Jerrod Hunter

 Jerrod Hunter

Jerrod Hunter

  • Courses4
  • Reviews20

Biography

J. Sargeant Reynolds Community College - Biology


Resume

  • 2004

    Ph.D

    The GPiBS program is an interdisciplinary program that combines the expertise of over 120 participating faculty from six participating departments (Biochemistry & Molecular

    Biology

    Cell Biology

    Microbiology & Immunology

    Neuroscience

    Pathology and Physiology) to provide students with the breadth of knowledge and technical acumen.

    Cell Biology (Molecular Biology

    Neuroscience

    Genetics)

  • 1997

    B.S.

    Biochemistry

  • Western Blotting

    ELISA

    Microsoft Office

    Microscopy

    Immunohistochemistry

    Life Sciences

    Fluorescence

    Molecular Biology

    PCR

    Confocal Microscopy

    Fluorescence Microscopy

    Genetics

    PowerPoint

    Teaching

    Problem Solving

    Research

    DNA

    Cell Biology

    Protein Purification

    Photoshop

    Neuroligin-deficient mutants of C. elegans have sensory processing deficits and are hypersensitive to oxidative stress and mercury toxicity.

    James B. Rand

    Angie Duke

    Jessica M. Heatherly

    John R. McManus

    Gregory P. Mullen

    Neuroligins are postsynaptic cell adhesion proteins that bind specifically to presynaptic membrane proteins called neurexins. Mutations in human neuroligin genes are associated with autism spectrum disorders in some families. The nematode Caenorhabditis elegans has a single neuroligin gene (nlg-1)

    and approximately a sixth of C. elegans neurons

    including some sensory neurons

    interneurons and a subset of cholinergic motor neurons

    express a neuroligin transcriptional reporter. Neuroligin-deficient mutants of C. elegans are viable

    and they do not appear deficient in any major motor functions. However

    neuroligin mutants are defective in a subset of sensory behaviors and sensory processing

    and are hypersensitive to oxidative stress and mercury compounds; the behavioral deficits are strikingly similar to traits frequently associated with autism spectrum disorders. Our results suggest a possible link between genetic defects in synapse formation or function

    and sensitivity to environmental factors in the development of autism spectrum disorders.

    Neuroligin-deficient mutants of C. elegans have sensory processing deficits and are hypersensitive to oxidative stress and mercury toxicity.

    Charles Stewart

    Heather Rice

    Min Qi

    Quentin N Pye

    Tamara Potapova

    Kim Nguyen

    Shenyun Mou

    Molina Mhatre

    Haitham Abdel-Moaty

    Kenneth Hensley

    Detailed study of glial inflammation has been hindered by lack of cell culture systems that spontaneously demonstrate the \"neuroinflammatory phenotype\". Mice expressing a glycine → alanine substitution in cytosolic Cu

    Zn-superoxide dismutase (G93A-SOD1) associated with familial amyotrophic lateral sclerosis (ALS) demonstrate age-dependent neuroinflammation associated with broad-spectrum cytokine

    eicosanoid and oxidant production. In order to more precisely study the cellular mechanisms underlying glial activation in the G93A-SOD1 mouse

    primary astrocytes were cultured from 7 day mouse neonates. At this age

    G93A-SOD1 mice demonstrated no in vivo hallmarks of neuroinflammation. Nonetheless astrocytes cultured from G93A-SOD1 (but not wild-type human SOD1-expressing) transgenic mouse pups demonstrated a significant elevation in either the basal or the tumor necrosis alpha (TNFα)-stimulated levels of proinflammatory eicosanoids prostaglandin E2 (PGE2) and leukotriene B4 (LTB4); inducible nitric oxide synthase (iNOS) and •NO (indexed by nitrite release into the culture medium); and protein carbonyl products. Specific cytokine- and TNFα death-receptor-associated components were similarly upregulated in cultured G93A-SOD1 cells as assessed by multiprobe ribonuclease protection assays (RPAs) for their mRNA transcripts. Thus

    endogenous glial expression of G93A-SOD1 produces a metastable condition in which glia are more prone to enter an activated neuroinflammatory state associated with broad-spectrum increased production of paracrine-acting substances. These findings support a role for active glial involvement in ALS and may provide a useful cell culture tool for the study of glial inflammation.

    Primary glia expressing the G93A-SOD1 mutation present a neuroinflammatory phenotype and provide a cellular system for studies of glial inflammation.

    Rand JB

    Crowell JA

    Osborne JD

    Grundahl K

    Duke A

    Frisby DL

    Vu MH

    Mathews EA

    Mullen GP

    The cho-1 gene in Caenorhabditis elegans encodes a high-affinity plasma-membrane choline transporter believed to be rate limiting for acetylcholine (ACh) synthesis in cholinergic nerve terminals. We found that CHO-1 is expressed in most

    but not all cholinergic neurons in C. elegans. cho-1 null mutants are viable and exhibit mild deficits in cholinergic behavior; they are slightly resistant to the acetylcholinesterase inhibitor aldicarb

    and they exhibit reduced swimming rates in liquid. cho-1 mutants also fail to sustain swimming behavior; over a 33-min time course

    cho-1 mutants slow down or stop swimming

    whereas wild-type animals sustain the initial rate of swimming over the duration of the experiment. A functional CHO-1GFP fusion protein rescues these cho-1 mutant phenotypes and is enriched at cholinergic synapses. Although cho-1 mutants clearly exhibit defects in cholinergic behaviors

    the loss of cho-1 function has surprisingly mild effects on cholinergic neurotransmission. However

    reducing endogenous choline synthesis strongly enhances the phenotype of cho-1 mutants

    giving rise to a synthetic uncoordinated phenotype. Our results indicate that both choline transport and de novo synthesis provide choline for ACh synthesis in C. elegans cholinergic neurons

    Choline transport and de novo choline synthesis support acetylcholine biosynthesis in Caenorhabditis elegans cholinergic neurons

    Esmon CT

    Esmon NL

    Lupu F

    Ferrell GL

    Gu J

    Zheng X

    Li W

    Previous studies have shown that blocking endothelial protein C receptor (EPCR)-protein C interaction results in about an 88% decrease in circulating activated protein C (APC) levels generated in response to thrombin infusion and exacerbates the response to Escherichia coli. To determine whether higher levels of EPCR expression on endothelial cells might further enhance the activation of protein C and protect the host during septicemia

    we generated a transgenic mouse (Tie2-EPCR) line which placed the expression of EPCR under the control of the Tie2 promoter. The mice express abundant EPCR on endothelial cells not only on large vessels

    but also on capillaries where EPCR is generally low. Tie2-EPCR mice show higher levels of circulating APC after thrombin infusion. Upon infusion with factor Xa and phospholipids

    Tie2-EPCR mice generate more APC

    less thrombin and are protected from fibrin/ogen deposition compared with wild type controls. The Tie2-EPCR animals also generate more APC upon lipopolysaccharide (LPS) challenge and have a survival advantage. These results reveal that overexpression of EPCR can protect animals against thrombotic or septic challenge.

    Overexpressing endothelial cell protein C receptor alters the hemostatic balance and protects mice from endotoxin

    Neuroligin and neurexin are cell adhesion molecules that are sufficient to induce synaptogenesis in cultured mammalian cells (Fu et al.

    2003; Nam et al.

    2005). Mutations in neuroligin are associated with a subset of cases of the developmental disorder autism (Jamain et al.

    2003). We have tested transcriptional fusion constructs using the nlg-1 regulatory sequences to drive the expression of a YFP reporter. We found that YFP expression is limited to neurons in the head

    ventral nerve cord and tail. In double reporter studies

    GABAergic neurons do not express nlg-1. Instead

    nlg-1 is expressed in a portion of cholinergic cells

    particularly in the ventral nerve cord. In addition

    many of the nlg-1 positive cells in the head are neither cholinergic nor GABAergic. Surprisingly

    neuroligin knockout animals do not exhibit obvious cholinergic defects. Instead

    they exhibit phenotypes that are similar to those of an AMPA type glutamate receptor (glr-1) knockout. The neuroligin expressing cholinergic neurons also express glr-1 glutamate receptors

    and receive input from putative glutamate-releasing interneurons. Neuroligin knockout worms have a lower frequency of spontaneous reversal

    although when these worms do reverse

    the reversal is of the same duration as wildtype worms. This phenotype is similar to that of glr-1 mutants. Another behavioral phenotype of neuroligin knockout mutants is a defect in thermotaxis. Well fed wildtype worms placed on a thermal gradient preferentially track to the temperature at which they were raised. The nlg-1 and glr-1 knockout animals do not accumulate at a specific temperature; instead

    these worms move independently of ambient temperature. Our working hypothesis is that neuroligin is required for proper localization of glr-1. We are testing this hypothesis by introducing a glr-1::GFP functional fusion into a neuroligin knockout background to assess the effect of nlg-1 on glr-1::GFP localization.\n

    Neuroligin Is Widely Expressed In The C. elegans Nervous System

    And May Effect Glutamate Receptor Localization

    https://sites.google.com/site/drjerrodhunter/\nThis is a portal website for all of my online content.

    Hunter

    Jerrod

    Gettysburg College

    University of Richmond

    J. Sargeant Reynolds Community College

    Oklahoma Medical Research Foundation

    University of Oklahoma

    US Navy

    Oklahoma School of Science and Math

    University of Oklahoma Health Sciences Center

    ECPI University

    Oklahoma Medical Research Foundation

    Designing experiments

    performing experiments and interpreting results. Maintaining lab equipment

    reagents and laboratory animals. PCR

    molecular cloning

    ELISA

    microscopy and imaging

    genetics

    behavioral analysis antibody production.

    Oklahoma Medical Research Foundation

    Biology Professor

    I teach vertebrate and invertebrate biology to gifted high school juniors and seniors.\nI try to instill an appreciation for biology

    promote intellectual engagement with biology and help students become discerning observers of the world around them as a neurobiology instructor. I develop curricula

    lesson plans and tests while maintaining alignment throughout (Sometimes on vary short notice) including genetics

    neurobiology and zoology classes.\nI instruct

    motivate and inspire students

    Oklahoma School of Science and Math

    University of Richmond

    I teach Cell Biology and Genetics. I use an active learning approach to help learners develop knowledge and acumen in the methods and thought processes employed in modern biology and bio-medical research laboratories.

    Visiting Biology Lecturer

    Richmond

    Virginia Area

    Gettysburg PA

    Visiting Assistant Professor

    Gettysburg College

    Insured personnel and reactor safety as a Lead Engineering Laboratory Technician. Provided daily operational review/quality control of education accountability as it relates to imposed government regulatory requirements in a nuclear environment. Supervised and trained 115 men in regulatory compliance. Supervised six men in documentation of regulatory compliance

    US Navy

    Graduate student

    Expanded knowledge of synaptogenesis\nDesigning experiments

    performing experiments and interpreting results. Maintaining lab equipment

    reagents and laboratory animals. PCR

    molecular cloning

    ELISA

    microscopy and imaging

    genetics

    behavioral analysis.

    University of Oklahoma Health Sciences Center

    Adjunct Professor of Neurobiology

    I teach neurobiology to upper division undergraduates and graduate students.I try to instill an appreciation for biology

    promote intellectual engagement with biology and help students become discerning observers of the world around them as a neurobiology instructor.

    University of Oklahoma

    ECPI University

    Newport News

    Anatomy and Physiology

    Biology Instructor

    Richmond

    Virginia Area

    I teach Biology and Anatomy and Physiology. I use an active learning approach to help learners develop knowledge and acumen in the methods and thought processes employed in modern biology. I try to instill an appreciation for biology

    promote intellectual engagement with biology and help students become discerning observers of the world around them. I try to instruct

    motivate and inspire students

    Assistant Professor

    J. Sargeant Reynolds Community College

    Expand knowledge of synaptogenesis \nDesigning experiments

    performing experiments and interpreting results. Maintaining lab equipment

    reagents and laboratory animals. PCR

    molecular cloning

    ELISA

    microscopy and imaging

    genetics

    behavioral analysis

    Oklahoma Medical Research Foundation

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