Publications by authors named "Jaclyn E Smith"

4 Publications

  • Page 1 of 1

Depth-Dependent Response of Fecal Indicator Bacteria in Sediments to Changes in Water Column Nutrient Levels.

J Environ Qual 2019 Jul;48(4):1074-1081

Concentrations of in bottom sediments can influence the assessment of microbial stream water quality. Runoff events bring nutrients to streams that can support the growth of in sediments. The objective of this work was to evaluate depth-dependent changes in populations after nutrients are introduced to the water column. Bovine feces were collected fresh and mixed into sediment. Studies were performed in a microcosm system with continuous flow of synthetic stream water over inoculated sediment. Dilutions of autoclaved bovine manure were added to water on Day 16 at two concentrations, and KBr tracer was introduced into the water column to evaluate ion diffusion. Concentrations of , total coliforms, and total aerobic heterotrophic bacteria, along with orthophosphate-P and ammonium N, were monitored in water and sediment for 32 d. Sediment samples were analyzed in 0- to 1-cm and 1- to 3-cm sectioned depths. Concentrations of and total coliforms in top sediments were approximately one order of magnitude greater than in bottom sediments throughout the experiment. Introduction of nutrients to the water column triggered an increase of nutrient levels in both top and bottom sediments and increased concentrations of bacteria in the water. However, the added nutrients had a limited effect on in sediment where bacterial inactivation continued. Vertical gradients of concentrations in sediments persisted during the inactivation periods both before and after nutrient addition to the water column.
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http://dx.doi.org/10.2134/jeq2018.12.0450DOI Listing
July 2019

PKCε Inhibits Neuronal Dendritic Spine Development through Dual Phosphorylation of Ephexin5.

Cell Rep 2018 11;25(9):2470-2483.e8

Department of Biological Chemistry, The Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA; Solomon H. Snyder Department of Neuroscience, The Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA. Electronic address:

Protein kinase C (PKC)-dependent mechanisms promote synaptic function in the mature brain. However, the roles of PKC signaling during synapse development remain largely unknown. Investigating each brain-enriched PKC isoform in early neuronal development, we show that PKCε acutely and specifically reduces the number of dendritic spines, sites of eventual synapse formation on developing dendrites. This PKCε-mediated spine suppression is temporally restricted to immature neurons and mediated through the phosphorylation and activation of Ephexin5, a RhoA guanine nucleotide exchange factor (GEF) and inhibitor of hippocampal synapse formation. Our data suggest that PKCε acts as an early developmental inhibitor of dendritic spine formation, in contrast to its emerging pro-synaptic roles in mature brain function. Moreover, we identify a substrate of PKCε, Ephexin5, whose early-elevated expression in developing neurons may in part explain the mechanism by which PKCε plays seemingly opposing roles that depend on neuronal maturity.
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http://dx.doi.org/10.1016/j.celrep.2018.11.005DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6371982PMC
November 2018

Nasal neuron PET imaging quantifies neuron generation and degeneration.

J Clin Invest 2017 Feb 23;127(2):681-694. Epub 2017 Jan 23.

Olfactory dysfunction is broadly associated with neurodevelopmental and neurodegenerative diseases and predicts increased mortality rates in healthy individuals. Conventional measurements of olfactory health assess odor processing pathways within the brain and provide a limited understanding of primary odor detection. Quantification of the olfactory sensory neurons (OSNs), which detect odors within the nasal cavity, would provide insight into the etiology of olfactory dysfunction associated with disease and mortality. Notably, OSNs are continually replenished by adult neurogenesis in mammals, including humans, so OSN measurements are primed to provide specialized insights into neurological disease. Here, we have evaluated a PET radiotracer, [11C]GV1-57, that specifically binds mature OSNs and quantifies the mature OSN population in vivo. [11C]GV1-57 monitored native OSN population dynamics in rodents, detecting OSN generation during postnatal development and aging-associated neurodegeneration. [11C]GV1-57 additionally measured rates of neuron regeneration after acute injury and early-stage OSN deficits in a rodent tauopathy model of neurodegenerative disease. Preliminary assessment in nonhuman primates suggested maintained uptake and saturable binding of [18F]GV1-57 in primate nasal epithelium, supporting its translational potential. Future applications for GV1-57 include monitoring additional diseases or conditions associated with olfactory dysregulation, including cognitive decline, as well as monitoring effects of neuroregenerative or neuroprotective therapeutics.
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http://dx.doi.org/10.1172/JCI89162DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5272198PMC
February 2017

Identification of FHL1 as a therapeutic target for Duchenne muscular dystrophy.

Hum Mol Genet 2014 Feb 18;23(3):618-36. Epub 2013 Sep 18.

Department of Biochemistry and Molecular Biology, Monash University, Clayton, VIC 3800, Australia.

Utrophin is a potential therapeutic target for the fatal muscle disease, Duchenne muscular dystrophy (DMD). In adult skeletal muscle, utrophin is restricted to the neuromuscular and myotendinous junctions and can compensate for dystrophin loss in mdx mice, a mouse model of DMD, but requires sarcolemmal localization. NFATc1-mediated transcription regulates utrophin expression and the LIM protein, FHL1 which promotes muscle hypertrophy, is a transcriptional activator of NFATc1. By generating mdx/FHL1-transgenic mice, we demonstrate that FHL1 potentiates NFATc1 activation of utrophin to ameliorate the dystrophic pathology. Transgenic FHL1 expression increased sarcolemmal membrane stability, reduced muscle degeneration, decreased inflammation and conferred protection from contraction-induced injury in mdx mice. Significantly, FHL1 expression also reduced progressive muscle degeneration and fibrosis in the diaphragm of aged mdx mice. FHL1 enhanced NFATc1 activation of the utrophin promoter and increased sarcolemmal expression of utrophin in muscles of mdx mice, directing the assembly of a substitute utrophin-glycoprotein complex, and revealing a novel FHL1-NFATc1-utrophin signaling axis that can functionally compensate for dystrophin.
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http://dx.doi.org/10.1093/hmg/ddt449DOI Listing
February 2014
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