Assessment of Sediment Contamination in Casco Bay

EXECUTIVE SUMMARY Contaminant concentrations of sediment samples collected approximately 10 years apart are compared in an attempt to establish current status of contaminant concentrations in Casco Bay, to determine whether contaminant concentrations are increasing, decreasing or remain unchanged, and to examine any changes in the geographical distribution of contaminants. This process is complicated by the potential of re-suspension of older sediment back to the surface, the non-homogeneity of sediments, low concentrations for some analytes and variability of different analytical methods. In spite of these complications several trends are observed. As expected, most of the contaminants appear to be decreasing in concentrations. Total PAH concentrations in the sediment are an exception. When comparing total PAH concentration in 1991 and 2001, there is neither an increase nor a decrease when the analytical uncertainties are considered. The continuing increased use of fossil fuels that may add additional PAH to the sediments appears to be balanced by increasing controls that lower PAH inputs. Total pesticides as well as 4,4-DDE, 4,4-DDD and total DDTs indicate a decrease from 1991 to 2000/2001. Total PCB concentrations also suggest a decrease over this time period. Silver is the only trace element increasing in concentration at most sampling sites from 1991 to 2001. The reason for this difference is not clear. Concentrations decreased at the majority of the sampling sites for cadmium, chromium, mercury, nickel, and selenium with no apparent difference for arsenic, copper lead and zinc. Tributyltin and total butyltin concentrations decreased over the time period from 1994 to 2000/2001. The overall indication for dioxin/furans is no change between sampling periods. The planar PCB indicates no change (PCB 77) or decreasing concentrations (PCB 126). With the many complicating factors, the interpretation of these data needs to be done with care. There is no indication from these data that any of the contaminants measured has increased by more than a factor of 2. At most Casco Bay sites and for most analytes there is either no change or a decrease. There are sites where increases are apparent and many of these sites are at the shallow water sites or at the Inner Bay sites where concentrations are higher and new inputs are more likely Sediments from the Inner Bay region of Casco Bay; closest to Portland, ME; contain the highest levels of trace metals, PCBs, DDTs, and chlordane. For contaminants other than PAH (and these only at a few locations) and PCBs at one location, the levels of contamination in Casco Bay would not be considered high on a national basis, based on Macauley et al. (1994). The geographical distribution of most contaminants remains similar to those determined in 1991/1994. There are generally higher contaminant concentrations in the vicinity of Portland and other populated and industrial areas. Toxicity tests for selected sites and comparison of 2 contamination concentrations to ERL or ERM indicate the sediments are not toxic. The overall conclusion based on the available data is that the contaminant loading for Casco Bay, as a whole, is decreasing or remaining the same and these concentrations are not likely to adversely affect the biota. The geographic distribution of sediment contaminants is generally confirmed in the analysis of mussel tissue by the Casco Bay Estuary Project and the Maine Department of Environmental Protection (DEP) (Doggett, DEP, personal communication)

Electromagnetic Fluctuations during Fast Reconnection in a Laboratory Plasma

Clear evidence for a positive correlation is established between the magnitude of magnetic fluctuations in the lower-hybrid frequency range and enhancement of reconnection rates in a well-controlled laboratory plasma. The fluctuations belong to the right-hand polarized whistler wave branch, propagating obliquely to the reconnecting magnetic field, with a phase velocity comparable to the relative drift velocity between electrons and ions. The short coherence length and large variation along the propagation direction indicate their strongly nonlinear nature in three dimensions.Comment: 4 pages, 6 figures, submitted to Phys. Rev. Let

Chronic cisplatin treatment promotes enhanced damage repair and tumor progression in a mouse model of lung cancer

Chemotherapy resistance is a major obstacle in cancer treatment, yet the mechanisms of response to specific therapies have been largely unexplored in vivo. Employing genetic, genomic, and imaging approaches, we examined the dynamics of response to a mainstay chemotherapeutic, cisplatin, in multiple mouse models of human non-small-cell lung cancer (NSCLC). We show that lung tumors initially respond to cisplatin by sensing DNA damage, undergoing cell cycle arrest, and inducing apoptosis—leading to a significant reduction in tumor burden. Importantly, we demonstrate that this response does not depend on the tumor suppressor p53 or its transcriptional target, p21. Prolonged cisplatin treatment promotes the emergence of resistant tumors with enhanced repair capacity that are cross-resistant to platinum analogs, exhibit advanced histopathology, and possess an increased frequency of genomic alterations. Cisplatin-resistant tumors express elevated levels of multiple DNA damage repair and cell cycle arrest-related genes, including p53-inducible protein with a death domain (Pidd). We demonstrate a novel role for PIDD as a regulator of chemotherapy response in human lung tumor cells.National Institutes of Health (U.S.) (grant 5-UO1-CA84306)National Cancer Institute (U.S.) (CA034992

Synaptic Dysbindin-1 Reductions in Schizophrenia Occur in an Isoform-Specific Manner Indicating Their Subsynaptic Location

Background: An increasing number of studies report associations between variation in DTNBP1, a top candidate gene in schizophrenia, and both the clinical symptoms of the disorder and its cognitive deficits. DTNBP1 encodes dysbindin-1, reduced levels of which have been found in synaptic fields of schizophrenia cases. This study determined whether such synaptic reductions are isoform-specific. Methodology/Principal Findings: Using Western blotting of tissue fractions, we first determined the synaptic localization of the three major dysbindin-1 isoforms (A, B, and C). All three were concentrated in synaptosomes of multiple brain areas, including auditory association cortices in the posterior half of the superior temporal gyrus (pSTG) and the hippocampal formation (HF). Tests on the subsynaptic tissue fractions revealed that each isoform is predominantly, if not exclusively, associated with synaptic vesicles (dysbindin-1B) or with postsynaptic densities (dysbindin-1A and -1C). Using Western blotting on pSTG (n = 15) and HF (n = 15) synaptosomal fractions from schizophrenia cases and their matched controls, we discovered that synaptic dysbindin-1 is reduced in an isoform-specific manner in schizophrenia without changes in levels of synaptophysin or PSD-95. In pSTG, about 92% of the schizophrenia cases displayed synaptic dysbindin-1A reductions averaging 48% (p = 0.0007) without alterations in other dysbindin-1 isoforms. In the HF, by contrast, schizophrenia cases displayed normal levels of synaptic dysbindin-1A, but 67% showed synaptic reductions in dysbindin-1B averaging 33% (p = 0.0256), while 80% showed synaptic reductions in dysbindin-1C averaging 35% (p = 0.0171). Conclusions/Significance: Given the distinctive subsynaptic localization of dysbindin-1A, -1B, and -1C across brain regions, the observed pSTG reductions in dysbindin-1A are postsynaptic and may promote dendritic spine loss with consequent disruption of auditory information processing, while the noted HF reductions in dysbindin-1B and -1C are both presynaptic and postsynaptic and could promote deficits in spatial working memory

Analyses of Water Samples From the Deepwater Horizon Oil Spill: Documentation of the Subsurface Plume

Surface and subsurface water samples were collected in the vicinity of the Deepwater Horizon (DWH) wellhead in the Gulf of Mexico. Samples were extracted with dichloromethane and analyzed for a toxic component, polycyclic aromatic hydrocarbons (PAHs), using total scanning fluorescence (TSF) and by gas chromatography/mass spectrometry (GC/MS). An aliquot of fresh, floating oil from a surface sample was used as a DWH oil reference standard. Twelve of 19 samples collected from 24 May 2010 to 6 June 2010 on the R/V Walton Smith cruise contained TSF maximum intensities above background (0.7 µg L À1 based on 1 L sample size). These 12 samples had total petroleum hydrocarbon (TPH) concentrations as measured by quantitative gas chromatography flame ionization detector (FID) ranging from 2 to 442 µg L À1 . Quantitative GC/MS analysis of these 12 samples resulted in total PAH concentrations ranging from 0.01 to 59 µg L À1 . Low molecular weight, more water-soluble naphthalene and alkylated naphthalene dominated the PAH composition patterns for 11 of the 12 water samples. Sample 12 exhibited substantially reduced concentrations of naphthalenes relative to other PAH compounds. The total PAH concentrations were positively correlated (R 2 = 0.80) with the TSF maximum intensity (MI). TSF is a simple, rapid technique providing an accurate prediction of the amount of PAH present in a sample. TSFderived estimates of the relative contribution of PAH present in the oil provided evidence that PAH represented~10% of the higher molecular weight TPH. The subsurface oil plume was confirmed by the analyses of discrete water samples for TSF, TPH, and PAH

The state of the Martian climate

60°N was +2.0°C, relative to the 1981–2010 average value (Fig. 5.1). This marks a new high for the record. The average annual surface air temperature (SAT) anomaly for 2016 for land stations north of starting in 1900, and is a significant increase over the previous highest value of +1.2°C, which was observed in 2007, 2011, and 2015. Average global annual temperatures also showed record values in 2015 and 2016. Currently, the Arctic is warming at more than twice the rate of lower latitudes

Low Pathogenic Avian Influenza Isolates from Wild Birds Replicate and Transmit via Contact in Ferrets without Prior Adaptation

Direct transmission of avian influenza viruses to mammals has become an increasingly investigated topic during the past decade; however, isolates that have been primarily investigated are typically ones originating from human or poultry outbreaks. Currently there is minimal comparative information on the behavior of the innumerable viruses that exist in the natural wild bird host. We have previously demonstrated the capacity of numerous North American avian influenza viruses isolated from wild birds to infect and induce lesions in the respiratory tract of mice. In this study, two isolates from shorebirds that were previously examined in mice (H1N9 and H6N1 subtypes) are further examined through experimental inoculations in the ferret with analysis of viral shedding, histopathology, and antigen localization via immunohistochemistry to elucidate pathogenicity and transmission of these viruses. Using sequence analysis and glycan binding analysis, we show that these avian viruses have the typical avian influenza binding pattern, with affinity for cell glycoproteins/glycolipids having terminal sialic acid (SA) residues with α 2,3 linkage [Neu5Ac(α2,3)Gal]. Despite the lack of α2,6 linked SA binding, these AIVs productively infected both the upper and lower respiratory tract of ferrets, resulting in nasal viral shedding and pulmonary lesions with minimal morbidity. Moreover, we show that one of the viruses is able to transmit to ferrets via direct contact, despite its binding affinity for α 2,3 linked SA residues. These results demonstrate that avian influenza viruses, which are endemic in aquatic birds, can potentially infect humans and other mammals without adaptation. Finally this work highlights the need for additional study of the wild bird subset of influenza viruses in regard to surveillance, transmission, and potential for reassortment, as they have zoonotic potential

Lives saved with vaccination for 10 pathogens across 112 countries in a pre-COVID-19 world.

BackgroundVaccination is one of the most effective public health interventions. We investigate the impact of vaccination activities for Haemophilus influenzae type b, hepatitis B, human papillomavirus, Japanese encephalitis, measles, Neisseria meningitidis serogroup A, rotavirus, rubella, Streptococcus pneumoniae, and yellow fever over the years 2000-2030 across 112 countries.MethodsTwenty-one mathematical models estimated disease burden using standardised demographic and immunisation data. Impact was attributed to the year of vaccination through vaccine-activity-stratified impact ratios.ResultsWe estimate 97 (95%CrI[80, 120]) million deaths would be averted due to vaccination activities over 2000-2030, with 50 (95%CrI[41, 62]) million deaths averted by activities between 2000 and 2019. For children under-5 born between 2000 and 2030, we estimate 52 (95%CrI[41, 69]) million more deaths would occur over their lifetimes without vaccination against these diseases.ConclusionsThis study represents the largest assessment of vaccine impact before COVID-19-related disruptions and provides motivation for sustaining and improving global vaccination coverage in the future.FundingVIMC is jointly funded by Gavi, the Vaccine Alliance, and the Bill and Melinda Gates Foundation (BMGF) (BMGF grant number: OPP1157270 / INV-009125). Funding from Gavi is channelled via VIMC to the Consortium's modelling groups (VIMC-funded institutions represented in this paper: Imperial College London, London School of Hygiene and Tropical Medicine, Oxford University Clinical Research Unit, Public Health England, Johns Hopkins University, The Pennsylvania State University, Center for Disease Analysis Foundation, Kaiser Permanente Washington, University of Cambridge, University of Notre Dame, Harvard University, Conservatoire National des Arts et Métiers, Emory University, National University of Singapore). Funding from BMGF was used for salaries of the Consortium secretariat (authors represented here: TBH, MJ, XL, SE-L, JT, KW, NMF, KAMG); and channelled via VIMC for travel and subsistence costs of all Consortium members (all authors). We also acknowledge funding from the UK Medical Research Council and Department for International Development, which supported aspects of VIMC's work (MRC grant number: MR/R015600/1).JHH acknowledges funding from National Science Foundation Graduate Research Fellowship; Richard and Peggy Notebaert Premier Fellowship from the University of Notre Dame. BAL acknowledges funding from NIH/NIGMS (grant number R01 GM124280) and NIH/NIAID (grant number R01 AI112970). The Lives Saved Tool (LiST) receives funding support from the Bill and Melinda Gates Foundation.This paper was compiled by all coauthors, including two coauthors from Gavi. Other funders had no role in study design, data collection, data analysis, data interpretation, or writing of the report. All authors had full access to all the data in the study and had final responsibility for the decision to submit for publication