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Software development tools for the CDF MX scanner
This paper discuses the design of the high level assembler and diagnostic control program developed for the MX, a high speed, custom designed computer used in the CDF data acquisition system at Fermilab. These programs provide a friendly productive environment for the development of software on the MX. Details of their implementation and special features, and some of the lessons learned during their development are included
DECam integration tests on telescope simulator
The Dark Energy Survey (DES) is a next generation optical survey aimed at
measuring the expansion history of the universe using four probes: weak
gravitational lensing, galaxy cluster counts, baryon acoustic oscillations, and
Type Ia supernovae. To perform the survey, the DES Collaboration is building
the Dark Energy Camera (DECam), a 3 square degree, 570 Megapixel CCD camera
which will be mounted at the Blanco 4-meter telescope at the Cerro Tololo
Inter- American Observatory. DES will survey 5000 square degrees of the
southern galactic cap in 5 filters (g, r, i, z, Y). DECam will be comprised of
74 250 micron thick fully depleted CCDs: 62 2k x 4k CCDs for imaging and 12 2k
x 2k CCDs for guiding and focus. Construction of DECam is nearing completion.
In order to verify that the camera meets technical specifications for DES and
to reduce the time required to commission the instrument, we have constructed a
full sized telescope simulator and performed full system testing and
integration prior to shipping. To complete this comprehensive test phase we
have simulated a DES observing run in which we have collected 4 nights worth of
data. We report on the results of these unique tests performed for the DECam
and its impact on the experiments progress.Comment: Proceedings of the 2nd International Conference on Technology and
Instrumentation in Particle Physics (TIPP 2011). To appear in Physics
Procedia. 8 pages, 3 figure
Duox, Flotillin-2, and Src42A Are Required to Activate or Delimit the Spread of the Transcriptional Response to Epidermal Wounds in Drosophila
The epidermis is the largest organ of the body for most animals, and the first line of defense against invading pathogens. A breach in the epidermal cell layer triggers a variety of localized responses that in favorable circumstances result in the repair of the wound. Many cellular and genetic responses must be limited to epidermal cells that are close to wounds, but how this is regulated is still poorly understood. The order and hierarchy of epidermal wound signaling factors are also still obscure. The Drosophila embryonic epidermis provides an excellent system to study genes that regulate wound healing processes. We have developed a variety of fluorescent reporters that provide a visible readout of wound-dependent transcriptional activation near epidermal wound sites. A large screen for mutants that alter the activity of these wound reporters has identified seven new genes required to activate or delimit wound-induced transcriptional responses to a narrow zone of cells surrounding wound sites. Among the genes required to delimit the spread of wound responses are Drosophila Flotillin-2 and Src42A, both of which are transcriptionally activated around wound sites. Flotillin-2 and constitutively active Src42A are also sufficient, when overexpressed at high levels, to inhibit wound-induced transcription in epidermal cells. One gene required to activate epidermal wound reporters encodes Dual oxidase, an enzyme that produces hydrogen peroxide. We also find that four biochemical treatments (a serine protease, a Src kinase inhibitor, methyl-Γ-cyclodextrin, and hydrogen peroxide) are sufficient to globally activate epidermal wound response genes in Drosophila embryos. We explore the epistatic relationships among the factors that induce or delimit the spread of epidermal wound signals. Our results define new genetic functions that interact to instruct only a limited number of cells around puncture wounds to mount a transcriptional response, mediating local repair and regeneration
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