Effect of groundwater-lake interactions on the distribution of arsenic in a freshwater beach

This thesis presents field measurements and numerical modeling that provide insight into the nearshore geochemical conditions and groundwater flows controlling the mobility of arsenic (As) in a freshwater beach aquifer and its potential discharge to Lake Erie. Field measurements were performed via shore-normal monitoring transects installed at beaches (Little Beach and Main Beach) located adjacent to a brownfield industrial harbour site that has elevated sediment and groundwater As concentrations. Detailed pore water chemistry analyses revealed elevated As (up to 0.056 mg/L) 1 - 2 m below the shoreline at all transect locations. The distributions of species in the aqueous and sedimentary phases suggest that As mobility is strongly linked with iron (Fe) redox cycling. Sediment analysis by sequential extraction revealed a layer of amorphous and crystalline Fe (hydr)oxides present at the sediment-water interface (SWI) near the shoreline. This Fe hydr(oxide) layer may be accumulating As and preventing its release to nearshore waters. Numerical modeling combined with vertical hydraulic gradient measurements indicated that wave-induced recirculation across the aquifer-lake interface was significant and this likely establishes the redox gradient that led to Fe (hydr)oxides precipitation at the SWI. Numerical and field results showed that the water infiltration/exfiltration across the groundwater-lake interface were sensitive to varying wave intensity and seasonal lake water level fluctuations. The source of As in the nearshore beach aquifers remains unknown. While Little Beach is adjacent to the East Headland of the industrial site where elevated As has been recorded, Main Beach is disconnected hydraulically from the East Headland. If the elevated dissolved As observed is from a natural geogenic source, this findings of this thesis may have widespread implications for As cycling in the nearshore areas of the Great Lakes. Finally, while this study focused on As, the nearshore geochemistry and subsurface flows investigated are be pertinent to understanding the discharge of other chemicals (e.g., nitrate, ammonium, phosphorous) to nearshore inland coastal waters via the groundwater pathway

CpG islands influence chromatin structure via the CpG-binding protein Cfp1

CpG islands (CGIs) are prominent in the mammalian genome owing to their GC-rich base composition and high density of CpG dinucleotides(1,2). Most human gene promoters are embedded within CGIs that lack DNA methylation and coincide with sites of histone H3 lysine 4 trimethylation (H3K4me3), irrespective of transcriptional activity(3,4). In spite of these intriguing correlations, the functional significance of non-methylated CGI sequences with respect to chromatin structure and transcription is unknown. By performing a search for proteins that are common to all CGIs, here we show high enrichment for Cfp1, which selectively binds to non-methylated CpGs in vitro(5,6). Chromatin immunoprecipitation of a mono-allelically methylated CGI confirmed that Cfp1 specifically associates with non-methylated CpG sites in vivo. High throughput sequencing of Cfp1-bound chromatin identified a notable concordance with non-methylated CGIs and sites of H3K4me3 in the mouse brain. Levels of H3K4me3 at CGIs were markedly reduced in Cfp1-depleted cells, consistent with the finding that Cfp1 associates with the H3K4 methyltransferase Setd1 (refs 7, 8). To test whether non-methylated CpG-dense sequences are sufficient to establish domains of H3K4me3, we analysed artificial CpG clusters that were integrated into the mouse genome. Despite the absence of promoters, the insertions recruited Cfp1 and created new peaks of H3K4me3. The data indicate that a primary function of non-methylated CGIs is to genetically influence the local chromatin modification state by interaction with Cfp1 and perhaps other CpG-binding proteins

A922 Sequential measurement of 1 hour creatinine clearance (1-CRCL) in critically ill patients at risk of acute kidney injury (AKI)

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