Bernd Fritzsch, Ph.D. - US grants
Affiliations: | University of Iowa, Iowa City, IA |
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High-probability grants
According to our matching algorithm, Bernd Fritzsch is the likely recipient of the following grants.| Years | Recipients | Code | Title / Keywords | Matching score |
|---|---|---|---|---|
| 2002 — 2004 | Fritzsch, Bernd | R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Cellular Interactions During Ear Development @ Creighton University DESCRIPTION (provided by applicant): In this application we want to resolve some of the molecular and cellular interactions that lead to the formation of the two main sensorineuronal cell types of the ear, the hair cell for mechanoelectric transduction and the sensory neurons for conduction of information from the hair cells to the brain. Using morphological (e.g. immunohistochemistry and DiI labeling) and molecular biological approaches (e.g. in situ hybridization, and RTPCR) we will analyze aspects of 1) cell survival, 2) general cell fate determination, and 3) organ specific cell fate determination. In AIM 1 we will scrutinize the role played by both location and amount of neurotrophin expression in patterning inner ear innervation. Inner ear sensory neurons express both trkB and trkC receptors. This unique feature will allow us to analyze in a BDNF null mutant simultaneously carrying a neurotrophin transgene (NT3 tgBDNF) for the first time in vivo how both concentration and distribution of a neurotrophin affect the patterning of normal and aberrant nerve fibers. In AIM 2 we will examine the molecular and cellular interactions of the principle neurogenic bHLH genes expressed in the ear; ngn1, Math1 and NeuroD. We will examine a possible clonal relationship between sensory neurons and hair cells and how the absence of varying combinations of proneuronal bHLH genes affects ear development, in particular the gene expression patterns in supporting cells. In contrast to the brain, this analysis is feasible because only two bHLH genes (Math1, ngn1) determine two neuron-like cells (hair cells, sensory neurons). We will interbreed mutants of ngn1, Math1, and NeuroD to study how ngn1 affects Math1, how ngn1 affects NeuroD, how Math1 affects NeuroD and how double nulls for both ngn1 and Math1 affect formation of the remaining ear. In AIM 3 we will analyze how BF1 and FGF10 affect the formation of organ specific sensory neurons and sensory epithelia absent in these mutants. We will characterize the expression of the bHLH genes, ngn1 and Math1, in null mutants of BF1 and FGF10. Such information can guide future research on regeneration of these cells in patients suffering sensorineuronal hearing loss and other areas of neuroscience less amenable to such investigations. |
0.957 |
| 2006 — 2010 | Fritzsch, Bernd | R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Dissecting the Ear Neurosensory Development. @ University of Iowa DESCRIPTION (provided by applicant): The neurosensory components of the ear that extract vestibular and auditory information and conduct it to the brain are hair cells and sensory neurons. Our short term goal is to analyze in vivo the molecular biology of neurosensory cell formation and survival that generates the most crucial cell types of the ear and connects them. Our long term goal is to use this information for neurosensory regeneration and to guide growing afferents to reach either regenerated hair cells or stimulating electrodes of cochlear implants. We will focus in this application on three steps required to develop and connect hair cells and sensory neurons. These are neurosensory fate determination, neurosensory fate acquisition and neurosensory connection formation. All of these events are influenced by a cascade of genes expressed in the growing otocyst. We will concentrate on the role of three genes and their possible interactions that determine the neurosensory region of the ear using composite mutant mice that are null or heterozygous for various combinations of three genes (Aim1). We will continue our investigation on the role of the three major bHLH genes in various combinations that are null or heterozygous or in newly generated transgenic line to dissect the molecular mechanisms of hair cell and sensory neuron fate acquisition (Aim2). Aim3 will extend our investigations into neonates and postnatal mice on the role of neurotrophins for neuronal fiber guidance through the use of transgenic misexpression and targeted elimination of neurotrophins in the ear. AIM 1 will specify the role of FgflO, Gata3 and Foxgl in neurosensory development of the ear. These three factors are known to interact in neurosensory development in the central and peripheral nervous systems of mice and flies, but their interactions in the ear are not clarified. AIM 2 will test the molecular interactions of bHLH genes (Atohl, Neurogl, Neurodl) in hair cell and sensory neuron development. Identifying multipotent precursors, that can be manipulated to generate all neurosensory cells could greatly benefit current attempts of restoring neurosensory hearing loss. AIM 3 will molecularly dissect the role of neurotrophins in neonatal and postnatal fiber reorganization using conditional Bdnf ear mutations in combination with transgenic misexpressors. Such information is crucial to govern the use of neurotrophins for regeneration, plasticity and maintenance of adult innervation. |
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| 2010 — 2014 | Dailey, Michael E [⬀] Fritzsch, Bernd |
P30Activity Code Description: To support shared resources and facilities for categorical research by a number of investigators from different disciplines who provide a multidisciplinary approach to a joint research effort or from the same discipline who focus on a common research problem. The core grant is integrated with the center's component projects or program projects, though funded independently from them. This support, by providing more accessible resources, is expected to assure a greater productivity than from the separate projects and program projects. |
@ University of Iowa Anatomy; Auditory system; base; Cells; Collaborations; Computer software; Computers; Data Analyses; Data Collection; Electron Microscopy; Ensure; experience; forging; Funding; Gene Expression; Gene Proteins; Genes; genetic manipulation; Goals; Histology; Image; image processing; immunocytochemistry; improved; In Situ Hybridization; In Vitro; in vivo; Individual; Label; Laboratories; Learning; Light; Molecular; mouse model; National Institute on Deafness and Other Communication Disorders; novel; Online Systems; Performance; Phenotype; Physiology; Process; protein expression; Protocols documentation; Research; Research Personnel; Research Project Grants; Services; Structure; Technical Expertise; Techniques; Time; tissue culture; tissue processing; Tissues; Training; web site; Work |
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| 2014 — 2019 | Cole, Renee Fritzsch, Bernd Florman, Jean Jacobson, Wayne |
N/AActivity Code Description: No activity code was retrieved: click on the grant title for more information |
Tile: Transform, Interact, Learn, and Engage For Success in Stem Education @ University of Iowa This project is preparing for institution-wide transformation of teaching and learning practices at a large public research university. It is continuing to expand a process that has already begun, building infrastructure around a core initiative called TILE (Transform, Interact, Learn, and Engage for success in STEM education). TILE requires faculty implementers to invest in professional development and the University to invest in technology-rich classrooms. TILE classrooms are remodeled after the SCALE-UP classrooms used in physics and other disciplines in the physical sciences that have been proven to be effective learning environments when paired with appropriate pedagogy. SCALE-UP (Student-Centered Active Learning Environment for Undergraduate Programs) is a mature, proven evidence-based method of education that puts students in small groups around circular tables and engages them in active construction of knowledge. Using computers, they pull information from the Internet to use in active solving problems. In SCALE-UP the task of getting disciplinary content is shifted to the internet and the process of solving difficult problems occurs in small groups during class time, where students help one another and are guided by expert instructors. This model is currently in use in more than 100 institutions of higher education. Appropriate pedagogy is learned by faculty instructors through a professional development program at the university that has already been designed and implemented by the Center for Teaching and the Office of Information Technology Services. |
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| 2018 — 2020 | Fritzsch, Bernd Yamoah, Ebenezer N [⬀] |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Mechanisms of Growth Factor Responsiveness in the Aging Auditory System @ University of Nevada Reno Abstract: During hearing development, auditory neurons are wired correctly, both qualitatively and quantitatively, with specific types of spiral ganglion neurons (SGN; auditory afferents) and cochlear nucleus (CN) nerve fibers. Maturation of the auditory neural pathway ensues along the functional tonotopic frequency axis, apparently correlating with time and space/location-dependent gradients in neurotrophins (NTs). In addition, the SGNs develop cochleotopic responses to sound and achieve cochleotopic projections to the cochlear nuclei (CN). The activity of SGNs maintains the number, size and functions of cells in the CN. Previous studies suggest that this process is regulated in part by neurotrophic factors (e.g. brain-derived neurotrophic factor (BDNF)). Expression data show that BDNF expression undergo developmental and age-dependent shifts in their cellular and longitudinal patterns of expression in the auditory pathway. This pattern was proposed to dictate distinct apico- basal function of auditory neuron electrical properties, in turn requirements for cochleotopic and central auditory neuron fine tuning. Despite the appeal of the NT-gradient and age-dependent hypothesis for auditory neural properties, this idea rests on correlative evidence, disputed by some. We seek to unequivocally test and clarify the NT-gradient predictions, and to understand BDNF-mediated auditory functional plasticity and how it sculpts age-related hearing loss (ARHL). We hypothesize that gradual decline in BDNF signaling is one of the common cause for ARHL. We will unravel the function of BDNF in auditory neuronal plasticity using well-characterized cre lines (e.g. Rosa26-creER; Fgf8-cre, Atoh1-cre) to selectively reduce or eliminate BDNF in floxed lines, to study the long- term influence of BDNF levels on auditory signal processing in aging mice. In Aim 1, we will quantify BDNF signaling expression in the auditory system, determine the source/s and the ensuing age-related changes in the auditory neural pathway. Single molecule fluorescent in situ hybridization (SmFISH) and immunocytochemical techniques will be used to quantify mRNA and protein expression and the age-related changes of BDNF. Additionally, age-related changes in BDNF-receptors expression will be quantified. In Aim 2, we will determine BDNF-mediated auditory plasticity with partial or delayed loss of BDNF. These goals will be accomplished using inducible cre lines (e.g. Rosa26-creER) to eliminate all BDNF at various stages of aging from ~3-week to 2-year old mice. We will determine the age-related cellular properties of auditory neurons (e.g. SGNs). Finally, in Aim 3, we will identify BDNF-mediated neural and synaptic plasticity with partial and delayed loss of BDNF. We will use the animal models outlined in Aim 2 to identify changes in synaptic function at the calyx of Held, due to BDNF loss/decline. This central auditory synapse, originates in the ventral cochlear nucleus (VCN), and project contralaterally to the medial nucleus of the trapezoid body (MNTB), and is found to undergo morphological and molecular alterations during aging. We will also examine CN functional changes. Thus, we will resolve how the expression of BDNF impacts SGN/VCN/MNTB functions during aging, providing evidence for BDNF signaling as a common cause for auditory decline. This knowledge will inform efforts to use BDNF in therapeutic strategies to preserve auditory neuron viability and function after ARHL. |
0.976 |