Dark energy and curvature from a future baryonic acoustic oscillation survey using the Lyman-alpha forest

We explore the requirements for a Lyman-alpha forest (LyaF) survey designed to measure the angular diameter distance and Hubble parameter at 2~<z~<4 using the standard ruler provided by baryonic acoustic oscillations (BAO). The goal would be to obtain a high enough density of sources to probe the three-dimensional density field on the scale of the BAO feature. A percent-level measurement in this redshift range can almost double the Dark Energy Task Force Figure of Merit, relative to the case with only a similar precision measurement at z~1, if the Universe is not assumed to be flat. This improvement is greater than the one obtained by doubling the size of the z~1 survey, with Planck and a weak SDSS-like z=0.3 BAO measurement assumed in each case. Galaxy BAO surveys at z~1 may be able to make an effective LyaF measurement simultaneously at minimal added cost, because the required number density of quasars is relatively small. We discuss the constraining power as a function of area, magnitude limit (density of quasars), resolution, and signal-to-noise of the spectra. For example, a survey covering 2000 sq. deg. and achieving S/N=1.8 per Ang. at g=23 (~40 quasars per sq. deg.) with an R~>250 spectrograph is sufficient to measure both the radial and transverse oscillation scales to 1.4% from the LyaF (or better, if fainter magnitudes and possibly Lyman-break galaxies can be used). At fixed integration time and in the sky-noise-dominated limit, a wider, noisier survey is generally more efficient; the only fundamental upper limit on noise being the need to identify a quasar and find a redshift. Because the LyaF is much closer to linear and generally better understood than galaxies, systematic errors are even less likely to be a problem.Comment: 18 pages including 6 figures, submitted to PR

Two Membrane-Associated Tyrosine Phosphatase Homologs Potentiate C. elegans AKT-1/PKB Signaling

Akt/protein kinase B (PKB) functions in conserved signaling cascades that regulate growth and metabolism. In humans, Akt/PKB is dysregulated in diabetes and cancer; in Caenorhabditis elegans, Akt/PKB functions in an insulin-like signaling pathway to regulate larval development. To identify molecules that modulate C. elegans Akt/PKB signaling, we performed a genetic screen for enhancers of the akt-1 mutant phenotype (eak). We report the analysis of three eak genes. eak-6 and eak-5/sdf-9 encode protein tyrosine phosphatase homologs; eak-4 encodes a novel protein with an N-myristoylation signal. All three genes are expressed primarily in the two endocrine XXX cells, and their predicted gene products localize to the plasma membrane. Genetic evidence indicates that these proteins function in parallel to AKT-1 to inhibit the FoxO transcription factor DAF-16. These results define two membrane-associated protein tyrosine phosphatase homologs that may potentiate C. elegans Akt/PKB signaling by cell autonomous and cell nonautonomous mechanisms. Similar molecules may modulate Akt/PKB signaling in human endocrine tissues

Two Membrane-Associated Tyrosine Phosphatase Homologs Potentiate C. elegans AKT-1/PKB Signaling

Akt/protein kinase B (PKB) functions in conserved signaling cascades that regulate growth and metabolism. In humans, Akt/PKB is dysregulated in diabetes and cancer; in Caenorhabditis elegans, Akt/PKB functions in an insulin-like signaling pathway to regulate larval development. To identify molecules that modulate C. elegans Akt/PKB signaling, we performed a genetic screen for enhancers of the akt-1 mutant phenotype (eak). We report the analysis of three eak genes. eak-6 and eak-5/sdf-9 encode protein tyrosine phosphatase homologs; eak-4 encodes a novel protein with an N-myristoylation signal. All three genes are expressed primarily in the two endocrine XXX cells, and their predicted gene products localize to the plasma membrane. Genetic evidence indicates that these proteins function in parallel to AKT-1 to inhibit the FoxO transcription factor DAF-16. These results define two membrane-associated protein tyrosine phosphatase homologs that may potentiate C. elegans Akt/PKB signaling by cell autonomous and cell nonautonomous mechanisms. Similar molecules may modulate Akt/PKB signaling in human endocrine tissues

Effects of C aenorhabditis elegans sgk‐1 mutations on lifespan, stress resistance, and DAF ‐16/ F ox O regulation

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/100177/1/acel12120.pd

First direct observation of a nearly ideal graphene band structure

Angle-resolved photoemission and X-ray diffraction experiments show that multilayer epitaxial graphene grown on the SiC(000-1) surface is a new form of carbon that is composed of effectively isolated graphene sheets. The unique rotational stacking of these films cause adjacent graphene layers to electronically decouple leading to a set of nearly independent linearly dispersing bands (Dirac cones) at the graphene K-point. Each cone corresponds to an individual macro-scale graphene sheet in a multilayer stack where AB-stacked sheets can be considered as low density faults.Comment: 5 pages, 4 figure

Release of cholesterol-rich particles from the macrophage plasma membrane during movement of filopodia and lamellipodia.

Cultured mouse peritoneal macrophages release large numbers of ~30-nm cholesterol-rich particles. Here, we show that those particles represent fragments of the plasma membrane that are pulled away and left behind during the projection and retraction of filopodia and lamellipodia. Consistent with this finding, the particles are enriched in proteins found in focal adhesions, which attach macrophages to the substrate. The release of particles is abolished by blocking cell movement (either by depolymerizing actin with latrunculin A or by inhibiting myosin II with blebbistatin). Confocal microscopy and NanoSIMS imaging studies revealed that the plasma membrane-derived particles are enriched in 'accessible cholesterol' (a mobile pool of cholesterol detectable with the modified cytolysin ALO-D4) but not in sphingolipid-sequestered cholesterol [a pool detectable with ostreolysin A (OlyA)]. The discovery that macrophages release cholesterol-rich particles during cellular locomotion is likely relevant to cholesterol efflux and could contribute to extracellular cholesterol deposition in atherosclerotic plaques

Increased Epithelial Expression of CTGF and S100A7 with Elevated Subepithelial Expression of IL-1β in Trachomatous Trichiasis.

PURPOSE: To characterize the histological appearance and expression of pro-inflammatory mediators, growth factors, matrix metalloproteinases and biomarkers of epithelial-mesenchymal transition (EMT) in healthy control and trachomatous trichiasis (TT) conjunctival tissue. METHODS: Conjunctival biopsies were taken from 20 individuals with TT and from 16 individuals with healthy conjunctiva, which served as controls. Study participants were of varying ethnicity and were living in a trachoma-endemic region of northern Tanzania. Formalin-fixed paraffin-embedded tissue sections were stained using hematoxylin and eosin or by immunohistochemistry using antibodies against: IL-1β, IL-6, IL-17A, IL-22, CXCL5, S100A7, cleaved caspase 1 (CC1), PDGF, CTGF, TGFβ2, MMP7, MMP9, E-cadherin, vimentin, and αSMA. RESULTS: Tissue from TT cases had a greater inflammatory cell infiltrate relative to controls and greater disruption of collagen structure. CTGF and S100A7 were more highly expressed in the epithelium and IL-1β was more highly expressed in the substantia propria of TT cases relative to controls. Latent TGFβ2 was slightly more abundant in the substantia propria of control tissue. No differences were detected between TT cases and controls in the degree of epithelial atrophy, the number of myofibroblasts or expression of EMT biomarkers. CONCLUSIONS: These data indicate that the innate immune system is active in the immunopathology of trachoma, even in the absence of clinical inflammation. CTGF might provide a direct link between inflammation and fibrosis and could be a suitable target for therapeutic treatment to halt the progression of trachomatous scarring