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  1. Article: Intentional Excellence in the Baldwin Wallace University Neuroscience Program.

    Morris, Jacqueline K / Peppers, Kieth / Mickley, G Andrew

    Journal of undergraduate neuroscience education : JUNE : a publication of FUN, Faculty for Undergraduate Neuroscience

    2015  Volume 13, Issue 3, Page(s) A146–9

    Abstract: The Society for Neuroscience recognized Baldwin Wallace University's (BWU) undergraduate Neuroscience program as their Program of the Year for 2012. This award acknowledged the "accomplishments of a neuroscience department or program for excellence in ... ...

    Abstract The Society for Neuroscience recognized Baldwin Wallace University's (BWU) undergraduate Neuroscience program as their Program of the Year for 2012. This award acknowledged the "accomplishments of a neuroscience department or program for excellence in educating neuroscientists and providing innovative models to which other programs can aspire." The Neuroscience program grew out of students interested in studying the biological basis of behavior. BWU's neuroscience major is research-intensive, and all students are required to produce an empirically-based senior thesis. This requirement challenges program resources, and the demand for faculty attention is high. Thus, we developed an intentional 3-step peer mentoring system that encourages our students to collaborate with and learn from, not only faculty, but each other. Peer mentoring occurs in the curriculum, faculty research labs, and as students complete their senior theses. As the program has grown with over 80 current majors, we have developed a new Neuroscience Methods course to train students on the safety, ethics, and practice of research in the neuroscience laboratory space. Students in this course leave with the skills and knowledge to assist senior level students with their theses and to begin the process of developing their own projects in the laboratory. Further, our students indicate that their "peer mentorship was excellent," "helped them gain confidence," and "allowed them to be more successful in their research."
    Language English
    Publishing date 2015-07-07
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2577251-X
    ISSN 1544-2896
    ISSN 1544-2896
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Decrease in levels of the evolutionarily conserved microRNA miR-124 affects oligodendrocyte numbers in Zebrafish, Danio rerio.

    Morris, Jacqueline K / Chomyk, Anthony / Song, Ping / Parker, Nate / Deckard, Sadie / Trapp, Bruce D / Pimplikar, Sanjay W / Dutta, Ranjan

    Invertebrate neuroscience : IN

    2015  Volume 15, Issue 3, Page(s) 4

    Abstract: Oligodendrocytes produce multi-lamellar myelin membranes that surround axons in the central nervous system (CNS). Preservation and generation of myelin are potential therapeutic targets for dysmyelinating and demyelinating diseases. MicroRNAs (miRNAs) ... ...

    Abstract Oligodendrocytes produce multi-lamellar myelin membranes that surround axons in the central nervous system (CNS). Preservation and generation of myelin are potential therapeutic targets for dysmyelinating and demyelinating diseases. MicroRNAs (miRNAs) play a vital role in oligodendrocyte differentiation and overall CNS development. miR-124 is a well-conserved neuronal miRNA with important roles in neuronal differentiation and function. miR-124 levels increase following loss of myelin in both human and rodent brains. While the role of neuronal miR-124 in neurogenesis has been established, its effects on axonal outgrowth and oligodendrocytes are not currently known. We therefore explored the possible effect of selective knockdown of miR-124 in Danio rerio using a morpholino-based knockdown approach. No morphological abnormalities or loss of motor neurons were detected despite loss of axonal outgrowth. Morpholino-based knockdown of miR-124 led to reciprocal increases in mRNA levels of target genes that inhibit axonal and dendritic projections. Importantly, loss of miR-124 led to decreased oligodendrocyte cell numbers and myelination of axonal projections in the ventral hindbrain. Taken together, our results add a new dimension to the existing complexity of neuron-glial relationships and highlight the utility of Danio rerio as a model system to investigate such interactions.
    MeSH term(s) Animals ; Animals, Genetically Modified ; Dose-Response Relationship, Drug ; Embryo, Nonmammalian ; Gene Expression Regulation, Developmental/drug effects ; Gene Expression Regulation, Developmental/physiology ; Larva ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Morpholinos/pharmacology ; Oligodendroglia/drug effects ; Oligodendroglia/metabolism ; Zebrafish/anatomy & histology
    Chemical Substances MicroRNAs ; Morpholinos
    Language English
    Publishing date 2015-09
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2003354-0
    ISSN 1439-1104 ; 1354-2516
    ISSN (online) 1439-1104
    ISSN 1354-2516
    DOI 10.1007/s10158-015-0180-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Is phosphorylated tau unique to chronic traumatic encephalopathy? Phosphorylated tau in epileptic brain and chronic traumatic encephalopathy.

    Puvenna, Vikram / Engeler, Madeline / Banjara, Manoj / Brennan, Chanda / Schreiber, Peter / Dadas, Aaron / Bahrami, Ashkon / Solanki, Jesal / Bandyopadhyay, Anasua / Morris, Jacqueline K / Bernick, Charles / Ghosh, Chaitali / Rapp, Edward / Bazarian, Jeffrey J / Janigro, Damir

    Brain research

    2016  Volume 1630, Page(s) 225–240

    Abstract: Repetitive traumatic brain injury (rTBI) is one of the major risk factors for the abnormal deposition of phosphorylated tau (PT) in the brain and chronic traumatic encephalopathy (CTE). CTE and temporal lobe epilepsy (TLE) affect the limbic system, but ... ...

    Abstract Repetitive traumatic brain injury (rTBI) is one of the major risk factors for the abnormal deposition of phosphorylated tau (PT) in the brain and chronic traumatic encephalopathy (CTE). CTE and temporal lobe epilepsy (TLE) affect the limbic system, but no comparative studies on PT distribution in TLE and CTE are available. It is also unclear whether PT pathology results from repeated head hits (rTBI). These gaps prevent a thorough understanding of the pathogenesis and clinical significance of PT, limiting our ability to develop preventative and therapeutic interventions. We quantified PT in TLE and CTE to unveil whether a history of rTBI is a prerequisite for PT accumulation in the brain. Six postmortem CTE (mean 73.3 years) and age matched control samples were compared to 19 surgically resected TLE brain specimens (4 months-58 years; mean 27.6 years). No history of TBI was present in TLE or control; all CTE patients had a history of rTBI. TLE and CTE brain displayed increased levels of PT as revealed by immunohistochemistry. No age-dependent changes were noted, as PT was present as early as 4 months after birth. In TLE and CTE, cortical neurons, perivascular regions around penetrating pial vessels and meninges were immunopositive for PT; white matter tracts also displayed robust expression of extracellular PT organized in bundles parallel to venules. Microscopically, there were extensive tau-immunoreactive neuronal, astrocytic and degenerating neurites throughout the brain. In CTE perivascular tangles were most prominent. Overall, significant differences in staining intensities were found between CTE and control (P<0.01) but not between CTE and TLE (P=0.08). pS199 tau analysis showed that CTE had the most high molecular weight tangle-associated tau, whereas epileptic brain contained low molecular weight tau. Tau deposition may not be specific to rTBI since TLE recapitulated most of the pathological features of CTE.
    MeSH term(s) Adolescent ; Adult ; Aged ; Aged, 80 and over ; Brain/metabolism ; Brain/pathology ; Brain/surgery ; Brain Injury, Chronic/metabolism ; Brain Injury, Chronic/pathology ; Child ; Child, Preschool ; Enzyme-Linked Immunosorbent Assay ; Epilepsy/metabolism ; Epilepsy/pathology ; Epilepsy/surgery ; Female ; Humans ; Immunohistochemistry ; Infant ; Male ; Middle Aged ; Phosphorylation ; Young Adult ; tau Proteins/metabolism
    Chemical Substances MAPT protein, human ; tau Proteins
    Language English
    Publishing date 2016-01-01
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1200-2
    ISSN 1872-6240 ; 0006-8993
    ISSN (online) 1872-6240
    ISSN 0006-8993
    DOI 10.1016/j.brainres.2015.11.007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 161: Show issues Location:
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  4. Article: The 36K protein of zebrafish CNS myelin is a short-chain dehydrogenase.

    Morris, Jacqueline K / Willard, Belinda B / Yin, Xinghua / Jeserich, Gunnar / Kinter, Michael / Trapp, Bruce D

    Glia

    2004  Volume 45, Issue 4, Page(s) 378–391

    Abstract: Previous studies identified homologues to mammalian myelin genes expressed in the teleost central nervous system (CNS), including myelin basic protein (MBP), protein zero (P0), and a member of the proteolipid protein family, DM20. In addition, an ... ...

    Abstract Previous studies identified homologues to mammalian myelin genes expressed in the teleost central nervous system (CNS), including myelin basic protein (MBP), protein zero (P0), and a member of the proteolipid protein family, DM20. In addition, an uncharacterized 36-kDa (36K) protein is a major component of teleost myelin, but is not a major component of myelin in other species. In the present study, we sought to better understand myelin proteins and myelination in one teleost, zebrafish, by molecular characterization of the zebrafish 36K protein. Purified zebrafish CNS myelin was isolated and the amino acid sequences of peptides present in the 36-kDa band were determined by mass spectrometry. These sequences matched a previously uncharacterized EST in The Institute for Genome Research (TIGR) zebrafish database that is related to the short-chain dehydrogenase/reductase (SDR) protein family. In vitro expression of the zebrafish 36K cDNA in Neuro 2a cells resulted in a protein product that was recognized by a 36K polyclonal antibody. The zebrafish 36K mRNA and protein expression patterns were determined and correlated to other known myelin gene expression profiles. In addition, we determined by in situ hybridization that a human 36K homologue (FLJ13639) is expressed in oligodendrocytes and neurons in the adult human cortex. This study identified a major myelin protein in zebrafish, 36K, as a member of the SDR superfamily; an expression pattern similar to other myelin genes was demonstrated.
    MeSH term(s) Amino Acid Sequence ; Animals ; Base Sequence ; Central Nervous System/embryology ; Central Nervous System/enzymology ; Central Nervous System/growth & development ; Gene Expression Regulation, Developmental/physiology ; Humans ; Molecular Sequence Data ; Molecular Weight ; Myelin Proteins/biosynthesis ; Myelin Proteins/genetics ; Nerve Tissue Proteins/biosynthesis ; Nerve Tissue Proteins/genetics ; Oxidoreductases/biosynthesis ; Oxidoreductases/genetics ; Sequence Homology, Amino Acid ; Zebrafish ; Zebrafish Proteins/biosynthesis ; Zebrafish Proteins/genetics
    Chemical Substances Myelin Proteins ; Nerve Tissue Proteins ; Zebrafish Proteins ; Oxidoreductases (EC 1.-)
    Language English
    Publishing date 2004-03
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 639414-0
    ISSN 1098-1136 ; 0894-1491
    ISSN (online) 1098-1136
    ISSN 0894-1491
    DOI 10.1002/glia.10338
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2345: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  5. Article: A disorganized innervation of the inner ear persists in the absence of ErbB2.

    Morris, Jacqueline K / Maklad, Adel / Hansen, Laura A / Feng, Feng / Sorensen, Christian / Lee, Kuo-Fen / Macklin, Wendy B / Fritzsch, Bernd

    Brain research

    2006  Volume 1091, Issue 1, Page(s) 186–199

    Abstract: ErbB2 protein is essential for the development of Schwann cells and for the normal fiber growth and myelin formation of peripheral nerves. We have investigated the fate of the otocyst-derived inner ear sensory neurons in the absence of ErbB2 using ErbB2 ... ...

    Abstract ErbB2 protein is essential for the development of Schwann cells and for the normal fiber growth and myelin formation of peripheral nerves. We have investigated the fate of the otocyst-derived inner ear sensory neurons in the absence of ErbB2 using ErbB2 null mutants. Afferent innervation of the ear sensory epithelia shows numerous fibers overshooting the organ of Corti, followed by a reduction of those fibers in near term embryos. This suggests that mature Schwann cells do not play a role in targeting or maintaining the inner ear innervation. Comparable to the overshooting of nerve fibers, sensory neurons migrate beyond their normal locations into unusual positions in the modiolus. They may miss a stop signal provided by the Schwann cells that are absent as revealed with detailed histology. Reduction of overshooting afferents may be enhanced by a reduction of the neurotrophin Ntf3 transcript to about 25% of wild type. Ntf3 transcript reductions are comparable to an adult model that uses a dominant negative form of ErbB4 expressed in the supporting cells and Schwann cells of the organ of Corti. ErbB2 null mice retain afferents to inner hair cells possibly because of the prominent expression of the neurotrophin Bdnf in developing hair cells. Despite the normal presence of Bdnf transcript, afferent fibers are disoriented near the organ of Corti. Efferent fibers do not form an intraganglionic spiral bundle in the absence of spiral ganglia and appear reduced and disorganized. This suggests that either ErbB2 mediated alterations in sensory neurons or the absence of Schwann cells affects efferent fiber growth to the organ of Corti.
    MeSH term(s) Animals ; Body Patterning ; Cochlear Nerve/cytology ; Cochlear Nerve/embryology ; Ear, Inner/innervation ; Ear, Inner/physiology ; Humans ; Mice ; Mice, Knockout ; Neurons, Afferent/physiology ; Receptor, ErbB-2/deficiency ; Receptor, ErbB-2/genetics
    Chemical Substances Receptor, ErbB-2 (EC 2.7.10.1)
    Language English
    Publishing date 2006-04-21
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 1200-2
    ISSN 1872-6240 ; 0006-8993
    ISSN (online) 1872-6240
    ISSN 0006-8993
    DOI 10.1016/j.brainres.2006.02.090
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    Zs.A 161: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  6. Article: ErbB2 is required for ductal morphogenesis of the mammary gland.

    Jackson-Fisher, Amy J / Bellinger, Gary / Ramabhadran, Rajani / Morris, Jacqueline K / Lee, Kuo-Fen / Stern, David F

    Proceedings of the National Academy of Sciences of the United States of America

    2004  Volume 101, Issue 49, Page(s) 17138–17143

    Abstract: The ERBB2/HER2/NEU receptor tyrosine kinase gene is amplified in up to 30% of human breast cancers. The frequent and specific selection of this receptor kinase gene for amplification in breast cancer implies that it has important normal functions in the ... ...

    Abstract The ERBB2/HER2/NEU receptor tyrosine kinase gene is amplified in up to 30% of human breast cancers. The frequent and specific selection of this receptor kinase gene for amplification in breast cancer implies that it has important normal functions in the mammary gland. To investigate the functions of ErbB2 during normal mouse mammary gland development, we transplanted mammary buds from genetically rescued ErbB2(-/-) embryos that express ErbB2 in the cardiac muscle. ErbB2(-/-) mammary buds transplanted to a wild-type mammary fat pad support outgrowth of an epithelial tree that advances only slowly through the mammary fat pad at puberty. This penetration defect is associated with structural defects in terminal end buds, characterized by a decrease in body cell number, an increased presence of cap-like cells in the prelumenal compartment, and the presence of large luminal spaces. Lobuloalveolar development was not affected in glands that developed from ErbB2(-/-) transplanted tissue. The results may have implications for the aggressive phenotypes associated with ERBB2-overexpressing mammary carcinomas.
    MeSH term(s) Animals ; Epithelium/abnormalities ; Epithelium/growth & development ; Female ; Mammary Glands, Animal/growth & development ; Mammary Glands, Animal/pathology ; Mammary Glands, Animal/transplantation ; Mammary Neoplasms, Animal/etiology ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Mice, Transgenic ; Rats ; Receptor, ErbB-2/deficiency ; Receptor, ErbB-2/genetics ; Receptor, ErbB-2/physiology
    Chemical Substances Receptor, ErbB-2 (EC 2.7.10.1)
    Language English
    Publishing date 2004-11-29
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.0407057101
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    Zs.A 1148: Show issues Location:
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