Mapping historical forest biomass for stock-change assessments at parcel to landscape scales

Understanding historical forest dynamics, specifically changes in forest biomass and carbon stocks, has become critical for assessing current forest climate benefits and projecting future benefits under various policy, regulatory, and stewardship scenarios. Carbon accounting frameworks based exclusively on national forest inventories are limited to broad-scale estimates, but model-based approaches that combine these inventories with remotely sensed data can yield contiguous fine-resolution maps of forest biomass and carbon stocks across landscapes over time. Here we describe a fundamental step in building a map-based stock-change framework: mapping historical forest biomass at fine temporal and spatial resolution (annual, 30m) across all of New York State (USA) from 1990 to 2019, using freely available data and open-source tools. Using Landsat imagery, US Forest Service Forest Inventory and Analysis (FIA) data, and off-the-shelf LiDAR collections we developed three modeling approaches for mapping historical forest aboveground biomass (AGB): training on FIA plot-level AGB estimates (direct), training on LiDAR-derived AGB maps (indirect), and an ensemble averaging predictions from the direct and indirect models. Model prediction surfaces (maps) were tested against FIA estimates at multiple scales. All three approaches produced viable outputs, yet tradeoffs were evident in terms of model complexity, map accuracy, saturation, and fine-scale pattern representation. The resulting map products can help identify where, when, and how forest carbon stocks are changing as a result of both anthropogenic and natural drivers alike. These products can thus serve as inputs to a wide range of applications including stock-change assessments, monitoring reporting and verification frameworks, and prioritizing parcels for protection or enrollment in improved management programs.Comment: Manuscript: 24 pages, 7 figures; Supplements: 12 pages, 5 figures; Submitted to Forest Ecology and Managemen

Noradrenergic α1 Receptor Antagonist Treatment Attenuates Positive Subjective Effects of Cocaine in Humans: A Randomized Trial

Preclinical research implicates dopaminergic and noradrenergic mechanisms in mediating the reinforcing effects of drugs of abuse, including cocaine. The objective of this study was to evaluate the impact of treatment with the noradrenergic α(1) receptor antagonist doxazosin on the positive subjective effects of cocaine.Thirteen non-treatment seeking, cocaine-dependent volunteers completed this single-site, randomized, placebo-controlled, within-subjects study. In one study phase volunteers received placebo and in the other they received doxazosin, with the order counterbalanced across participants. Study medication was masked by over-encapsulating doxazosin tablets and matched placebo lactose served as the control. Study medication treatment was initiated at 1 mg doxazosin or equivalent number of placebo capsules PO/day and increased every three days by 1 mg. After receiving 4 mg doxazosin or equivalent number of placebo capsules participants received masked doses of 20 and 40 mg cocaine IV in that order with placebo saline randomly interspersed to maintain the blind.Doxazosin treatment was well tolerated and doxazosin alone produced minimal changes in heart rate and blood pressure. During treatment with placebo, cocaine produced dose-dependent increases in subjective effect ratings of "high", "stimulated", "like cocaine", "desire cocaine", "any drug effect", and "likely to use cocaine if had access" (p<.001). Doxazosin treatment significantly attenuated the effects of 20 mg cocaine on ratings of "stimulated", "like cocaine", and "likely to use cocaine if had access" (p<.05). There were trends for doxazosin to reduce ratings of "stimulated", "desire cocaine", and "likely to use cocaine if had access" (p<.10).Medications that block noradrenergic α₁ receptors, such as doxazosin, may be useful as treatments for cocaine dependence, and should be evaluated further.Clinicaltrials.gov NCT01062945

Structural neuroanatomy of tinnitus and hyperacusis in semantic dementia

Introduction Tinnitus and hyperacusis are common symptoms of excessive auditory perception in the general population; however, their anatomical substrates and disease associations continue to be defined. Patients with semantic dementia (SemD) frequently repor

Degradation of cognitive timing mechanisms in behavioural variant frontotemporal dementia.

The current study examined motor timing in frontotemporal dementia (FTD), which manifests as progressive deterioration in social, behavioural and cognitive functions. Twenty-patients fulfilling consensus clinical criteria for behavioural variant FTD (bvFTD), 11 patients fulfilling consensus clinical criteria for semantic-variant primary progressive aphasia (svPPA), four patients fulfilling criteria for nonfluent/agrammatic primary progressive aphasia (naPPA), eight patients fulfilling criteria for Alzheimer׳s disease (AD), and 31 controls were assessed on both an externally- and self-paced finger-tapping task requiring maintenance of a regular, 1500 ms beat over 50 taps. Grey and white matter correlates of deficits in motor timing were examined using voxel-based morphometry (VBM) and diffusion tensor imaging (DTI). bvFTD patients exhibited significant deficits in aspects of both externally- and self-paced tapping. Increased mean inter-response interval (faster than target tap time) in the self-paced task was associated with reduced grey matter volume in the cerebellum bilaterally, right middle temporal gyrus, and with increased axial diffusivity in the right superior longitudinal fasciculus, regions and tracts which have been suggested to be involved in a subcortical-cortical network of structures underlying timing abilities. This suggests that such structures can be affected in bvFTD, and that impaired motor timing may underlie some characteristics of the bvFTD phenotype

Developmental regulation of tau splicing is disrupted in stem cell-derived neurons from frontotemporal dementia patients with the 10 + 16 splice-site mutation in MAPT

The alternative splicing of the tau gene, MAPT, generates six protein isoforms in the adult human CNS. Tau splicing is developmentally regulated and dysregulated in disease. Mutations in MAPT that alter tau splicing cause frontotemporal dementia (FTD) with tau pathology, providing evidence for a causal link between altered tau splicing and disease. The use of induced pluripotent stem cell (iPSC) derived neurons has revolutionized the way we model neurological disease in vitro. However, as most tau mutations are located within or around the alternatively spliced exon 10, it is important that iPSC-neurons splice tau appropriately in order to be used as disease models. To address this issue, we analysed the expression, and splicing of tau in iPSC-derived cortical neurons from control patients and FTD patients with the 10+16 intronic mutation in MAPT. We show that control neurons only express the fetal tau isoform (0N3R), even at extended time points of 100 days in vitro. Neurons from FTD patients with the 10+16 mutation in MAPT express both 0N3R and 0N4R tau isoforms, demonstrating that this mutation overrides the developmental regulation of exon 10 inclusion in our in vitro model. Further, at extended time-points of 365 days in vitro, we observe a switch in tau splicing to include six tau isoforms as seen the adult human CNS. Our results demonstrate the importance of neuronal maturity for use in in vitro modeling and provide a system that will be important for understanding the functional consequences of altered tau splicing

The Maunakea Spectroscopic Explorer Book 2018

(Abridged) This is the Maunakea Spectroscopic Explorer 2018 book. It is intended as a concise reference guide to all aspects of the scientific and technical design of MSE, for the international astronomy and engineering communities, and related agencies. The current version is a status report of MSE's science goals and their practical implementation, following the System Conceptual Design Review, held in January 2018. MSE is a planned 10-m class, wide-field, optical and near-infrared facility, designed to enable transformative science, while filling a critical missing gap in the emerging international network of large-scale astronomical facilities. MSE is completely dedicated to multi-object spectroscopy of samples of between thousands and millions of astrophysical objects. It will lead the world in this arena, due to its unique design capabilities: it will boast a large (11.25 m) aperture and wide (1.52 sq. degree) field of view; it will have the capabilities to observe at a wide range of spectral resolutions, from R2500 to R40,000, with massive multiplexing (4332 spectra per exposure, with all spectral resolutions available at all times), and an on-target observing efficiency of more than 80%. MSE will unveil the composition and dynamics of the faint Universe and is designed to excel at precision studies of faint astrophysical phenomena. It will also provide critical follow-up for multi-wavelength imaging surveys, such as those of the Large Synoptic Survey Telescope, Gaia, Euclid, the Wide Field Infrared Survey Telescope, the Square Kilometre Array, and the Next Generation Very Large Array.Comment: 5 chapters, 160 pages, 107 figure

Creation of an Open-Access, Mutation-Defined Fibroblast Resource for Neurological Disease Research

Our understanding of the molecular mechanisms of many neurological disorders has been greatly enhanced by the discovery of mutations in genes linked to familial forms of these diseases. These have facilitated the generation of cell and animal models that can be used to understand the underlying molecular pathology. Recently, there has been a surge of interest in the use of patient-derived cells, due to the development of induced pluripotent stem cells and their subsequent differentiation into neurons and glia. Access to patient cell lines carrying the relevant mutations is a limiting factor for many centres wishing to pursue this research. We have therefore generated an open-access collection of fibroblast lines from patients carrying mutations linked to neurological disease. These cell lines have been deposited in the National Institute for Neurological Disorders and Stroke (NINDS) Repository at the Coriell Institute for Medical Research and can be requested by any research group for use in in vitro disease modelling. There are currently 71 mutation-defined cell lines available for request from a wide range of neurological disorders and this collection will be continually expanded. This represents a significant resource that will advance the use of patient cells as disease models by the scientific community

Creation of an Open-Access, Mutation-Defined Fibroblast Resource for Neurological Disease Research

Our understanding of the molecular mechanisms of many neurological disorders has been greatly enhanced by the discovery of mutations in genes linked to familial forms of these diseases. These have facilitated the generation of cell and animal models that can be used to understand the underlying molecular pathology. Recently, there has been a surge of interest in the use of patient-derived cells, due to the development of induced pluripotent stem cells and their subsequent differentiation into neurons and glia. Access to patient cell lines carrying the relevant mutations is a limiting factor for many centres wishing to pursue this research. We have therefore generated an open-access collection of fibroblast lines from patients carrying mutations linked to neurological disease. These cell lines have been deposited in the National Institute for Neurological Disorders and Stroke (NINDS) Repository at the Coriell Institute for Medical Research and can be requested by any research group for use in in vitro disease modelling. There are currently 71 mutation-defined cell lines available for request from a wide range of neurological disorders and this collection will be continually expanded. This represents a significant resource that will advance the use of patient cells as disease models by the scientific community

International Nonregimes: A Research Agenda1

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/146934/1/j.1468-2486.2007.00672.x.pd

Complementarity and Institutional Change: How Useful a Concept?

The concept of institutional complementarity – i.e. the idea that the co-existence of two or more institutions enhances the functioning of each – is increasingly used to explain why institutions are resistant to change and why introducing new institutions into a system often leads to unintended consequences or failure to achieve the intended objective. While the concept is appealing and intuitive, in reality its utility for explaining change is less than straightforward. This paper utilizes examples from comparative political economy to, first, unpack and delineate the concept and address the issue of how to measure the strength or ‘binding force’ of complementarities. Second, it assesses the utility of the concept for explaining institutional change. It is suggested that one’s view of the methods and utility of measuring complementarity will hinge importantly on one’s general theory of institutions and institutional change. In the end, while institutional complementarities are significant, assessing their causal effect on institutional change is difficult and ambiguous in most instances. A better understanding requires that we embed complementarities within a more general theory of institutional change which takes a broader view of the ways in which institutions interconnect and change.Das Konzept der institutionellen Komplementarität – d.h. die Idee, dass zwei oder mehr Institutionen sich gegenseitig stützen und ihre Funktionsfähigkeit erhöhen – gilt mehr und mehr als Erklärung dafür, dass Institutionen gegen Veränderungen resistent sind und das Einführen neuer Institutionen in ein bestehendes System oft unerwartete Konsequenzen oder nicht darin erfolgreich sind, das gewünschte Ziel zu erreichen. Obwohl das Konzept attraktiv und intuitiv ist, ist sein Erklärungsnutzen nicht offensichtlich. In diesem Aufsatz werden Beispiele aus der vergleichenden politischen Ökonomie verwendet, um zunächst den Inhalt des Konzeptes zu umschreiben und die Frage zu stellen, wie die Stärke bzw. „Bindungskraft“ von Komplementaritäten zu messen sind. Dann bewertet er den Nutzen des Konzeptes zur Erklärung von institutionellem Wandel. Dabei ist darauf hinzuweisen, dass es stark vom Hintergrund des Betrachters, seiner allgemeinen Theorie von Institutionen und institutionellem Wandel, abhängt, welchen Blickwinkel er in Bezug auf die Einschätzung der Methoden und des Nutzen der Komplementaritätsmessung einnimmt. Abschließend stellt sich heraus, dass institutionelle Komplementaritäten wichtig sind, es aber in den meisten Fällen schwierig und unklar bleibt, ihren kausalen Effekt auf institutionellen Wandel zu bewerten. Zum besseren Verständnis ist es notwendig, dass das Konzept der Komplementaritäten in eine allgemeine Theorie des institutionellen Wandels eingebettet wird, die eine breitere Sicht über die Art und Weise zulässt, wie Institutionen untereinander verbunden sind und sich verändern