44 research outputs found

    Variable climatic conditions dominate recent phytoplankton dynamics in Chesapeake Bay

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    Variable climatic conditions strongly influence phytoplankton dynamics in estuaries globally. Our study area is Chesapeake Bay, a highly productive ecosystem providing natural resources, transportation, and recreation for nearly 16 million people inhabiting a 165,000-km2 watershed. Since World War II, nutrient over-enrichment has led to multiple ecosystem impairments caused by increased phytoplankton biomass as chlorophyll-a (chl-a). Doubled nitrogen (N) loadings from 1945–1980 led to increased chl-a, reduced water clarity, and low dissolved oxygen (DO), while decreased N loadings from 1981–2012 suggest modest improvement. The recent 30+ years are characterized by high inter-annual variability of chl-a, coinciding with irregular dry and wet periods, complicating the detection of long-term trends. Here, we synthesize time-series data for historical and recent N loadings (TN, NO2 + NO3), chl-a, floral composition, and net primary productivity (NPP) to distinguish secular changes caused by nutrient over-enrichment from spatio-temporal variability imposed by climatic conditions. Wet years showed higher chl-a, higher diatom abundance, and increased NPP, while dry years showed lower chl-a, lower diatom abundance, and decreased NPP. Our findings support a conceptual model wherein variable climatic conditions dominate recent phytoplankton dynamics against a backdrop of nutrient over-enrichment, emphasizing the need to separate these effects to gauge progress toward improving water quality in estuaries

    High and low levels of an NTRK2-driven genetic profile affect motor- and cognition-associated frontal gray matter in prodromal Huntington’s disease

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    This study assessed how BDNF (brain-derived neurotrophic factor) and other genes involved in its signaling influence brain structure and clinical functioning in pre-diagnosis Huntington’s disease (HD). Parallel independent component analysis (pICA), a multivariate method for identifying correlated patterns in multimodal datasets, was applied to gray matter concentration (GMC) and genomic data from a sizeable PREDICT-HD prodromal cohort (N = 715). pICA identified a genetic component highlighting NTRK2, which encodes BDNF’s TrkB receptor, that correlated with a GMC component including supplementary motor, precentral/premotor cortex, and other frontal areas (p < 0.001); this association appeared to be driven by participants with high or low levels of the genetic profile. The frontal GMC profile correlated with cognitive and motor variables (Trail Making Test A (p = 0.03); Stroop Color (p = 0.017); Stroop Interference (p = 0.04); Symbol Digit Modalities Test (p = 0.031); Total Motor Score (p = 0.01)). A top-weighted NTRK2 variant (rs2277193) was protectively associated with Trail Making Test B (p = 0.007); greater minor allele numbers were linked to a better performance. These results support the idea of a protective role of NTRK2 in prodromal HD, particularly in individuals with certain genotypes, and suggest that this gene may influence the preservation of frontal gray matter that is important for clinical functioning.This project was supported by 1U01NS082074 (V.C. and J.T., co-principal investigators) from the National Institutes of Health, National Institute of Neurological Disorders and Stroke. The PREDICT-HD study was supported by NIH/NINDS grant 5R01NS040068 awarded to J.P.; CHDI Foundation, Inc., A3917 and 6266 awarded to J.P.; Cognitive and Functional Brain Changes in Preclinical Huntington’s Disease (HD) 5R01NS054893 awarded to J.P.; 4D Shape Analysis for Modeling Spatiotemporal Change Trajectories in Huntington’s 1U01NS082086; Functional Connectivity in Premanifest Huntington’s Disease 1U01NS082083; and Basal Ganglia Shape Analysis and Circuitry in Huntington’s Disease 1U01NS082085 awarded to Christopher A. Ross

    Program- and service-level costs of seven screening, brief intervention, and referral to treatment programs

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    Jeremy W Bray,1 Erin Mallonee,2 William Dowd,2 Arnie Aldridge,2 Alexander J Cowell,2 Janice Vendetti31Department of Economics, Bryan School of Business and Economics, University of North Carolina at Greensboro, Greensboro, NC, USA; 2RTI International, Research Triangle Park, NC, USA; 3Department of Community Medicine and Health Care, School of Medicine, UCONN Health, Farmington, CT, USAAbstract: This paper examines the costs of delivering screening, brief intervention, and referral to treatment (SBIRT) services within the first seven demonstration programs funded by the US Substance Abuse and Mental Health Services Administration. Service-level costs were estimated and compared across implementation model (contracted specialist, inhouse specialist, inhouse generalist) and service delivery setting (emergency department, hospital inpatient, outpatient). Program-level costs were estimated and compared across grantee recipient programs. Service-level data were collected through timed observations of SBIRT service delivery. Program-level data were collected during key informant interviews using structured cost interview guides. At the service level, support activities that occur before or after engaging the patient comprise a considerable portion of the cost of delivering SBIRT services, especially short duration services. At the program level, average costs decreased as more patients were screened. Comparing across program and service levels, the average annual operating costs calculated at the program level often exceeded the cost of actual service delivery. Provider time spent in support of service provision may comprise a large share of the costs in some cases because of potentially substantial fixed and quasifixed costs associated with program operation. The cost structure of screening, brief intervention, and referral to treatment is complex and discontinuous of patient flow, causing annual operating costs to exceed the costs of actual service provision for some settings and implementation models.Keywords: screening, brief intervention, brief treatment, SBIRT, cos

    Etiology of growth hormone deficiency in little, Ames, and Snell dwarf mice.

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    There are three recessive genes (little, Snell, and Ames) which cause dwarfism and GH deficiency in mice. These genes are nonallelic, and in the case of little mice, GH deficiency is isolated, while Snell and Ames dwarfs have deficiencies of GH as well as other anterior pituitary hormones. Previous reports in which restriction endonuclease analyses were used suggested that the GH genes are grossly intact in each of these types of dwarfs. In this report, ultrastructural studies of the anterior pituitary glands of little mice showed a deficiency or absence of secretory granules within somatotropes, while Snell and Ames dwarf pituitaries lacked identifiable somatotropes. Furthermore, there were deficiencies of GH precursor RNA and mRNA in total RNA from little pituitaries, while GH transcripts appeared to be absent in total RNA from Snell or Ames dwarf pituitaries. Thus, the primary defect in little mice may be in the production of GH transcripts, while GH deficiency in Snell and Ames dwarfs is probably due to defects other than alterations of the GH genes
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