Browsing by Author "Connors, Liam"

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    Methane oxidation and methylotroph population dynamics in groundwater mesocosms
    (Society for Applied Microbiology and John Wiley & Sons Ltd., 2020-01) Kuloyo, Olukayode; Ruff, S Emil; Cahill, Aaron; Connors, Liam; Zorz, Jackie K; Hrabe de Angelis, Isabella; Nightingale, Michael; Mayer, Bernhard; Strous, Marc
    Extraction of natural gas from unconventional hydrocarbon reservoirs by hydraulic fracturing raises concerns about methane migration into groundwater. Microbial methane oxidation can be a significant methane sink. Here, we inoculated replicated, sand-packed, continuous mesocosms with groundwater from a field methane release experiment. The mesocosms experienced thirty-five weeks of dynamic methane, oxygen and nitrate concentrations. We determined concentrations and stable isotope signatures of methane, carbon dioxide and nitrate and monitored microbial community composition of suspended and attached biomass. Methane oxidation was strictly dependent on oxygen availability and led to enrichment of 13 C in residual methane. Nitrate did not enhance methane oxidation under oxygen limitation. Methylotrophs persisted for weeks in the absence of methane, making them a powerful marker for active as well as past methane leaks. Thirty-nine distinct populations of methylotrophic bacteria were observed. Methylotrophs mainly occurred attached to sediment particles. Abundances of methanotrophs and other methylotrophs were roughly similar across all samples, pointing at transfer of metabolites from the former to the latter. Two populations of Gracilibacteria (Candidate Phyla Radiation) displayed successive blooms, potentially triggered by a period of methane famine. This study will guide interpretation of future field studies and provides increased understanding of methylotroph ecophysiology.
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    Prenatal Exposure to a Low Dose of BPS Causes Sex-Dependent Alterations to Vascular Endothelial Function in Adult Offspring
    (2022-06) Connors, Liam; Thompson, Jennifer; Cole, William; Habibi, Hamid; Ahmed, Sofia
    Background: Bisphenol A (BPA) is among the world’s most ubiquitous industrial chemicals, used as a plasticizer in the manufacture of plastics and epoxy resins. Bisphenols interfere with estrogen receptor (ER) signaling, which modulates vascular function through stimulation of nitric oxide (NO) production by endothelial nitric oxide synthase (eNOS). After regulatory agencies declared BPA to be a toxic substance in 2010, manufacturers turned to substitutes such as bisphenol S (BPS). BPS can cross into the placenta, and it accumulates in the fetal compartment to a greater extent than BPA, potentially interfering with key developmental events. Little is known regarding the developmental impact of exposure to BPA analogues, particularly with respect to vascular development and later-life vascular function. Objective: To determine if prenatal BPS exposure influences vascular health in adulthood through modulation of NO production. Methods: Mesenteric arteries were excised from 12-week-old male and female C57BL/6 mice prenatally exposed to 250 nM BPS and mounted on a pressure myograph. Contractile and dilatory function was assessed by generating concentration-response curves to phenylephrine (Phe) and the endothelium-dependent dilator, acetylcholine (ACh). Wire myography was used to assess dilatory responses of aortic rings after acute exposure to BPS in the bath in the presence or absence of pharmacological inhibitors of eNOS and ER. Results: Vessels isolated from prenatally-exposed males did not exhibit changes in their dilatory or contractile responses. Whereas increased ACh dilation and increased sensitivity to Phe were observed in microvessels from female BPS-exposed mice. The increase in dilation was blocked by inhibition of eNOS. Aortic rings isolated from female mice and acutely exposed to BPS had increased dilatory responses to ACh that were eliminated with inhibition of eNOS or ER. Conclusions: Prenatal BPS exposure leads to endothelium-dependent alterations of vascular function in a sex-specific manner that appears to be modulated by interaction with ER.