Probing reionization with Lyman-alpha emission lines

Lyman-alpha emission from high-redshift galaxies may be a powerful probe of the ionization history of the IGM at z>6: the observed Lyman-alpha emission line is sensitive to the neutral fraction of IGM hydrogen in the range 0.1-1. We present calculations of observed Lyman-alpha emission lines from z>6 galaxies, illustrating the effect of varying the many free parameters associated with the emitting galaxy, its halo, and the IGM around the galaxy. In particular, we use a dynamic model of the IGM that includes the effect of IGM infall toward the emitting galaxy. Galactic winds may play a crucial role in determining observed Lyman-alpha line fluxes. We compare our model predictions with observations of two z=6.5 galaxies and conclude that, if galactic winds are allowed for, existing observations place no constraint on the neutral fraction of the IGM at z=6.5. Future space-based observations will constrain the importance of galactic winds; if winds are unimportant for the observed z=6.5 galaxies, our models suggest that the IGM neutral fraction at z=6.5 is <~0.1.Comment: 17 pages, 25 figures, submitted to MNRA

In the Beginning: The First Sources of Light and the Reionization of the Universe

The formation of the first stars and quasars marks the transformation of the universe from its smooth initial state to its clumpy current state. In popular cosmological models, the first sources of light began to form at redshift 30 and reionized most of the hydrogen in the universe by redshift 7. Current observations are at the threshold of probing the hydrogen reionization epoch. The study of high-redshift sources is likely to attract major attention in observational and theoretical cosmology over the next decade.Comment: Final revision: 136 pages, including 42 figures; to be published in Physics Reports 2001. References updated, and a few minor corrections made. In this submission, several figures were compressed, resulting in just a slight reduction in quality; a postscript file with the full figures is available at http://www.cita.utoronto.ca/~barkana/review.htm

Transcriptional factor snail controls tumor neovascularization, growth and metastasis in mouse model of human ovarian carcinoma

Abstract Background Snail, a transcriptional factor and repressor of E-cadherin is well known for its role in cellular invasion. It can regulate epithelial to mesenchymal transition (EMT) during embryonic development and in epithelial cells. Snail also mediates tumor progression and metastases. Silencing of Snail and its associate member Slug in human A2780 ovarian epithelial carcinoma cell line was investigated to identify its role in tumor neovascularization. Methods Live cell sialidase, WST-1 cell viability and immunohistochemistry assays were used to evaluate sialidase activity, cell survival and the expression levels of tumor E-cadherin, N-cadherin, VE-cadherin, and host endothelial CD31+(PECAM-1) cells in archived paraffin-embedded ovarian A2780, A2780 Snail shRNA GIPZ lentiviral knockdown (KD) and A2780 Slug shRNA GIPZ lentiviral KD tumors grown in RAGxCγ double mutant mice. Results Oseltamivir phosphate (OP), anti-Neu1 antibodies and MMP-9 specific inhibitor blocked Neu1 activity associated with epidermal growth factor (EGF) stimulated A2780 ovarian epithelial carcinoma cells. Silencing Snail in A2780 cells abrogated the Neu1 activity following EGF stimulation of the cells compared to A2780 and A2780 Slug KD cells. OP treatment of A2780 and cisplatin-resistant A2780cis cells reproducibly and dose-dependently abated the cell viability with a LD50 of 7 and 4 μm, respectively, after 48 h of incubation. Heterotopic xenografts of A2780 and A2780 Slug KD tumors developed robust and bloody tumor vascularization in RAG2xCγ double mutant mice. OP treatment at 50 mg/kg daily intraperitoneally did not significantly impede A2780 tumor growth rate but did cause a significant reduction of lung metastases compared with the untreated and OP 30mg/kg cohorts. Silencing Snail in A2780 tumor cells completely abrogated tumor vascularization, tumor growth and spread to the lungs in RAGxCγ double mutant mice. A2780 and A2780 Slug KD tumors expressed high levels of human N- and VE-cadherins, and host CD31+ endothelial cells, while A2780 Snail KD tumors expressed E-cadherin and reduced host CD31+ cells. OP 50mg/kg cohort tumors had reduced numbers of host CD31+ cells compared to a higher expression levels of CD31+ cells in tumors from the untreated control and OP 30mg/kg cohorts. Conclusion Snail transcriptional factor is an important intermediate player in human ovarian tumor neovascularization