The Large Array Survey Telescope -- System Overview and Performances

The Large Array Survey Telescope (LAST) is a wide-field visible-light telescope array designed to explore the variable and transient sky with a high cadence. LAST will be composed of 48, 28-cm f/2.2 telescopes (32 already installed) equipped with full-frame backside-illuminated cooled CMOS detectors. Each telescope provides a field of view (FoV) of 7.4 deg^2 with 1.25 arcsec/pix, while the system FoV is 355 deg^2 in 2.9 Gpix. The total collecting area of LAST, with 48 telescopes, is equivalent to a 1.9-m telescope. The cost-effectiveness of the system (i.e., probed volume of space per unit time per unit cost) is about an order of magnitude higher than most existing and under-construction sky surveys. The telescopes are mounted on 12 separate mounts, each carrying four telescopes. This provides significant flexibility in operating the system. The first LAST system is under construction in the Israeli Negev Desert, with 32 telescopes already deployed. We present the system overview and performances based on the system commissioning data. The Bp 5-sigma limiting magnitude of a single 28-cm telescope is about 19.6 (21.0), in 20 s (20x20 s). Astrometric two-axes precision (rms) at the bright-end is about 60 (30)\,mas in 20\,s (20x20 s), while absolute photometric calibration, relative to GAIA, provides ~10 millimag accuracy. Relative photometric precision, in a single 20 s (320 s) image, at the bright-end measured over a time scale of about 60 min is about 3 (1) millimag. We discuss the system science goals, data pipelines, and the observatory control system in companion publications.Comment: Submitted to PASP, 15p

Clinical Trials in Head Injury

Traumatic brain injury (TBI) remains a major public health problem globally. In the United States the incidence of closed head injuries admitted to hospitals is conservatively estimated to be 200 per 100,000 population, and the incidence of penetrating head injury is estimated to be 12 per 100,000, the highest of any developed country in the world. This yields an approximate number of 500,000 new cases each year, a sizeable proportion of which demonstrate signficant long-term disabilities. Unfortunately, there is a paucity of proven therapies for this disease. For a variety of reasons, clinical trials for this condition have been difficult to design and perform. Despite promising pre-clinical data, most of the trials that have been performed in recent years have failed to demonstrate any significant improvement in outcomes. The reasons for these failures have not always been apparent and any insights gained were not always shared. It was therefore feared that we were running the risk of repeating our mistakes. Recognizing the importance of TBI, the National Institute of Neurological Disorders and Stroke (NINDS) sponsored a workshop that brought together experts from clinical, research, and pharmaceutical backgrounds. This workshop proved to be very informative and yielded many insights into previous and future TBI trials. This paper is an attempt to summarize the key points made at the workshop. It is hoped that these lessons will enhance the planning and design of future efforts in this important field of research.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/63185/1/089771502753754037.pd

3, 3′-Diindolylmethane Exhibits Antileukemic Activity In Vitro and In Vivo through a Akt-Dependent Process

3,3′-diindolylmethane (DIM), one of the active products derived from Brassica plants, is a promising antitumor agent. The present study indicated that DIM significantly induced apoptosis in U937 human leukemia cells in dose- and time-dependent manners. These events were also noted in other human leukemia cells (Jurkat and HL-60) and primary human leukemia cells (AML) but not in normal bone marrow mononuclear cells. We also found that DIM-induced lethality is associated with caspases activation, myeloid cell leukemia-1 (Mcl-1) down-regulation, p21cip1/waf1 up-regulation, and Akt inactivation accompanied by c-jun NH2-terminal kinase (JNK) activation. Enforced activation of Akt by a constitutively active Akt construct prevented DIM-mediated caspase activation, Mcl-1 down-regulation, JNK activation, and apoptosis. Conversely, DIM lethality was potentiated by the PI3K inhibitor LY294002. Interruption of the JNK pathway by pharmacologic or genetic approaches attenuated DIM-induced caspases activation, Mcl-1 down-regulation, and apoptosis. Lastly, DIM inhibits tumor growth of mouse U937 xenograft, which was related to induction of apoptosis and inactivation of Akt, as well as activation of JNK. Collectively, these findings suggest that DIM induces apoptosis in human leukemia cell lines and primary human leukemia cells, and exhibits antileukemic activity in vivo through Akt inactivation and JNK activation