmetric and global even though infection of the CNS results in a non-necrotizing encephalitis characterized by widely scattered foci of virus-infected cells with mononuclear cell infiltrates. These findings suggested that inflammation induced by MCMV infection could underlie deficits in CNS development. We investigated the contribution of host inflammatory responses to abnormal cerebellar development by modulating inflammatory responses in infected mice with glucocorticoids. Treatment of infected animals with glucocorticoids decreased activation of CNS mononuclear cells and expression of inflammatory cytokines (TNF-α, IFN-β and IFNγ) in the CNS while minimally impacting CNS virus replication. Glucocorticoid treatment also limited morphogenic abnormalities and normalized the expression of developmentally regulated genes within the cerebellum. Importantly, GNPC proliferation deficits were normalized in MCMV infected mice following glucocorticoid treatment. Our findings argue that host inflammatory responses to MCMV infection contribute to deficits in CNS development in MCMV infected mice and suggest that similar mechanisms of disease could be responsible for the abnormal CNS development in human infants infected in-utero with HCMV
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