Uranium: The problem, or the solution?

Abstract only availableUranium is of great importance as a nuclear fuel and is used to generate electrical power, produce isotopes, and to make weapons. The possibility of developing a realistic flow scheme for nuclear fuel reprocessing or separation for segregation is one that the Chemistry Department at MU consistently looks into. One way to better optimize waste extraction is to possibly bind two separate functional groups to uranyl(VI) [UO22+] so that the reactions will occur selectively. The product of interest is a mixed uranyl iodide/amide and is a novel uranium compound generated for further study. This is accomplished with the following reactions. UO3 --TfOTf--- UO2(OTf)2 UO2I2(THF)3 + 2KOTfUO2(OTf)2 + 2KI ---THF---- UO2I[N(SiMe3)] + KIUO2I2(THF)3 + K[N(SiMe3)3] ----THF- After completing the reactions under an inert atmosphere, an orange product formed. The next step in this research requires NMR analysis and X-Ray crystallography to determine if this product is the target molecule desired.NSF-REU Radiochemistr

52 Genetic Loci Influencing Myocardial Mass.

BACKGROUND: Myocardial mass is a key determinant of cardiac muscle function and hypertrophy. Myocardial depolarization leading to cardiac muscle contraction is reflected by the amplitude and duration of the QRS complex on the electrocardiogram (ECG). Abnormal QRS amplitude or duration reflect changes in myocardial mass and conduction, and are associated with increased risk of heart failure and death. OBJECTIVES: This meta-analysis sought to gain insights into the genetic determinants of myocardial mass. METHODS: We carried out a genome-wide association meta-analysis of 4 QRS traits in up to 73,518 individuals of European ancestry, followed by extensive biological and functional assessment. RESULTS: We identified 52 genomic loci, of which 32 are novel, that are reliably associated with 1 or more QRS phenotypes at p < 1 × 10(-8). These loci are enriched in regions of open chromatin, histone modifications, and transcription factor binding, suggesting that they represent regions of the genome that are actively transcribed in the human heart. Pathway analyses provided evidence that these loci play a role in cardiac hypertrophy. We further highlighted 67 candidate genes at the identified loci that are preferentially expressed in cardiac tissue and associated with cardiac abnormalities in Drosophila melanogaster and Mus musculus. We validated the regulatory function of a novel variant in the SCN5A/SCN10A locus in vitro and in vivo. CONCLUSIONS: Taken together, our findings provide new insights into genes and biological pathways controlling myocardial mass and may help identify novel therapeutic targets

Nfib Promotes Metastasis through a Widespread Increase in Chromatin Accessibility

Metastases are the main cause of cancer deaths, but the mechanisms underlying metastatic progression remain poorly understood. We isolated pure populations of cancer cells from primary tumors and metastases from a genetically engineered mouse model of human small cell lung cancer (SCLC) to investigate the mechanisms that drive the metastatic spread of this lethal cancer. Genome-wide characterization of chromatin accessibility revealed the opening of large numbers of distal regulatory elements across the genome during metastatic progression. These changes correlate with copy number amplification of the Nfib locus, and differentially accessible sites were highly enriched for Nfib transcription factor binding sites. Nfib is necessary and sufficient to increase chromatin accessibility at a large subset of the intergenic regions. Nfib promotes pro-metastatic neuronal gene expression programs and drives the metastatic ability of SCLC cells. The identification of widespread chromatin changes during SCLC progression reveals an unexpected global reprogramming during metastatic progression