Chesapeake Bay Shoreline Study: Headland Breakwaters and Pocket Beaches for Shoreline Erosion Control Final Report

The Chesapeake Bay Shoreline Study is a cooperative project of the Commonwealth of Virginia, the Norfolk District of the U.S. Army Corps of Engineers, and the Virginia Institute of Marine Science. The project consists of three modeling and five monitoring sites located on the tributary estuarine shores of the Virginia portion of Chesapeake Bay. The purpose of the study is to examine more closely gapped-offshore-headland breakwaters and the headland concept for the abatement of estuarine shoreline erosion. Headland breakwaters provide fixed points along a shore between which a series of stable pocket beaches can develop. These structures may represent a lower cost approach to control shoreline erosion as well as provide an environmental edge between what we perceive as land and marine resources

Public Beach Assessment Report Central Beach and Castlewood Park Beach Colonial Beach, Virginia

The purpose of this report is to document the recent history of Colonial Beach’s Potomac River shoreline as well as assess the historical shoreline evolution and status of the beach zone. Review of previously-published literature, field survey data, aerial photos, and computer modeling were used to address the study objectives

Chesapeake Bay Dune Systems: Evolution and Status

The goals of this study were to locate, classify, and enumerate the existing jurisdictional dunes and dune fields within the eight localities listed in the Act. These include the counties of Accomack, Lancaster, Mathews, Northampton, and Northumberland and the cities of Hampton, Norfolk, and Virginia Beach. Only Chesapeake Bay and river sites are considered in this study

KArLE: In-Situ Geochronology on the Mars 2020 Rover with KArLE (The Potassium-Argon Laser Experiment)

No abstract availabl

Using C. elegans to discover therapeutic compounds for ageing-associated neurodegenerative diseases

Age-associated neurodegenerative disorders such as Alzheimer’s disease are a major public health challenge, due to the demographic increase in the proportion of older individuals in society. However, the relatively few currently approved drugs for these conditions provide only symptomatic relief. A major goal of neurodegeneration research is therefore to identify potential new therapeutic compounds that can slow or even reverse disease progression, either by impacting directly on the neurodegenerative process or by activating endogenous physiological neuroprotective mechanisms that decline with ageing. This requires model systems that can recapitulate key features of human neurodegenerative diseases that are also amenable to compound screening approaches. Mammalian models are very powerful, but are prohibitively expensive for high-throughput drug screens. Given the highly conserved neurological pathways between mammals and invertebrates, Caenorhabditis elegans has emerged as a powerful tool for neuroprotective compound screening. Here we describe how C. elegans has been used to model various human ageing-associated neurodegenerative diseases and provide an extensive list of compounds that have therapeutic activity in these worm models and so may have translational potential

Transcriptional and Post-Transcriptional Regulation of SPAST, the Gene Most Frequently Mutated in Hereditary Spastic Paraplegia

Hereditary spastic paraplegias (HSPs) comprise a group of neurodegenerative disorders that are characterized by progressive spasticity of the lower extremities, due to axonal degeneration in the corticospinal motor tracts. HSPs are genetically heterogeneous and show autosomal dominant inheritance in ∼70–80% of cases, with additional cases being recessive or X-linked. The most common type of HSP is SPG4 with mutations in the SPAST gene, encoding spastin, which occurs in 40% of dominantly inherited cases and in ∼10% of sporadic cases. Both loss-of-function and dominant-negative mutation mechanisms have been described for SPG4, suggesting that precise or stoichiometric levels of spastin are necessary for biological function. Therefore, we hypothesized that regulatory mechanisms controlling expression of SPAST are important determinants of spastin biology, and if altered, could contribute to the development and progression of the disease. To examine the transcriptional and post-transcriptional regulation of SPAST, we used molecular phylogenetic methods to identify conserved sequences for putative transcription factor binding sites and miRNA targeting motifs in the SPAST promoter and 3′-UTR, respectively. By a variety of molecular methods, we demonstrate that SPAST transcription is positively regulated by NRF1 and SOX11. Furthermore, we show that miR-96 and miR-182 negatively regulate SPAST by effects on mRNA stability and protein level. These transcriptional and miRNA regulatory mechanisms provide new functional targets for mutation screening and therapeutic targeting in HSP