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Title: Murine strain differences in beta-endorphin immunoreactivity.
Creator: Wong, Donna M., Florida Atlantic University, Lasiter, Phillip S.
Abstract/Description: The murine strains BALB and C57 differ in behavioral sensitivity to opioid alkaloids, beta-endorphin, and met-/leu-enkephalin. Possible differences in levels of endogenous "opioid peptides" have not been evaluated in the BALB and C57 murine genotypes by the use of immunohistochemical procedures. Antisera to synthetic ovine beta-endorphin was used to examine neuropil and somatic immunoreactivity in various diencephalic and telencephalic areas within three strains of inbred mice, BALB/c, C57BL...
Show moreThe murine strains BALB and C57 differ in behavioral sensitivity to opioid alkaloids, beta-endorphin, and met-/leu-enkephalin. Possible differences in levels of endogenous "opioid peptides" have not been evaluated in the BALB and C57 murine genotypes by the use of immunohistochemical procedures. Antisera to synthetic ovine beta-endorphin was used to examine neuropil and somatic immunoreactivity in various diencephalic and telencephalic areas within three strains of inbred mice, BALB/c, C57BL and the heterogenous strain (CF1). Results indicate that quantitative differences exist between these strains in the number of immunoreactive cells present in the arcuate nucleus of the hypothalamus and in neuropil straining. These observations indicate that behavioral differences in opioid responsivity may relate to differences in either the number of parent somata in the arcuate nucleus and/or the organization and/or trajectory of efferent projections arising from arcuate nucleus neurons.
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Date Issued: 1988
PURL: http://purl.flvc.org/fcla/dt/14452
Subject Headings: Mice as laboratory animals, Endorphins, Mice--Immunology
Format: Document (PDF)

Title: Energy metabolism and slow skeletal troponin I phosphorylation in cardiac troponin I null mouse heart.
Creator: Jia, Yuanyuan, Florida Atlantic University, Huang, Xupei, Charles E. Schmidt College of Medicine, Department of Biomedical Science
Abstract/Description: Troponin I (TnI) plays an important role in cardiac muscle contraction. Two TnI genes (cardiac and slow skeletal TnI) are predominantly expressed in the heart. In cTnI knockout mice, myocardial TnI deficiency results in a diastolic dysfunction and a sudden death in homozygous mutants. In the present studies, energy metabolism has been analyzed in myocardial cells from cTnI null hearts. Our results have demonstrated that damaged relaxation and increased Ca2+-independent force production in...
Show moreTroponin I (TnI) plays an important role in cardiac muscle contraction. Two TnI genes (cardiac and slow skeletal TnI) are predominantly expressed in the heart. In cTnI knockout mice, myocardial TnI deficiency results in a diastolic dysfunction and a sudden death in homozygous mutants. In the present studies, energy metabolism has been analyzed in myocardial cells from cTnI null hearts. Our results have demonstrated that damaged relaxation and increased Ca2+-independent force production in cTnI null hearts stimulated myofibril MgATPase activities accompanied by the increase of mitochondria quantity and ATPase activities. In addition, an increase of ssTnI phosphorylation level has been observed in cTnI null hearts. The results indicate that TnI deficiency can cause the disturbance of energy metabolism and some protein overphosphorylation.
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Date Issued: 2003
PURL: http://purl.flvc.org/fcla/dt/12998
Subject Headings: Mice as laboratory animals, Mice--Metabolism, Energy metabolism, Mitochondria
Format: Document (PDF)

Title: Heading in the right direction: the behavior and brain mechanisms of directional navigation.
Creator: Williams, Sidney Beth., Charles E. Schmidt College of Science, Department of Psychology
Abstract/Description: The mechanisms that rodents employ to navigate through their environment have been greatly studied. Cognitive mapping theory suggests that animals use distal cues in the environment to navigate to a goal location (place navigation). However, others have found that animals navigate in a particular direction to find a goal (directional navigation). The rodent brain contains head direction cells (HD cells) that discharge according to the head direction of the animal. Navigation by heading...
Show moreThe mechanisms that rodents employ to navigate through their environment have been greatly studied. Cognitive mapping theory suggests that animals use distal cues in the environment to navigate to a goal location (place navigation). However, others have found that animals navigate in a particular direction to find a goal (directional navigation). The rodent brain contains head direction cells (HD cells) that discharge according to the head direction of the animal. Navigation by heading direction is disrupted by lesions of the anterodorsal thalamic nuclei (ADN), many of which are HD cells. Aim 1 tested whether male C57BL/6J mice exhibit direction or place navigation in the Morris water maze. Aim 2 tested the effects of temporary inactivation of the ADN on directional navigation. Together, these data indicate that C57BL/6J mice also exhibit preference for directional navigation and suggest that the ADN may be crucial for this form of spatial navigation.
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Date Issued: 2009
PURL: http://purl.flvc.org/FAU/186774
Subject Headings: Mice as laboratory animals, Animal navigation, Spatial behavior in animals, Cognition in animals
Format: Document (PDF)

Title: Evaluation of cardiac function in cTnI(R192H) transgenic mice and cTni knockout mice with High-Resolution Ultrasound Imaging and Doppler Echocardiography.
Creator: Liu, Jing, Huang, Xupei, Florida Atlantic University, Charles E. Schmidt College of Medicine, Department of Biomedical Science
Abstract/Description: Troponin I is a contractile protein and plays an important role in cardiac function. We have generated cTnl knockout and cTnI(R192H) transgenic mouse models. All of cTnl knockout homozygous mice die at 17-18 days after birth. Some of cTnI(R192H) transgenic mice die at early life stages, some mice develop heart failure at late stages. High-resolution ultrasound imaging and Doppler echocardiography have been used to evaluate cardiac function on cTnl deficient mice and cTnl(R192H) transgenic...
Show moreTroponin I is a contractile protein and plays an important role in cardiac function. We have generated cTnl knockout and cTnI(R192H) transgenic mouse models. All of cTnl knockout homozygous mice die at 17-18 days after birth. Some of cTnI(R192H) transgenic mice die at early life stages, some mice develop heart failure at late stages. High-resolution ultrasound imaging and Doppler echocardiography have been used to evaluate cardiac function on cTnl deficient mice and cTnl(R192H) transgenic mice. cTnI mice have damaged relaxation with gradually decreased E/A ratio(E/A<1). FS and cardiac output dramatically decrease on 17-day-o1d cTnI mice indicating severe cardiac dysfunction. We find that the damaged heart function is correspondent with the Tnl expression level decline. 6-8 weeks transgenic mice have shown that the dimension of left and right atria increase. In 15-month-old transgenic mice, the E/A ratio shows a pseudonormal pattern indicating a diastolic dysfunction. This study demonstrate that damaged heart function is tightly associated with Tnl levels in the heart.
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Date Issued: 2006
PURL: http://purl.flvc.org/fau/fd/FA00000789
Subject Headings: Transgenic mice, Mice as laboratory animals, Coronary heart disease--Seriodiagnosis, Congestive heart failure--Pathophysiology
Format: Document (PDF)

Title: Which Way is It? Spatial Navigation and the Genetics of Head Direction Cells.
Creator: Lora, Joan C., Stackman, Robert W., Florida Atlantic University, Charles E. Schmidt College of Science, Department of Psychology
Abstract/Description: From locating a secure home, foraging for food, running away from predators, spatial navigation is an integral part of everyday life. Multiple brain regions work together to form a three-dimensional representation of our environment; specifically, place cells, grid cells, border cells & head direction cells are thought to interact and influence one another to form this cognitive map. Head direction (HD) cells fire as the animal moves through space, according to directional orientation of the...
Show moreFrom locating a secure home, foraging for food, running away from predators, spatial navigation is an integral part of everyday life. Multiple brain regions work together to form a three-dimensional representation of our environment; specifically, place cells, grid cells, border cells & head direction cells are thought to interact and influence one another to form this cognitive map. Head direction (HD) cells fire as the animal moves through space, according to directional orientation of the animal’s head with respect to the laboratory reference frame, and are therefore considered to represent the directional sense. Interestingly, inactivation of head direction cell-containing brain regions has mixed consequences on spatial behavior. Current methods of identifying HD cells are limited to in vivo electrophysiological recordings in a dry-land environment. We first developed a dry-land version of the MWM in order to carry out behavioral-recording paired studies. Additionally, to learn about HD cells function we quantified expression of neuronal activation marker (c-Fos), and L-amino acid transporter 4 (Lat4) in neurons found within the HD cell dense anterodorsal thalamic nucleus (ADN) in mice after exploratory behavior in an open field, or forward unidirectional movement on a treadmill. We hypothesize that the degree to which ADN neurons are activated during exploratory behavior is influenced by the range of heading directions sampled. Additionally, we hypothesize that c-Fos and Lat4 are colocalized within ADN neurons following varying amounts of head direction exposure. Results indicate that following free locomotion of mice in an open field arena, which permitted access to 360° of heading, a greater number of ADN neurons express c-Fos protein compared to those exposed to a limited range of head directions during locomotion in a treadmill. These findings suggest that the degree of ADN neuronal activation was dependent upon the range of head directions sampled. We observed a high degree of colocalization of c-Fos and Lat4 within ADN suggesting that Lat4 may be a useful tool to manipulate neuronal activity of HD cells. Identifying genetic markers specific to ADN helps provide an essential understanding of the spatial navigation system, and supports development of therapies for cognitive disorders affecting navigation.
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Date Issued: 2017
PURL: http://purl.flvc.org/fau/fd/FA00004931, http://purl.flvc.org/fau/fd/FA00004931
Subject Headings: Psychobiology., Spatial behavior in animals., Mice as laboratory animals., Navigation--Psychological aspects., Computational intelligence.
Format: Document (PDF)

Title: Assessment of anatomical structures and hemodynamic function of cTnI[193His] transgenic mice with micro-echocardiography.
Creator: Gobara, Nariman., Charles E. Schmidt College of Medicine
Abstract/Description: Transgenic mice were generated to express a restrictive cardiomyopathy (RCM) human cardiac troponin I (cTnI) R192H mutation in the heart. My study's objective was to assess cardiac function during the development of diastolic dysfunction and to gain insight into the pathophysiological impact of the RCM cTnI mutation. Cardiac function was monitored in cTnI193His mice and wild-type littermates for a period of 12 months. It progressed gradually from abnormal relaxation to diastolic dysfunction...
Show moreTransgenic mice were generated to express a restrictive cardiomyopathy (RCM) human cardiac troponin I (cTnI) R192H mutation in the heart. My study's objective was to assess cardiac function during the development of diastolic dysfunction and to gain insight into the pathophysiological impact of the RCM cTnI mutation. Cardiac function was monitored in cTnI193His mice and wild-type littermates for a period of 12 months. It progressed gradually from abnormal relaxation to diastolic dysfunction characterized with micro- echocardiography by a reversed E/A ratio, increased deceleration time, and prolonged isovolumetric relaxation time. The negative impact of cTnI193His on cardiac function was further demonstrated in isolated mouse working heart preparations. Dobutamine stimulation increased heart rate in cTnI193His mice but did not improve CO. The cTnI193His mice had a phenotype similar to that in human RCM patients carrying the cTnI mutation characterized morphologically by enlarged atria and restricted ventricle and functionally by diastolic dysfunction.
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Date Issued: 2009
PURL: http://purl.flvc.org/FAU/186680
Subject Headings: Mice as laboratory animals, Biochemical markers, Diagnostic use, Cardiovascular system, Pathophysiology, Coronary heart disease, Molecular diagnosis
Format: Document (PDF)

Title: Analyses of neuronal replacement in the neuron-depleted olfactory systems in adult mice.
Creator: Liu, Huan, Charles E. Schmidt College of Medicine
Abstract/Description: New neurons are continuously generated in the olfactory system of adult mice, including olfactory sensory neurons (OSNs) in the olfactory epithelium (OE) and interneurons, produced in the subventricular zone (SVZ) and migrated toward olfactory bulb (OB) along rostral migratory stream (RMS). The present study observed the effects of target neuron loss on the life-span and maturation of adult-born OSNs in the OE and on the proliferation, migration and differentiation of SVZ stem cells in the...
Show moreNew neurons are continuously generated in the olfactory system of adult mice, including olfactory sensory neurons (OSNs) in the olfactory epithelium (OE) and interneurons, produced in the subventricular zone (SVZ) and migrated toward olfactory bulb (OB) along rostral migratory stream (RMS). The present study observed the effects of target neuron loss on the life-span and maturation of adult-born OSNs in the OE and on the proliferation, migration and differentiation of SVZ stem cells in the forebrain after eliminating bulb neurons. We found the life-span of newborn neurons in the absence of synaptic targets was shortened, but the timing of maturation was not delayed. In addition, SVZ cells continued to divide and migrate to the damaged bulb, and the migration of newborn cells in the RMS on the contralateral side was delayed at 2 weeks post-BrdU. Also, the proliferation of cells in dentate gyrus of the hippocampus was not affected by OB damage at 3 weeks post-lesion, though lesion affects occurred in the adult SVZ/RMS.
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Date Issued: 2008
PURL: http://purl.flvc.org/fcla/dt/172671
Subject Headings: Mice as laboratory animals, Neurotransmitter receptors, Sensory neurons, Testing, Cellular control mechanisms
Format: Document (PDF)

Title: Influence of small conductance calcium-activated potassium channels (SK,Kca2) on long-term memory: global and local analysis across time- and task- dependent measures.
Creator: Vick, Kyle A., Charles E. Schmidt College of Science, Department of Psychology
Abstract/Description: Small conductance calcium-activated potassium (SK) channels are found ubiquitously throughout the brain and modulate the encoding of learning and memory. Systemic injection of 1-ethyl-2-benzimidalzolinoe (EBIO), a SK channel activator, impairs the encoding of novel object memory and locomotion but spares fear memory encoding in C57BL/6NHsd mice. The memory impairments discovered were not due to non-cognitive performance confounds such as ataxia, anxiety, attention or analgesia. Further...
Show moreSmall conductance calcium-activated potassium (SK) channels are found ubiquitously throughout the brain and modulate the encoding of learning and memory. Systemic injection of 1-ethyl-2-benzimidalzolinoe (EBIO), a SK channel activator, impairs the encoding of novel object memory and locomotion but spares fear memory encoding in C57BL/6NHsd mice. The memory impairments discovered were not due to non-cognitive performance confounds such as ataxia, anxiety, attention or analgesia. Further investigation with intra-hippocampal application of EBIO revealed SK channels in dorsal CA1 contribute to the encoding deficits seen systemically, but do not account for the full extent of the impairment. Concentrated activation of dorsal CA1 SK channels do not influence fear memory encoding or locomotor impairments. Taken together, these data indicate SK channels, especially in the dorsal hippocampus, have a modulatory role on novel object memory encoding, but not retrieval; however, pharmacological activation of hippocampal SK channels does not appear to influence fear memory encoding.
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Date Issued: 2009
PURL: http://purl.flvc.org/FAU/192991
Subject Headings: Mice as laboratory animals, Cellular signal transduction, Memory, Research, Biological transport, Research, Potassium channels, Physiological effect
Format: Document (PDF)

Title: The effect of small conductance calcium-activated potassium channels on emotional learning and memory.
Creator: Sanguinetti, Shannon, Stackman, Robert W., Florida Atlantic University, Charles E. Schmidt College of Science, Department of Psychology
Abstract/Description: Small conductance Ca2+-activated K+ (SK) channels have been shown to alter the encoding of spatial and non-spatial memory in the hippocampus by shaping glutamatergic postsynaptic potentials and modulating NMDA receptor-dependent synaptic plasticity. When activated, dendritic SK channels reduce hippocampal neuronal excitability and LTP. Similar SK channel properties have been demonstrated in lateral amygdala (LA) pyramidal neurons. Additionally, induction of synaptic plasticity and beta...
Show moreSmall conductance Ca2+-activated K+ (SK) channels have been shown to alter the encoding of spatial and non-spatial memory in the hippocampus by shaping glutamatergic postsynaptic potentials and modulating NMDA receptor-dependent synaptic plasticity. When activated, dendritic SK channels reduce hippocampal neuronal excitability and LTP. Similar SK channel properties have been demonstrated in lateral amygdala (LA) pyramidal neurons. Additionally, induction of synaptic plasticity and beta-adrenoreceptor activation in LA pyramidal neurons causes PKA-mediated internalization of SK channels from the postsynaptic density. Chronic activation of the amygdala through repetitive stressful stimuli can lead to excitatory synaptic strengthening that may create permanent hyper-excitability in its circuitry. This mechanism may contribute to a number of mood and anxiety disorders. The selective influence of SK channels in the LA on anxiety and fear conditioning are not known. The thesis project outlined herein examined whether SK channel blockade by bee venom peptide, apamin, during a repetitive acute fear conditioning paradigm was sufficient to alter fear memory encoding and the resulting behavioral outcome. Following the final fear memory test session, mice were tested in the open field immediately after the second fear conditioning test session. The findings indicate that intracranial LA microinfusions of apamin did not affect memory encoding or subsequent anxiety.
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Date Issued: 2015
PURL: http://purl.flvc.org/fau/fd/FA00004543, http://purl.flvc.org/fau/fd/FA00004543
Subject Headings: Biological transport -- Research, Cellular signal transduction, Memory -- Research, Mice as laboratory animals, Potassium channels -- Physiological effect
Format: Document (PDF)

Title: Representation of object-in-context within mouse hippocampal neuronal activity.
Creator: Asgeirsdottir, Herborg Nanna, Charles E. Schmidt College of Science, Department of Psychology
Abstract/Description: The rodent hippocampus is critical for processing spatial memory but its contribution to non-spatial, specifically object memory is debated. The cognitive map theory of hippocampal function states that the hippocampus stores relationships of goal locations (places) to discrete items (objects) encountered within environments. Dorsal CA1 place cells were recorded in male C57BL/6J mice performing three variations of the novel object recognition paradigm to define "object-in-context"...
Show moreThe rodent hippocampus is critical for processing spatial memory but its contribution to non-spatial, specifically object memory is debated. The cognitive map theory of hippocampal function states that the hippocampus stores relationships of goal locations (places) to discrete items (objects) encountered within environments. Dorsal CA1 place cells were recorded in male C57BL/6J mice performing three variations of the novel object recognition paradigm to define "object-in-context" representation of hippocampal neuronal activity that may support object memory. Results indicate, (i) that place field stability is higher when polarizing environmental cues are provided during object recognition; (ii) hippocampal place fields remain stable throughout the novel object recognition testing without a polarizing cue; and (iii) time dependent effects on stability when objects were dissociated from the context. These data indirectly support that the rodent hippocampus processes object memory, and challenge the view that "object-in-context" representations are formed when mice perform novel object recognition task.
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Date Issued: 2013
PURL: http://purl.flvc.org/fcla/dt/3362339
Subject Headings: Mice as laboratory animals, Hippocampus (Brain), Neurotransmitter receptors, Cellular control mechanisms, Cellular signal transduction
Format: Document (PDF)

Title: Selective Activation of the SK1 Subtype of Small Conductance Ca2+ Activated K+ Channels by GW542573X in C57BL6J Mice Impairs Hippocampal-dependent Memory.
Creator: Rice Kuchera, Claire A., Stackman, Robert W., Florida Atlantic University, Charles E. Schmidt College of Science, Department of Psychology
Abstract/Description: SK channels are small conductance Ca2+-activated K+ channels expressed throughout the CNS. SK channels modulate the excitability of hippocampal CA1 neurons by affecting afterhyperpolarization and shaping excitatory postsynaptic responses. Such SK-mediated effects on activity-dependent neuronal excitability and synaptic strength are thought to underlie the modulatory influence of SK channels on memory encoding. Here,the effect of a new SK1 selective activator, GW542573X, on hippocampal...
Show moreSK channels are small conductance Ca2+-activated K+ channels expressed throughout the CNS. SK channels modulate the excitability of hippocampal CA1 neurons by affecting afterhyperpolarization and shaping excitatory postsynaptic responses. Such SK-mediated effects on activity-dependent neuronal excitability and synaptic strength are thought to underlie the modulatory influence of SK channels on memory encoding. Here,the effect of a new SK1 selective activator, GW542573X, on hippocampal-dependent object memory, contextual and cued conditioning, and trace fear conditioning was examined. The results demonstrated that pre- but not post-training systemic administration of GW542573X impaired object memory and trace fear memory in mice 24 h after training. Contextual and cued fear memory were not disrupted. These current data suggest that activation of SK1 subtype-containing SK channels impairs long-term memory. These results are consistent with converging evidence that SK channel activation suppressed behaviorally triggered synaptic plasticity necessary for encoding hippocampal-dependent memory.
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Date Issued: 2015
PURL: http://purl.flvc.org/fau/fd/FA00004541, http://purl.flvc.org/fau/fd/FA00004541
Subject Headings: Cellular control mechanisms, Cognitive neuroscience, Cognitive psychology, Hippocampus (Brain), Mice as laboratory animals, Neurotransmitter receptors
Format: Document (PDF)

Title: Roles of troponin I in heart development and cardiac function.
Creator: Du, Jianfeng., Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: Two major troponin I (TnI) genes, fetal TnI (ssTnI) and adult TnI (cTnI), are expressed in the mammalian heart under the control of a developmentally regulated program. In this study, the up-stream domain (~1,800 bp) of mouse fetal TnI gene has been cloned and characterized. There is a high homology of this region among mouse, rat and human. Transfection assays indicated that conserved GA-rich sequences, CREB and a CCAAT box within the first 300 bp upstream of the transcription start site...
Show moreTwo major troponin I (TnI) genes, fetal TnI (ssTnI) and adult TnI (cTnI), are expressed in the mammalian heart under the control of a developmentally regulated program. In this study, the up-stream domain (~1,800 bp) of mouse fetal TnI gene has been cloned and characterized. There is a high homology of this region among mouse, rat and human. Transfection assays indicated that conserved GA-rich sequences, CREB and a CCAAT box within the first 300 bp upstream of the transcription start site were critical for the gene expression. Electrophoretic mobility shift assays (EMSAs) and chromatin immunoprecipitation (ChIP) assays revealed binding proteins to CREB site in nuclear extracts from myocardial cells. Thyroid hormone (T3) caused a significant inhibitory effect on ssTnI expression in myocardial cells. Cardiac troponin I (cTnI) mutations have been linked to the development of restrictive cardiomyopathy (RCM) in human patients. We modeled one mutation in human cTnI Cv terminus, arginine1 92 histidine (R192H) by cardiac specific expression of the mutated protein (cTnI193His in mouse sequence) in transgenic mice. The main functional alteration detected in cTnI193His mice by ultrasound cardiac imaging examinations was impaired cardiac relaxation manifested by a decreased left ventricular end diastolic dimension (LVEDD) and an increased end diastolic dimension in both atria. Echocardiography revealed a series of changes on the transgenic mice including a reversed E-to-A ratio, increased deceleration time, and prolonged isovolumetric relaxation time. At the age of 12 months, cardiac output in cTnI193His mice was significantly declined, and some transgenic mice showed congestive heart failure. The negative impact of cTnI193His on ventricular contraction and relaxation was further demonstrated in isolated mouse working heart preparations., Dobutamine stimulation increased heart rate in cTnI193His mice but did not improve CO.The cTnI193His mice had a phenotype similar to that in human RCM patients carrying the cTnI mutation. The results demonstrate a critical role of the COOH-terminal domain of cTnI in the diastolic function of cardiac muscle. This mouse model provides us with a tool to further investigate the pathophysiology and the development of RCM.
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Date Issued: 2008
PURL: http://purl.flvc.org/FAU/186287
Subject Headings: Mice as laboratory animals, Biochemical markers, Diagnostic use, Heart, Diseases, Molecular diagnosis, Cardiovascular system, Pathophysiology
Format: Document (PDF)

Title: Pathogenesis of idiopathic restrictive cardiomyopathy.
Creator: Li, Yuejin, Charles E. Schmidt College of Medicine, Department of Biomedical Science
Abstract/Description: Restrictive cardiomyopathy (RCM) is a heart muscle disease, characterized by diastolic dysfunction. The present dissertation is to understand the mechanisms underlyijng the initiation of diastolic dysfunction and the fast disease progression to early death in a RCM mouse model, the transgenic cTnI193His mouse... These data showed that myocardial ischemia occurred after diastolic dysfunction and before systolic dysfunction which proceeded congestive heart failure. The results demonstrate that...
Show moreRestrictive cardiomyopathy (RCM) is a heart muscle disease, characterized by diastolic dysfunction. The present dissertation is to understand the mechanisms underlyijng the initiation of diastolic dysfunction and the fast disease progression to early death in a RCM mouse model, the transgenic cTnI193His mouse... These data showed that myocardial ischemia occurred after diastolic dysfunction and before systolic dysfunction which proceeded congestive heart failure. The results demonstrate that myocardial ischemia causing cardiomycete death is a link between the initial diastolic dysfunction and late-stage systolic dysfunction, and accelerates the disease progression to fatal heart failure in the early age.
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Date Issued: 2011
PURL: http://purl.flvc.org/fcla/dt/3362045
Subject Headings: Mice as laboratory animals, Heart conduction system, Cardiovascular system, Diseases, Genetic aspects
Format: Document (PDF)

Title: Unraveling the mysteries of Sjogren's syndrome: a closer look at the effects of hormones and genetics over time using the NOD.B10.H2b mouse model.
Creator: Seamon, Vanessa., Charles E. Schmidt College of Medicine, Department of Integrated Medical Science
Abstract/Description: Sjogren's Syndrome (SS) is characterized by lymphocytic infiltration, destruction and dysfunction of the lacrimal and salivary glands and the presence of serum autoantibodies. Although, approximately 0.5% of the population suffers from SS, there is a female predominance of 9:1 compared with males. Most women with SS are postmenopausal; however, not all women who are post-menopausal develop SS. Therefore, we postulate that a decrease in the circulating levels of hormones creates an environment...
Show moreSjogren's Syndrome (SS) is characterized by lymphocytic infiltration, destruction and dysfunction of the lacrimal and salivary glands and the presence of serum autoantibodies. Although, approximately 0.5% of the population suffers from SS, there is a female predominance of 9:1 compared with males. Most women with SS are postmenopausal; however, not all women who are post-menopausal develop SS. Therefore, we postulate that a decrease in the circulating levels of hormones creates an environment favorable to the development of SS in a predisposed genetic background. In order to carry out our studies, we used the NOD.B10.H2b mouse model of SS, and ovariectomized (OVX) them as a model for the post-menopausal condition. We removed the lacrimal glands and measured the gene expression and protein levels of several cytokines and chemokines known to be upregulated in patients with SS such as : lL-1B, IL-10, INF-y, TNFa, CCL9 and CXCL13., We also stained for markers of B cells (B220+) and T cells (CD4+ and CD8+), and counted positively stained cleaved caspase-3 cells as an indication of apoptosis. These experiments were done 3, 7 and 21 days post-OVX and compared to sham operated animals. In order to determine whether the changes observed with OVX were triggered mainly by a genetic pre-disposition, a non-prediposed OVX and sham operated mouse (C57BL/10) was used as control. We found that gene expression of IL-1B, IL-10 and IF-y were upregulated in the lacrimal glands of the OVX NOD.B10.H2b mice at 3 days post-OVX compared with sham operated animals. Gene expression of IL-1B, IL-10, IFN-y, TNF-a, CCL9 and CXCL13, and protein levels of IL-1B, IL-10 and CCL9 were upregulated in the OVX NOD.B10.H2b mice at 7 days post-OVX compared to sham operated animals., Also, at 7 days, an increase in B220+ B cells and an increase in cleaved caspase-3 were also observed in the OVX NOD.B10.H2b mice lacrimal glands compared to sham operated animals. At 21 days, protein levels of IL-10 were also highly upregulated in the OVX NOD.B10.H2b mice, together with an increase of B220+ B cells, a slight increase in the CD4/CD8 ratio and an increase on the number of caspase-3 positive cells. No changes were observed in any of the above parameters measured in the OVX C57BL/10 mice compared to the sham operated group, supporting our hypothesis that both, genetics and a decrease in the levels of hormones are necessary for SS to occur.
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Date Issued: 2009
PURL: http://purl.flvc.org/FAU/215292
Subject Headings: Sjèogren's syndrome, Immunological aspects, Sjèogren's syndrome, Animal models, Mice as laboratory animals, Gene expression, Salivary glands, Diseases, Histopathology
Format: Document (PDF)

Title: Cell-surface glycan-lectin interactions for biomedical applications.
Creator: Rodriguez Benavente, Maria Carolina, Lepore, Salvatore D., Cudic, Predrag, Charles E. Schmidt College of Science, Department of Chemistry and Biochemistry
Abstract/Description: Carbohydrate recognition is one of the most sophisticated recognition processes in biological systems, mediating many important aspects of cell-cell recognition, such as inflammation, cell differentiation, and metastasis. Consequently, lectin-glycan interactions have been intensively studied in order to mimic their actions for potential bioanalytical and biomedical applications. Galectins, a class of ß-galactoside-specific animal lectins, have been strongly implicated in inflammation and...
Show moreCarbohydrate recognition is one of the most sophisticated recognition processes in biological systems, mediating many important aspects of cell-cell recognition, such as inflammation, cell differentiation, and metastasis. Consequently, lectin-glycan interactions have been intensively studied in order to mimic their actions for potential bioanalytical and biomedical applications. Galectins, a class of ß-galactoside-specific animal lectins, have been strongly implicated in inflammation and cancer. Galectin-3 is involved in carbohydrate-mediated metastatic cell heterotypic and homotypic adhesion via interaction with Thomsen-Friedenreich (TF) antigen on cancer-associated MUC1. However, the precise mechanism by which galectin-3 recognizes TF antigen is poorly understood. Our thermodynamic studies have shown that the presentation of the carbohydrate ligand by MUC1-based peptide scaffolds can have a major impact on recognition, and may facilitate the design of more potent and specific galectin-3 inhibitors that can be used as novel chemical tools in dissecting the precise role of galectin-3 in cancer and inflammatory diseases. Another lectin, odorranalectin (OL), has been recently identified from Odorrana grahami skin secretions as the smallest cyclic peptide lectin, has a particular selectivity for L-fucose and very low toxicity and immunogenicity, rendering OL an excellent candidate for drug delivery to targeted sites, such as: (1) tumor-associated fucosylated antigens implicated in the pathogenesis of several cancers, for overcoming the nonspecificity of most anticancer agents; (2) the olfactory epithelium of nasal mucosa for enhanced delivery of peptide-based drugs to the brain.
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Date Issued: 2015
PURL: http://purl.flvc.org/fau/fd/FA00004405
Subject Headings: Biopharmaceutics, Carbohydrates -- Therapeutic use, Cell differentiation, Drug delivery systems, Glycoproteins, Glycoslation, Mice as laboratory animals, Peptides -- Derivatives, Pharmaceutical biotechnology
Format: Document (PDF)

Title: Modulation of adult neurogenesis in mouse models of neurodegenerative disease.
Creator: McCollum, Mark Harvey., Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: Adult neurogenesis is affected in neurodegenerative diseases and also represents an important therapeutic target. The goal of this dissertation research was to test the hypothesis that regeneration of neurons and glia in the adult brain can be manipulated by neurotrophic drugs in the context of two mouse models of neurodegenerative disease : Parkinson's disease and Huntington's disease.... These findings have implications for the pathophysiology of Huntington's disease and neurodegeneration...
Show moreAdult neurogenesis is affected in neurodegenerative diseases and also represents an important therapeutic target. The goal of this dissertation research was to test the hypothesis that regeneration of neurons and glia in the adult brain can be manipulated by neurotrophic drugs in the context of two mouse models of neurodegenerative disease : Parkinson's disease and Huntington's disease.... These findings have implications for the pathophysiology of Huntington's disease and neurodegeneration in general. Specific alterations to the SVZ neurogenic niche parallel some of the pre-motor symptoms of Parkinson's disease and Huntington's disease. This dissertation research contributes to the growing body of literature concerning the pharmacological modulation of SVZ-derived neurogenesis designed to attenuate the progressive loss of neurons in neurodegenerative diseases and perhaps delay the onset of symptoms.
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Date Issued: 2012
PURL: http://purl.flvc.org/FAU/3355626
Subject Headings: Mice as laboratory animals, Huntington's chorea, Genetic aspects, Huntington's chorea, Pathophysiology, Parkinson's disease, Pathophysiology, Parkinson's disease, Genetic aspects
Format: Document (PDF)

Title: cTnI N-Terminal deletion: an agent for rescuing restrictive cardiomyopathy, a disease caused by mutations of Cardiac Troponin I.
Creator: Getfield, Cecile A., Huang, Xupei, Florida Atlantic University, Charles E. Schmidt College of Medicine, Department of Biomedical Science
Abstract/Description: Restrictive cardiomyopathy (RCM) is represented in part by left ventricular stiffness and diastolic dysfunction. Missense mutations of the cardiac troponin I (cTnI) gene cause idiopathic RCM. These mutations are located in the C-terminus of cTnI and affect cardiac relaxation. Transgenic mouse models presenting the pathology observed in clinical patients with RCM have been generated previously and express the mutant cTnI in their hearts. RCM-linked mutations increase cardiac myofilament Ca2+...
Show moreRestrictive cardiomyopathy (RCM) is represented in part by left ventricular stiffness and diastolic dysfunction. Missense mutations of the cardiac troponin I (cTnI) gene cause idiopathic RCM. These mutations are located in the C-terminus of cTnI and affect cardiac relaxation. Transgenic mouse models presenting the pathology observed in clinical patients with RCM have been generated previously and express the mutant cTnI in their hearts. RCM-linked mutations increase cardiac myofilament Ca2+ sensitivity and promote diastolic dysfunction in the heart. Previous studies using double transgenic mice (cTnI/R193H/ND) showed that ventricular relaxation is enhanced in the cTnI/R193H transgenic mice. In this study, another double transgenic mouse model, (cTnI/R193H/ND/KO), provides an avenue to investigate its rescuing effects on RCMlinked mutations in the cTnI /R193H/KO mouse. Use of molecular biological techniques, transgenic animal developments and murine echocardiography in this study has culminated into a greater understanding of RCM and diastolic dysfunction.
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Date Issued: 2014
PURL: http://purl.flvc.org/fau/fd/FA00004196, http://purl.flvc.org/fau/fd/FA00004196
Subject Headings: Biochemical markers -- Diagnostic use, Cardiovascular system -- Pathophysiology, Coronary heart disease -- Molecular diagnosis, Mice as laboratory animals, Molecular biology
Format: Document (PDF)

Title: UP-regulation of inflammatory cytokines in the lacrimal glands of a predisposed mouse model of Sjèogren's syndrome (SS): the influence of sex hormones and a newly proposed mechanism for SS.
Creator: Czerwinski, Stefanie P.C., Charles E. Schmidt College of Medicine, Department of Biomedical Science
Abstract/Description: Sjèogren's Syndrome (SS) is a chronic, inflammatory autoimmune disease affecting mostly the exocrine cells of lacrimal and salivary glands, leading to diminished secretory function and resulting in keratoconjunctivitis sicca (dry eye disease) and/or stomatitis sicca (dry mouth disease). Despite several decades of studies focusing on autoimmune diseases and dry eye diseases, the exact etiology and mechanisms of SS remain unknown. Besides the fact that SS is often unreported, unrecognized and...
Show moreSjèogren's Syndrome (SS) is a chronic, inflammatory autoimmune disease affecting mostly the exocrine cells of lacrimal and salivary glands, leading to diminished secretory function and resulting in keratoconjunctivitis sicca (dry eye disease) and/or stomatitis sicca (dry mouth disease). Despite several decades of studies focusing on autoimmune diseases and dry eye diseases, the exact etiology and mechanisms of SS remain unknown. Besides the fact that SS is often unreported, unrecognized and untreated, today's therapies rely exclusively on treating the symptoms after disease progression; there exists neither prevention therapy nor cure for SS. In addition, SS has been diagnosed predominantly in post-menopausal women with the female to male ratio reaching 9:1, suggesting a role of ovarian sex hormones in the pathogenesis of SS. However, not all postmenopausal women develop SS, indicating the contribution of other factors such as a genetic background to the onset of SS. In the present study, ovariectomized (OVX) NOD.B10.H2b mice provide a model of menopause with a genetic predisposition to SS, as compared to non-predisposed C57BL/10 mice. Both strands of mice were either sham operated, OVX, OVX and treated with 17(Sb (Bestradiol (E2), or OVX and treated with dihydrotestosterone (DHT). Lacrimal glands were collected 3, 7, 21, and 30 days after surgery and processed for RNA analysis by rt-qPCR and protein assays by ELISA to evaluate cytokine expression and concentrations of IL- 1\U+fffd\, TNF-a, IFN-(Sd(B, IL-10, and IL-4 on a timeline. Overall, our results showed a significant increase in IL-1\U+fffd\ TNF-a, IL-10, and IL-4 expression and levels in the lacrimal glands of OVX NOD.B10.H2b mice as compared to sham operated animals, and treatment with E2 or DHT at time of OVX prevented the increase in cytokine expression and levels.
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Date Issued: 2013
PURL: http://purl.flvc.org/FAU/3360770
Subject Headings: Cytokines, Mice as laboratory animals, Dry eye syndromes, Immunological aspects, Sjèogren's syndrome, Immunological aspects, Medical genetics, Molecular immunology
Format: Document (PDF)

Title: Investigating the Role of CHI3L1 in Promoting Tumor Growth and Metastasis Using Mammary Tumor Models.
Creator: Libreros, Stephania, Iragavarapu-Charyulu, Vijaya, Florida Atlantic University, Charles E. Schmidt College of Medicine, Department of Biomedical Science
Abstract/Description: Metastasis is the primary cause of mortality in women with breast cancer. Recently, elevated serum levels of a glycoprotein known as chitinase-3 likeprotein- 1 (CHI3L1) has been correlated with poor prognosis and shorter survival of patients with cancer and inflammatory diseases. The biological and physiological functions of CHI3L1 in tumor progression have not yet been elucidated. In this document, we describe the role of CHI3L1 in tumor growth and metastasis and its relationship with...
Show moreMetastasis is the primary cause of mortality in women with breast cancer. Recently, elevated serum levels of a glycoprotein known as chitinase-3 likeprotein- 1 (CHI3L1) has been correlated with poor prognosis and shorter survival of patients with cancer and inflammatory diseases. The biological and physiological functions of CHI3L1 in tumor progression have not yet been elucidated. In this document, we describe the role of CHI3L1 in tumor growth and metastasis and its relationship with inflammation. Using well-established models of breast cancer, we show that CHI3L1 is increased in the serum of tumor bearing mice. We found that CHI3L1 levels are increased at both the “pre-metastatic” and “metastatic stage” and that tumor cells, splenic, alveolar and interstitial macrophages; and myeloid derived population produce CHI3L1. Furthermore, we demonstrated that CHI3L1 has an inhibitory role on the expression of interferon-gamma (IFN γ) by T cells, while enhancing the production of pro-inflammatory mediators by macrophages such as Cchemokine ligand 2 (CCL2/MCP-1), Chemokine CX motif ligand 2 (CXCL2/IL-8) and matrix metalloproteinase-9 (MMP-9), all of which promote tumor growth and metastasis. We demonstrated that in vivo treatment of tumor-bearing mice with chitin microparticles, a TH1 adjuvant and a substrate for CHI3L1, promoted immune effector functions with increased production of IFN-γ but decreased CCL2/MCP-1, CXCL2/IL-8 and MMP-9 expression by splenic and pulmonary macrophages. Significantly, in vivo administration of chitin microparticles decreased tumor growth and pulmonary metastasis in mammary tumor bearing mice. These results suggest that CHI3L1 may play a role in tumor progression. Inflammation plays a pivotal role during tumor progression and metastasis by promoting the production of pro-inflammatory molecules such as CHI3L1. However, little is known about how CHI3L1 expression can affect secondary sites to enhance metastasis. In these studies, we demonstrated that CHI3L1 alters the cellular composition and inflammatory mediators that aid in the establishment of a metastatic niche for the support of infiltrating tumor cells leading to accelerated tumor progression. Since previous studies showed that CHI3L1 modulates inflammation, we determined the role of CHI3L1 in the context of pre-existing inflammation and metastasis. We found that CHI3L1 deficient mice with preexisting inflammation had decreased pro-inflammatory mediators, and significant reduction in tumor volume and metastasis compared to wild type controls. Preexisting inflammation and CHI3L1 may be driving the establishment of a premetastatic milieu in the lungs and aiding in the establishment of metastasis. Understanding the role of CHI3L1 in inflammation during tumor progression could result in the design of targeted therapies for breast cancer patients.
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Date Issued: 2015
PURL: http://purl.flvc.org/fau/fd/FA00004517, http://purl.flvc.org/fau/fd/FA00004517
Subject Headings: Biopharmaceutics, Breast -- Cancer -- Etiology, Breast -- Cancer -- Molecular aspects, Cell differentiation, Chitinase, Glycoproteins -- Metabolism, Inflammation, Mice as laboratory animals
Format: Document (PDF)

Title: Effects of target neuron loss on olfactory sensory neurons in adult mice.
Creator: Ardiles, Yona., Florida Atlantic University, Guthrie, Kathleen M.
Abstract/Description: Olfactory sensory neurons (OSN) expressing the same odor receptor (OR) project their axons to topographically fixed glomeruli in the olfactory bulb (OB). This topographic map results from axon guidance mechanisms determined by ORs, glia and molecular guidance cues. The present study examined the organization of mature OSNs expressing the P2 OR in adult mice after ablation of bulb neurons with N-methyl-D-aspartate (NMDA). Rapid neuronal degeneration was followed by progressive laminar...
Show moreOlfactory sensory neurons (OSN) expressing the same odor receptor (OR) project their axons to topographically fixed glomeruli in the olfactory bulb (OB). This topographic map results from axon guidance mechanisms determined by ORs, glia and molecular guidance cues. The present study examined the organization of mature OSNs expressing the P2 OR in adult mice after ablation of bulb neurons with N-methyl-D-aspartate (NMDA). Rapid neuronal degeneration was followed by progressive laminar disorganization of the OB and glomerular shrinkage. P2 axon targeting and convergence was maintained within degenerating glomeruli for up to 2 weeks. After that time, fewer P2 axons were observed in the lesioned OB with fewer P2 neurons in the olfactory epithelium (OE). By 3 weeks, the mature OSN population was reduced and the immature population was increased. These results suggest that bulbar synaptic contacts do not maintain sensory axon convergence in the adult, but regulate neuronal survival in the OE.
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Date Issued: 2004
PURL: http://purl.flvc.org/fcla/dt/13166
Subject Headings: Sensory neurons--Testing, Senses and sensation, Neurotransmitter receptors, Mice as laboratory animals, Smell--Research--Methodology
Format: Document (PDF)

Mice as laboratory animals (21)	+ -
Cellular control mechanisms (5)	+ -
Neurotransmitter receptors (5)	+ -
Cellular signal transduction (4)	+ -
Cardiovascular system (3)	+ -

Diseases (3)	+ -
Pathophysiology (3)	+ -
Biochemical markers (2)	+ -
Biochemical markers -- Diagnostic use (2)	+ -
Biopharmaceutics (2)	+ -
Cardiovascular system -- Pathophysiology (2)	+ -
Cell differentiation (2)	+ -
Coronary heart disease -- Molecular diagnosis (2)	+ -
Diagnostic use (2)	+ -
Genetic aspects (2)	+ -
Hippocampus (Brain) (2)	+ -
Immunological aspects (2)	+ -
Mice as laboratory animals. (2)	+ -
Molecular biology (2)	+ -
Molecular diagnosis (2)	+ -
Sjèogren's syndrome (2)	+ -
Animal models (1)	+ -
Animal navigation (1)	+ -
Association of ideas (1)	+ -
Biological transport (1)	+ -
Biological transport -- Research (1)	+ -
Breast -- Cancer -- Etiology (1)	+ -
Breast -- Cancer -- Molecular aspects (1)	+ -
Carbohydrates -- Therapeutic use (1)	+ -
Cellular control mechanisms. (1)	+ -

Florida Atlantic University (12)	+ -
Charles E. Schmidt College of Medicine (11)	+ -
Charles E. Schmidt College of Science (11)	+ -
Department of Biomedical Science (8)	+ -
Department of Psychology (7)	+ -

Stackman, Robert W. (5)	+ -
Huang, Xupei (3)	+ -
Department of Biological Sciences (2)	+ -
Guthrie, Kathleen M. (2)	+ -
Ardiles, Yona. (1)	+ -
Asgeirsdottir, Herborg Nanna (1)	+ -
Berger, Rachel A. (1)	+ -
Center for Complex Systems and Brain Sciences (1)	+ -
Cinalli, David A. (1)	+ -
Cohen, Sarah J. (1)	+ -
Cudic, Predrag (1)	+ -
Czerwinski, Stefanie P.C. (1)	+ -
Department of Chemistry and Biochemistry (1)	+ -
Department of Integrated Medical Science (1)	+ -
Du, Jianfeng. (1)	+ -
Getfield, Cecile A. (1)	+ -
Gobara, Nariman. (1)	+ -
Iragavarapu-Charyulu, Vijaya (1)	+ -
Jean-Charles, Pierre-Yves (1)	+ -
Jia, Yuanyuan (1)	+ -
Lasiter, Phillip S. (1)	+ -
Lepore, Salvatore D. (1)	+ -
Li, Yuejin (1)	+ -
Libreros, Stephania (1)	+ -
Liu, Huan (1)	+ -

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