17 research outputs found
Turbulence and galactic structure
Interstellar turbulence is driven over a wide range of scales by processes
including spiral arm instabilities and supernovae, and it affects the rate and
morphology of star formation, energy dissipation, and angular momentum transfer
in galaxy disks. Star formation is initiated on large scales by gravitational
instabilities which control the overall rate through the long dynamical time
corresponding to the average ISM density. Stars form at much higher densities
than average, however, and at much faster rates locally, so the slow average
rate arises because the fraction of the gas mass that forms stars at any one
time is low, ~10^{-4}. This low fraction is determined by turbulence
compression, and is apparently independent of specific cloud formation
processes which all operate at lower densities. Turbulence compression also
accounts for the formation of most stars in clusters, along with the cluster
mass spectrum, and it gives a hierarchical distribution to the positions of
these clusters and to star-forming regions in general. Turbulent motions appear
to be very fast in irregular galaxies at high redshift, possibly having speeds
equal to several tenths of the rotation speed in view of the morphology of
chain galaxies and their face-on counterparts. The origin of this turbulence is
not evident, but some of it could come from accretion onto the disk. Such high
turbulence could help drive an early epoch of gas inflow through viscous
torques in galaxies where spiral arms and bars are weak. Such evolution may
lead to bulge or bar formation, or to bar re-formation if a previous bar
dissolved. We show evidence that the bar fraction is about constant with
redshift out to z~1, and model the formation and destruction rates of bars
required to achieve this constancy.Comment: in: Penetrating Bars through Masks of Cosmic Dust: The Hubble Tuning
Fork strikes a New Note, Eds., K. Freeman, D. Block, I. Puerari, R. Groess,
Dordrecht: Kluwer, in press (presented at a conference in South Africa, June
7-12, 2004). 19 pgs, 5 figure
The Ionizing Radiation-Induced Bystander Effect: Evidence, Mechanism, and Significance
It has long been considered that the important biological effects of ionizing radiation are a direct consequence of unrepaired or misrepaired DNA damage occurring in the irradiated cells. It was presumed that no effect would occur in cells in the population that receive no direct radiation exposure. However, in vitro evidence generated over the past two decades has indicated that non-targeted cells in irradiated cell cultures also experience significant biochemical and phenotypic changes that are often similar to those observed in the targeted cells. Further, nontargeted tissues in partial body-irradiated rodents also experienced stressful effects, including oxidative and oncogenic effects. This phenomenon, termed the “bystander response,” has been postulated to impact both the estimation of health risks of exposure to low doses/low fluences of ionizing radiation and the induction of second primary cancers following radiotherapy. Several mechanisms involving secreted soluble factors, oxidative metabolism, gap-junction intercellular communication, and DNA repair, have been proposed to regulate radiation-induced bystander effects. The latter mechanisms are major mediators of the system responses to ionizing radiation exposure, and our knowledge of the biochemical and molecular events involved in these processes is reviewed in this chapter