56 research outputs found

    Gene Mitchell Gray Pioneer Award (2013)

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    Remediating a Toxic Town: Power, Place, and Justice in Anniston, Alabama

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    This dissertation examines a struggle for Environmental Justice over the long term to understand the impacts of current state-led strategies for achieving Environmental Justice. Recent geographic scholarship in Environmental Justice literatures suggests that state-centric strategies come with problems scholars have yet to fully comprehend. This dissertation, based on fieldwork and archival research in Anniston, Alabama, supports this claim with three main findings: 1) Corporations produce scaled identities to advantageously empower themselves and weather shifts in their profitability, while ordinary people are limited in their capacity to respond in kind to such unequal power arrangements. 2) Current legal solutions for Environmental Justice are not meeting the demands expressed by Environmental Justice movement actors, and in themselves demonstrate a resistance to solutions that would more fairly address a collective body of victims due to the normative economizing of neoliberalism. 3) The process of remediation is confined to limiting risks from the physical environment, even while the city itself continues to struggle. This can cause a source of pain and frustration for residents who remain in impacted areas, who wish to see a more holistic solution to resolving environmental injustice, including remediating a sense of place

    Justice, Truth, and Community Organizing in Boston, MA

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    In 2010, community organizers in Boston, MA began to lay the groundwork for a truth and reconciliation process about the long-term impacts of the violence and racism surrounding the desegregation/busing crisis in the 1970s. Organizers believe that the busing crisis still presents impediments to the ability of communities of color in Boston to live well and participate in public life. I contextualize their efforts first as a response to the failures of the liberal democratic reforms that marked the civil rights movement. Rather than truly reforming the structures that permit the existence of racialized inequalities, I argue that the liberal democratic state instead systematically preserves and enhances white privileged access to resources. The state does this by resolving crises in such a way that places racism and inequality outside the purview of state responsibility by constructing a “post-racist” sensibility. I demonstrate this by examining two seminal court cases in Boston: Morgan v. Hennigan and Wessman v. Boston School Committee. Second, in order to achieve equality, I argue that the notions of justice and rights must be expanded in order to achieve a positive conception of rights—one in which it is possible to advocate for the rights of groups rather than liberal individuals. Thus, I conceptualize the organizers’ efforts as a way to use a restorative conception of justice to assert a Right to the City, in terms of asserting a right to live well and participate in public life

    The Relationship Between Lifestyle and Eating Behaviors in College Students

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    A Research Methods Project supervised by Dr. Laura Wilson (Fall 2021)

    Bilateral Remote Ischemic Conditioning in Children:a two-center, double-blind, randomized controlled trial in young children undergoing cardiac surgery

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    Objective: The study objective was to determine whether adequately delivered bilateral remote ischemic preconditioning is cardioprotective in young children undergoing surgery for 2 common congenital heart defects with or without cyanosis.Methods: We performed a prospective, double-blind, randomized controlled trial at 2 centers in the United Kingdom. Children aged 3 to 36 months undergoing tetralogy of Fallot repair or ventricular septal defect closure were randomized 1:1 to receive bilateral preconditioning or sham intervention. Participants were followed up until hospital discharge or 30 days. The primary outcome was area under the curve for high-sensitivity troponin-T in the first 24 hours after surgery, analyzed by intention-to-treat. Right atrial biopsies were obtained in selected participants.Results: Between October 2016 and December 2020, 120 eligible children were randomized to receive bilateral preconditioning (n = 60) or sham intervention (n = 60). The primary outcome, area under the curve for high-sensitivity troponin-T, was higher in the preconditioning group (mean: 70.0 ± 50.9 μg/L/h, n = 56) than in controls (mean: 55.6 ± 30.1 μg/L/h, n = 58) (mean difference, 13.2 μg/L/h; 95% CI, 0.5-25.8; P = .04). Subgroup analyses did not show a differential treatment effect by oxygen saturations (pinteraction = .25), but there was evidence of a differential effect by underlying defect (pinteraction = .04). Secondary outcomes and myocardial metabolism, quantified in atrial biopsies, were not different between randomized groups.Conclusions: Bilateral remote ischemic preconditioning does not attenuate myocardial injury in children undergoing surgical repair for congenital heart defects, and there was evidence of potential harm in unstented tetralogy of Fallot. The routine use of remote ischemic preconditioning cannot be recommended for myocardial protection during pediatric cardiac surgery

    Estuarine sediment hydrocarbon-degrading microbial communities demonstrate resilience to nanosilver

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    Little is currently known about the potential impact of silver nanoparticles (AgNPs) on estuarine microbial communities. The Colne estuary, UK, is susceptible to oil pollution through boat traffic, and there is the potential for AgNP exposure via effluent discharged from a sewage treatment works located in close proximity. This study examined the effects of uncapped AgNPs (uAgNPs), capped AgNPs (cAgNPs) and dissolved Ag2SO4, on hydrocarbon-degrading microbial communities in estuarine sediments. The uAgNPs, cAgNPs and Ag2SO4 (up to 50 mg L−1) had no significant impact on hydrocarbon biodegradation (80–92% hydrocarbons were biodegraded by day 7 in all samples). Although total and active cell counts in oil-amended sediments were unaffected by silver exposure; total cell counts in non-oiled sediments decreased from 1.66 to 0.84 × 107 g−1 dry weight sediment (dws) with 50 mg L−1 cAgNPs and from 1.66 to 0.66 × 107 g−1 dws with 0.5 mg L−1 Ag2SO4 by day 14. All silver-exposed sediments also underwent significant shifts in bacterial community structure, and one DGGE band corresponding to a member of Bacteroidetes was more prominent in non-oiled microcosms exposed to 50 mg L−1 Ag2SO4 compared to non-silver controls. In conclusion, AgNPs do not appear to affect microbial hydrocarbon-degradation but do impact on bacterial community diversity, which may have potential implications for other important microbial-mediated processes in estuaries

    Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial

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    Background Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy

    Regulatory T Cells Expanded from Hiv-1-Infected Individuals Maintain Phenotype, Tcr Repertoire and Suppressive Capacity

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    While modulation of regulatory T cell (Treg) function and adoptive Treg transfer are being explored as therapeutic modalities in the context of autoimmune diseases, transplantation and cancer, their role in HIV-1 pathogenesis remains less well defined. Controversy persists regarding their beneficial or detrimental effects in HIV-1 disease, which warrants further detailed exploration. Our objectives were to investigate if functional CD4+ Tregs can be isolated and expanded from HIV-1-infected individuals for experimental or potential future therapeutic use and to determine phenotype and suppressive capacity of expanded Tregs from HIV-1 positive blood and tissue. Tregs and conventional T cell controls were isolated from blood and gut-associated lymphoid tissue of individuals with HIV-1 infection and healthy donors using flow-based cell-sorting. The phenotype of expanded Tregs was assessed by flow-cytometry and quantitative PCR. T-cell receptor ß-chain (TCR-β) repertoire diversity was investigated by deep sequencing. Flow-based T-cell proliferation and chromium release cytotoxicity assays were used to determine Treg suppressive function. Tregs from HIV-1 positive individuals, including infants, were successfully expanded from PBMC and GALT. Expanded Tregs expressed high levels of FOXP3, CTLA4, CD39 and HELIOS and exhibited a highly demethylated TSDR (Treg-specific demethylated region), characteristic of Treg lineage. The TCRß repertoire was maintained following Treg expansion and expanded Tregs remained highly suppressive in vitro. Our data demonstrate that Tregs can be expanded from blood and tissue compartments of HIV-1+ donors with preservation of Treg phenotype, function and TCR repertoire. These results are highly relevant for the investigation of potential future therapeutic use, as currently investigated for other disease states and hold great promise for detailed studies on the role of Tregs in HIV-1 infection.Elizabeth Glaser Pediatric AIDS Foundation (Pediatric HIV Vaccine Program Award MV-00-9-900-1429-0-00)Massachusetts General Hospital. Executive Committee on Research (MGH/ECOR Physician Scientist Development Award)National Institutes of Health (U.S.) (NIH NIAID (KO8 AI074405))National Institutes of Health (U.S.) (NIH NIAID AI074405-03S1)Massachusetts General Hospital (William F. Milton Fund)Harvard University. Center for AIDS Research (CFAR Scholar Award)Massachusetts General Hospital. Center for the Study Inflammatory Bowel Disease (P30DK043351)Harvard University. Center for AIDS Research (NIH funded program (5P30AI060354-09
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