A surface mooring for air–sea interaction research in the Gulf Stream. Part II : analysis of the observations and their accuracies

Author Posting. © American Meteorological Society, 2013. This article is posted here by permission of American Meteorological Society for personal use, not for redistribution. The definitive version was published in Journal of Atmospheric and Oceanic Technology 39 (2013): 450–469, doi:10.1175/JTECH-D-12-00078.1.A surface mooring was deployed in the Gulf Stream for 15 months to investigate the role of air–sea interaction in mode water formation and other processes. The accuracies of the near-surface meteorological and oceanographic measurements are investigated. In addition, the impacts of these measurement errors on the estimation and study of the air–sea fluxes in the Gulf Stream are discussed. Pre- and postdeployment calibrations together with in situ comparison between shipboard and moored sensors supported the identification of biases due to sensor drifts, sensor electronics, and calibration errors. A postdeployment field study was used to further investigate the performance of the wind sensors. The use of redundant sensor sets not only supported the filling of data gaps but also allowed an examination of the contribution of random errors. Air–sea fluxes were also analyzed and computed from both Coupled Ocean–Atmosphere Response Experiment (COARE) bulk parameterization and using direct covariance measurements. The basic conclusion is that the surface buoy deployed in the Gulf Stream to support air–sea interaction research was successful, providing an improved 15-month record of surface meteorology, upper-ocean variability, and air–sea fluxes with known accuracies. At the same time, the coincident deployment of mean meteorological and turbulent flux sensors proved to be a successful strategy to certify the validity of the bulk formula fluxes over the midrange of wind speeds and to support further work to address the present shortcomings of the bulk formula methods at the low and high wind speeds.The National Science Foundation (Grant OCE04-24536) funded this work, as part of the CLIVAR Mode Water Dynamics Experiment (CLIMODE). The Vetlesen Foundation is also acknowledged for the early support of S. Bigorre.2013-09-0

Absence of microglia promotes diverse pathologies and early lethality in Alzheimer’s disease mice

Microglia are strongly implicated in the development and progression of Alzheimer's disease (AD), yet their impact on pathology and lifespan remains unclear. Here we utilize a CSF1R hypomorphic mouse to generate a model of AD that genetically lacks microglia. The resulting microglial-deficient mice exhibit a profound shift from parenchymal amyloid plaques to cerebral amyloid angiopathy (CAA), which is accompanied by numerous transcriptional changes, greatly increased brain calcification and hemorrhages, and premature lethality. Remarkably, a single injection of wild-type microglia into adult mice repopulates the microglial niche and prevents each of these pathological changes. Taken together, these results indicate the protective functions of microglia in reducing CAA, blood-brain barrier dysfunction, and brain calcification. To further understand the clinical implications of these findings, human AD tissue and iPSC-microglia were examined, providing evidence that microglia phagocytose calcium crystals, and this process is impaired by loss of the AD risk gene, TREM2

The genomes of two key bumblebee species with primitive eusocial organization

Background: The shift from solitary to social behavior is one of the major evolutionary transitions. Primitively eusocial bumblebees are uniquely placed to illuminate the evolution of highly eusocial insect societies. Bumblebees are also invaluable natural and agricultural pollinators, and there is widespread concern over recent population declines in some species. High-quality genomic data will inform key aspects of bumblebee biology, including susceptibility to implicated population viability threats. Results: We report the high quality draft genome sequences of Bombus terrestris and Bombus impatiens, two ecologically dominant bumblebees and widely utilized study species. Comparing these new genomes to those of the highly eusocial honeybee Apis mellifera and other Hymenoptera, we identify deeply conserved similarities, as well as novelties key to the biology of these organisms. Some honeybee genome features thought to underpin advanced eusociality are also present in bumblebees, indicating an earlier evolution in the bee lineage. Xenobiotic detoxification and immune genes are similarly depauperate in bumblebees and honeybees, and multiple categories of genes linked to social organization, including development and behavior, show high conservation. Key differences identified include a bias in bumblebee chemoreception towards gustation from olfaction, and striking differences in microRNAs, potentially responsible for gene regulation underlying social and other traits. Conclusions: These two bumblebee genomes provide a foundation for post-genomic research on these key pollinators and insect societies. Overall, gene repertoires suggest that the route to advanced eusociality in bees was mediated by many small changes in many genes and processes, and not by notable expansion or depauperation

The evolution of free and bound waves during dispersive focusing in a numerical and physical flume

publisher: Elsevier articletitle: The evolution of free and bound waves during dispersive focusing in a numerical and physical flume journaltitle: Coastal Engineering articlelink: http://dx.doi.org/10.1016/j.coastaleng.2017.11.003 content_type: article copyright: © 2017 The Authors. Published by Elsevier B.V

Generation and application of a chimeric model to examine human microglia responses to amyloid pathology

Microglia are the primary cell type comprising the brain’s immune system and, as such, inflammatory responses in these cells have been implicated in essentially all diseases of the central nervous system. Historically, directly studying human microglia has been experimentally challenging, so much of what we understand has been inferred from the study of animal models despite species-specific genetic variation that underlies the inability of rodent microglia to fully recapitulate the human condition. However, recent advancements in the use of human induced pluripotent stem cells (iPSCs) to generate human microglia surrogates has ushered in a new era of microglia research. While the initial in vitro studies utilizing these iPSC-derived microglia (iMG) were revolutionary, subsequent work has demonstrated that these cells are highly sensitive to their environment and exhibit robust transcriptomic deficiencies when kept in isolation from the brain.Therefore, the development of a model that would allow for the examination of these cells within a surrogate brain environment was necessary for the continued development of our understanding of the roles of microglia in health and disease. By transplanting iPSC-derived hematopoietic progenitor cells into the postnatal brain of humanized, immune-deficient mice, transplanted cells were shown to undergo context-dependent differentiation into microglia and other CNS macrophages. Transcriptomic analyses showed that the resulting cells acquired an ex vivo human microglial gene signature and appropriately responded to acute and chronic inflammatory insults. Most notably, transplanted microglia exhibited robust transcriptional responses to Aβ plaques that only partially overlapped with that of murine microglia, revealing multiple human-specific Aβ-response genes. Further expansion of this model in conjunction with CRISPR gene editing technology has allowed for the direct interrogation of the Alzheimer’s disease (AD)-related triggering receptor expressed in myeloid cells 2 (TREM2) R47H genetic polymorphism. This study demonstrated that a key effect of the R47H mutation is an alteration in the distribution of microglia subpopulations and a reduction in plaque associated microglia. Furthermore, cells with the R47H mutation exhibit an inflammatory signature that is not present in WT cells, suggesting that their lack of responsiveness is also paired with inappropriate inflammation. Importantly, these results have highlighted aspects of the R47H mutation that have not previously been observed in mouse models. Finally, as disruption of activation states in response to amyloid pathology appeared to be a primary result of genetic mutation in xMG, further understanding the complex genetic interactions driving these states was a question of critical importance. Analysis of the epigenomic and transcriptomic landscapes of the individual xMG subpopulations that arise in response to amyloid pathology has provided insight into the chromatin structure and gene expression alterations that underlie the microglia response to Aβ plaques. What these data have begun to demonstrate is that the amyloid-responsive population of microglia appear to rely on chromatin modifications that allow transcription factors in the MiTF/TFE family to upregulate the expression of genes related to phagocytosis and lysosomal function. While there are still aspects of these results that have not been fully elucidated, future studies are underway that will determine the nature of these changes and their ability to drive microglial responses in AD. Taken as a whole, the development of the xMG model and application to the study of the early amyloid response has yielded important new insight into Alzheimer’s disease. While these experiments are only the first steps in what will hopefully become a much broader body of human microglia research, my dissertation work has demonstrated that the xMG model is a powerful tool for the future study of microglial homeostasis and disease-associated inflammatory responses