767 research outputs found

    Number 4 (June 1977)

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    A Status Report on the Bayou Darter, Etheostoma rubrum, and the Bayou Pierre System. By R.D. Suttkus and G. Clemmer, plus News Notes, 4 pp

    A Review of Graphite and Gold Surface Studies for Use as Substrates in Biological Scanning Tunneling Microscopy Studies

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    The current status of biological Scanning Tunneling Microscopy (STM) investigations and the importance of using a well-characterized substrate are discussed. The findings of over two years of experiments and over 1,000 images obtained on gold substrates prepared by a variety of different methods are statistically summarized and compared to a very flat reference substrate, highly oriented pyrolytic graphite (HOPG). In an effort to begin to corroborate STM results with those obtained from other more established techniques, the results of Auger Electron Spectroscopy (AES) and Electron Spectroscopy for Chemical Analysis (ESCA) of biomolecular STM samples are presented

    Janus kinase mutations in mice lacking PU.1 and Spi-B drive B cell leukemia through reactive oxygen species-induced DNA damage

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    Precursor B cell acute lymphoblastic leukemia (B-ALL) is caused by genetic lesions in developing B cells that function as drivers for the accumulation of additional mutations in an evolutionary selection process. We investigated secondary drivers of leukemogenesis in a mouse model of B-ALL driven by PU.1/Spi-B deletion (Mb1-CreΔPB). Whole-exome-sequencing analysis revealed recurrent mutations in Jak3 (encoding Janus kinase 3), Jak1, and Ikzf3 (encoding Aiolos). Mutations with a high variant-allele frequency (VAF) were dominated by C¡T transition mutations that were compatible with activation-induced cytidine deaminase, whereas the majority of mutations, with a low VAF, were dominated by C¡A transversions associated with 8-oxoguanine DNA damage caused by reactive oxygen species (ROS). The Janus kinase (JAK) inhibitor ruxolitinib delayed leukemia onset, reduced ROS and ROS-induced gene expression signatures, and altered ROS-induced mutational signatures. These results reveal that JAK mutations can alter the course of leukemia clonal evolution through ROS-induced DNA damage
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