5,521 research outputs found

    The Luminosity Function of Field Galaxies in the CNOC1 Redshift Survey

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    We have computed the luminosity function for 389 field galaxies from the Canadian Network for Observational Cosmology cluster redshift survey (CNOC1), over redshifts z = 0.2-0.6. We find Schechter parameters M^* - 5 log h = -19.6 \pm 0.3 and \alpha = -0.9 \pm 0.2 in rest-frame B_{AB}. We have also split our sample at the color of a redshifted but nonevolving Sbc galaxy, and find distinctly different luminosity functions for red and blue galaxies. Red galaxies have a shallow slope \alpha \approx -0.4 and dominate the bright end of the luminosity function, while blue galaxies have a steep \alpha \approx -1.4 and prevail at the faint end. Comparisons of the CNOC1 results to those from the Canada-France (CFRS) and Autofib redshift surveys show broad agreement among these independent samples, but there are also significant differences which will require larger samples to resolve. Also, in CNOC1 the red galaxy luminosity density stays about the same over the range z = 0.2-0.6, while the blue galaxy luminosity density increases steadily with redshift. These results are consistent with the trend of the luminosity density vs. redshift relations seen in the CFRS, though the normalizations of the luminosity densities appear to differ for blue galaxies. Comparison to the local luminosity function from the Las Campanas redshift survey (LCRS) shows that the luminosity density at z \approx 0.1 is only about half that seen at z \approx 0.4. A change in the luminosity function shape, particularly at the faint end, appears to be required to match the CNOC1 and LCRS luminosity functions, if galaxy evolution is the sole cause of the differences seen. However, it should be noted that the specific details of the construction of different surveys may complicate the comparison of results and so may need to be considered carefully.Comment: 22 pages, including 6 postscript figures, uses AASTEX v4.0 style files. Corrected minor typos and updated references. Results and conclusions unchanged. Final version to appear in the Astrophysical Journa

    Chain Formation by Spin Pentamers in eta-Na9V14O35

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    The nature of the gapped ground state in the quasi-one-dimensional compound eta-Na9V14O35 cannot easily be understood, if one takes into account the odd number of spins on each structural element. Combining the results of specific heat, susceptibility and electron spin resonance measurements we show that eta-Na9V14O35 exhibits a novel ground state where multi-spin objects build up a linear chain. These objects - pentamers - consist of five antiferromagnetically arranged spins with effective spin 1/2. Their spatial extent results in an exchange constant along the chain direction comparable to the one in the high-temperature state.Comment: 6 pages, 5 figure

    Functional rescue of dystrophin deficiency in mice caused by frameshift mutations using Campylobacter jejuni Cas9

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    Duchenne muscular dystrophy (DMD) is a fatal, X-linked muscle wasting disease caused by mutations in the DMD gene. In 51% of DMD cases, a reading frame is disrupted because of deletion of several exons. Here, we show that CjCas9 derived from Campylobacter jejuni can be used as a gene editing tool to correct an out-of-frame Dmd exon in Dmd knockout mice. Herein, we used Cas9 derived from S. pyogenes to generate Dmd knockout (KO) mice with a frameshift mutation in Dmd gene. Then, we expressed CjCas9, its single-guide RNA, and the eGFP gene in the tibialis anterior muscle of the Dmd KO mice using an all-in-one adeno-associated virus (AAV) vector. CjCas9 cleaved the target site in the Dmd gene efficiently in vivo and induced small insertions or deletions at the target site. This treatment resulted in conversion of the disrupted Dmd reading frame from out-of-frame to in-frame, leading to the expression of dystrophin in the sarcolemma. Importantly, muscle strength was enhanced in the CjCas9-treated muscles, without off-target mutations, indicating high efficiency and specificity of CjCas9. This work suggests that in vivo DMD frame correction, mediated by CjCas9 has great potential for the treatment of DMD and other neuromuscular diseases
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