186 research outputs found
Evaluating the role of sedimentâbacteria interactions on Escherichia coli concentrations at beaches in southern Lake Michigan
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/102640/1/jgrc20481.pd
Ultrasound evaluation of the abductor hallucis muscle: Reliability study
© 2008 Cameron et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution Licens
Characterization of magnesium requirement of human 5'-tyrosyl DNA phosphodiesterase mediated reaction
<p>Abstract</p> <p>Background</p> <p>Topo-poisons can produce an enzyme-DNA complex linked by a 3'- or 5'-phosphotyrosyl covalent bond. 3'-phosphotyrosyl bonds can be repaired by tyrosyl DNA phosphodiesterase-1 (TDP1), an enzyme known for years, but a complementary human enzyme 5'-tyrosyl DNA phosphodiesterase (hTDP2) that cleaves 5'-phosphotyrosyl bonds has been reported only recently. Although hTDP2 possesses both 3'- and 5'- tyrosyl DNA phosphodiesterase activity, the role of Mg<sup>2+ </sup>in its activity was not studied in sufficient details.</p> <p>Results</p> <p>In this study we showed that purified hTDP2 does not exhibit any 5'-phosphotyrosyl phosphodiesterase activity in the absence of Mg<sup>2+</sup>/Mn<sup>2+</sup>, and that neither Zn<sup>2+ </sup>or nor Ca<sup>2+ </sup>can activate hTDP2. Mg<sup>2+ </sup>also controls 3'-phosphotyrosyl activity of TDP2. In MCF-7 cell extracts and de-yolked zebrafish embryo extracts, Mg<sup>2+ </sup>controlled 5'-phosphotyrosyl activity. This study also showed that there is an optimal Mg<sup>2+ </sup>concentration above which it is inhibitory for hTDP2 activity.</p> <p>Conclusion</p> <p>These results altogether reveal the optimal Mg<sup>2+ </sup>requirement in hTDP2 mediated reaction.</p
Additive Anti-Tumor Effects of Lovastatin and Everolimus In Vitro through Simultaneous Inhibition of Signaling Pathways
This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are creditedThis work was supported by a research grant from the Ludwig-Maximilians University of Munich (Förderprogramm fĂŒr Forschung und Lehre [FöFoLe], grant number 865/829)
Observational Constraints on the Merger History of Galaxies since z â 6: Probabilistic Galaxy Pair Counts in the CANDELS Fields
Galaxy mergers are expected to have a significant role in the mass assembly
of galaxies in the early Universe, but there are very few observational
constraints on the merger history of galaxies at . We present the first
study of galaxy major mergers (mass ratios 1:4) in mass-selected samples
out to . Using all five fields of the HST/CANDELS survey and a
probabilistic pair count methodology that incorporates the full photometric
redshift posteriors and corrections for stellar mass completeness, we measure
galaxy pair-counts for projected separations between 5 and 30 kpc in stellar
mass selected samples at
and . We find that the major
merger pair fraction rises with redshift to proportional to
, with () for ().
Investigating the pair fraction as a function of mass ratio between 1:20 and
1:1, we find no evidence for a strong evolution in the relative numbers of
minor to major mergers out to . Using evolving merger timescales we find
that the merger rate per galaxy () rises rapidly from Gyr at to Gyr at for galaxies
at . The corresponding co-moving
major merger rate density remains roughly constant during this time, with rates
of Gyr Mpc. Based on the observed merger
rates per galaxy, we infer specific mass accretion rates from major mergers
that are comparable to the specific star-formation rates for the same mass
galaxies at - observational evidence that mergers are as important a
mechanism for building up mass at high redshift as in-situ star-formation.Comment: 36 pages, 17 figures. Accepted for publication in Ap
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Cancer therapy shapes the fitness landscape of clonal hematopoiesis.
Acquired mutations are pervasive across normal tissues. However, understanding of the processes that drive transformation of certain clones to cancer is limited. Here we study this phenomenon in the context of clonal hematopoiesis (CH) and the development of therapy-related myeloid neoplasms (tMNs). We find that mutations are selected differentially based on exposures. Mutations in ASXL1 are enriched in current or former smokers, whereas cancer therapy with radiation, platinum and topoisomerase II inhibitors preferentially selects for mutations in DNA damage response genes (TP53, PPM1D, CHEK2). Sequential sampling provides definitive evidence that DNA damage response clones outcompete other clones when exposed to certain therapies. Among cases in which CH was previously detected, the CH mutation was present at tMN diagnosis. We identify the molecular characteristics of CH that increase risk of tMN. The increasing implementation of clinical sequencing at diagnosis provides an opportunity to identify patients at risk of tMN for prevention strategies
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