The Fate of Terrestrial Dissolved Organic Matter in Ocean Margins Investigated Through Coupled Microbial-Photochemical Incubations of Vascular Plant Leachates

Rivers are the primary link between terrestrial and marine carbon reservoirs. Dissolved organic matter (DOM) contributes the majority of carbon flux between these environments. Understanding the influence of source, availability and transformations of dissolved organic carbon (DOC) in rivers and coastal ocean systems is important to determine the fate of DOM in the marine environment. Coupled microbial-photochemical incubations were used to analyze microbial and photochemical decomposition of plant leachates and to investigate DOM cycling in the Sacramento-San Joaquin River Delta/San Francisco Bay estuary. A wide range of chemical and optical parameters were tracked during coupled incubations including absorbance, fluorescence, enantiomeric amino acids, and neutral sugars measurements. Vascular plant leachates were characterized by high neutral sugar yields and low amino acid yields with variable THAA and THNS composition. Biomarkers that most accurately tracked vascular plant DOM and microbial DOM during coupled incubations were selected to apply to seasonal transects collected from the Sacramento-San Joaquin River Delta and San Francisco Bay, California. Enantiomeric amino acids and neutral sugars were used to investigate the composition and bioavailability of riverine DOM in this natural system. Biochemical trends in the Delta-Bay system were influenced by source inputs, wetlands, and environmental processes. Differences in DOM composition and concentration related to differences in regions, highlighting heterogenetic inputs, hydrology of the system, and in situ production of DOM. Furthermore, terrestrial DOM was already extensively degraded prior to entering the Delta and was largely refractory throughout the Bay. Neutral sugar yields in the transect were used to determine a median of ~10% terrestrial DOC labile fraction, and amino acid yields were used to determine a median of 5% in situ DOM labile fraction. Median total labile fraction in the Delta and Bay was 21% and was influenced by hydrological conditions in the estuary. Our study demonstrated the complexity of river delta and estuarine systems integrating complex varying sources and decomposition trends connected to seasons and flow regime. Bay systems were recognized as efficient filters of terrestrial DOM limiting its flux to the ocean and exerting a major control on air-sea CO2 fluxes, acidification and nutrient budgets in the estuary

Neurotoxicity

Neurotoxicity refers to the direct or indirect effect of chemicals that disrupt the nervous system of humans or animals. Numerous chemicals can produce neurotoxic diseases in humans, and many more are used as experimental tools to disturb or damage the nervous system of animals. Some act directly on neural cells, others interfere with metabolic processes on which the nervous system is especially dependent. Some disrupt neural function, others induce maldevelopment or damage to the adult nervous system. Perturbations may appear and disappear rapidly, evolve slowly over days or weeks and regress over months or years, or cause permanent deficits. Neurotoxicity is usually self-limiting after exposure ceases and rarely progressive in the absence of continued exposure, although there may be a significant delay between exposure and manifestation of neurotoxic effects

Study of policies and practices to inform the Massachusetts Department of Housing and Community Development

Thesis (M.C.P.)--Massachusetts Institute of Technology, Dept. of Urban Studies and Planning, 2009.Includes bibliographical references (leaves 70-73).Local housing authorities in the Commonwealth of Massachusetts currently manage over 50,000 state-aided public housing units on a consolidated, authority-wide level-a style of property management that does not allow for the detailed monitoring or assessment of each property within a local housing authority's portfolio. The private real estate sector and federal public housing authorities with more than 500 federal public housing units manage properties according to an asset management model in which the funding, budgeting, accounting, and management systems are conducted on a property-specific level. Recently adopted for federal public housing authorities, asset management is recognized as an effective tool for generating increased efficiency and accountability as well as improved financial and physical performance for individual properties. Some academics and professionals argue that public housing is fundamentally different from the private sector and should not adopt a private sector business practice. The differences cited include unique resident populations (one is high-need, low-income and the other is independent and financially stable) and the objectives of each sector (one is considered a public service and the other is profit-driven). This thesis investigates the models and mechanisms of two asset management models used in the public housing sector in order to best inform the Massachusetts Department of Housing and Community Development on how to move towards an asset management model for state-aided public housing.(cont.) First, strategic asset management employed by the social rented sectors of Europe and Australia is driven by four primary characteristics: market-oriented, systematic, comprehensive, and proactive. Second, the U.S. Department of Housing and Urban Development's asset management model for federal public housing authorities is technical and process-oriented with a focus on five core reform areas: property-based funding, budgeting, accounting, management, and performance assessment. Each case is informative in creating an asset management model for Massachusetts state-aided public housing that will increase efficiency and accountability, place a focus on property performance, and end the stigma and isolation of public housing.by Hannah Highton Creeley.M.C.P

Alcohol-induced apoptosis of oligodendrocytes in the fetal macaque brain

BACKGROUND: In utero exposure of the fetal non-human primate (NHP) brain to alcohol on a single occasion during early or late third-trimester gestation triggers widespread acute apoptotic death of cells in both gray and white matter (WM) regions of the fetal brain. In a prior publication, we documented that the dying gray matter cells are neurons, and described the regional distribution and magnitude of this cell death response. Here, we present new findings regarding the magnitude, identity and maturational status of the dying WM cells in these alcohol-exposed fetal NHP brains. RESULTS: Our findings document that the dying WM cells belong to the oligodendrocyte (OL) lineage. OLs become vulnerable when they are just beginning to generate myelin basic protein in preparation for myelinating axons, and they remain vulnerable throughout later stages of myelination. We found no evidence linking astrocytes, microglia or OL progenitors to this WM cell death response. The mean density (profiles per mm(3)) of dying WM cells in alcohol-exposed brains was 12.7 times higher than the mean density of WM cells dying by natural apoptosis in drug-naive control brains. CONCLUSIONS: In utero exposure of the fetal NHP brain to alcohol on a single occasion triggers widespread acute apoptotic death of neurons (previous study) and of OLs (present study) throughout WM regions of the developing brain. The rate of OL apoptosis in alcohol-exposed brains was 12.7 times higher than the natural OL apoptosis rate. OLs become sensitive to the apoptogenic action of alcohol when they are just beginning to generate constituents of myelin in their cytoplasm, and they remain vulnerable throughout later stages of myelination. There is growing evidence for a similar apoptotic response of both neurons and OLs following exposure of the developing brain to anesthetic and anticonvulsant drugs. Collectively, this body of evidence raises important questions regarding the role that neuro and oligo apoptosis may play in the human condition known as fetal alcohol spectrum disorder (FASD), and also poses a question whether other apoptogenic drugs, although long considered safe for pediatric/obstetric use, may have the potential to cause iatrogenic FASD-like developmental disability syndromes

Superoxide Production by a Manganese-Oxidizing Bacterium Facilitates Iodide Oxidation

The release of radioactive iodine (i.e., iodine-129 and iodine-131) from nuclear reprocessing facilities is a potential threat to human health. The fate and transport of iodine are determined primarily by its redox status, but processes that affect iodine oxidation states in the environment are poorly characterized. Given the difficulty in removing electrons from iodide (I(−)), naturally occurring iodide oxidation processes require strong oxidants, such as Mn oxides or microbial enzymes. In this study, we examine iodide oxidation by a marine bacterium, Roseobacter sp. AzwK-3b, which promotes Mn(II) oxidation by catalyzing the production of extracellular superoxide (O(2)(−)). In the absence of Mn(2+), Roseobacter sp. AzwK-3b cultures oxidized ∼90% of the provided iodide (10 μM) within 6 days, whereas in the presence of Mn(II), iodide oxidation occurred only after Mn(IV) formation ceased. Iodide oxidation was not observed during incubations in spent medium or with whole cells under anaerobic conditions or following heat treatment (boiling). Furthermore, iodide oxidation was significantly inhibited in the presence of superoxide dismutase and diphenylene iodonium (a general inhibitor of NADH oxidoreductases). In contrast, the addition of exogenous NADH enhanced iodide oxidation. Taken together, the results indicate that iodide oxidation was mediated primarily by extracellular superoxide generated by Roseobacter sp. AzwK-3b and not by the Mn oxides formed by this organism. Considering that extracellular superoxide formation is a widespread phenomenon among marine and terrestrial bacteria, this could represent an important pathway for iodide oxidation in some environments