Current Search: Pathology (x)
Pages
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Title
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Morbillivirus infection in free ranging Atlantic bottlenose dolphins (Tursiops truncatus) from the Southeastern United States: Seroepidemiologic and pathologic evidence of subclinical infection.
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Creator
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Bossart, Gregory D., Reif, John S., Schaefer, Adam M., Goldstein, Juli D., Fair, Patricia A., Saliki, Jeremiah T.
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Date Issued
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2009
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PURL
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http://purl.flvc.org/FCLA/DT/3174065
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Subject Headings
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Bottlenose dolphin, Serology, Veterinary serology, Forensic serology, Pathology, Veterinary clinical pathology, Forensic pathology
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Format
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Document (PDF)
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Title
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Cytopathology ofcutaneous viral papillomatosis in the killer whale Orcinus orca.
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Creator
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Bossart, Gregory D., Decker, Susan J., Ewing, Ruth Y., Harbor Branch Oceanographic Institute
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Date Issued
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2002
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PURL
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http://purl.flvc.org/fau/fd/FA00007318
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Subject Headings
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Killer whale, Orcinus orca, Papillomaviruses, Pathology, Cellular, Papilloma
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Format
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Document (PDF)
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Title
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Pathological findings in a rare mass stranding of Melon-Headed Whales (Peponocephala electra) in Florida.
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Creator
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Bossart, Gregory D., Hansen, Larry J., Goldstein, Juli D., Kilpatrick, David, Bechdel, Sarah E., Howells, Elisabeth M., Kroell, Kenny, de Sieyes, Malcolm, Stolen, Megan K., Durden, Wendy N., Reif, John S., Defran, R. H., McCulloch, Stephen D., Harbor Branch Oceanographic Institute
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Date Issued
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2007
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PURL
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http://purl.flvc.org/FCLA/DT/1925747
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Subject Headings
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Whales --Stranding, Peponocephala electra, Whales--Florida, Pathology
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Format
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Document (PDF)
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Title
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Sulindac enhances the killing of cancer cells exposed to oxidative stress.
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Creator
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Kreymerman, Alexander, Ayyanathan, Kasirajan, Kesaraju, Shailaja, Dawson-Scully, Ken, Weissbach, Herbert, Graduate College
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Date Issued
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2011-04-08
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PURL
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http://purl.flvc.org/fcla/dt/3164545
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Subject Headings
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Nonsteroidal anti-inflammatory agents, Oxidative stress, Mitochondrial pathology
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Format
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Document (PDF)
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Title
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A comparison of parents' perceptions and speech/language pathologists' perceptions of selected social competency needs of speech/language impaired preschool children in Broward County, Florida.
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Creator
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Thornton, Robin Elizabeth, Florida Atlantic University, College of Education, Department of Educational Leadership and Research Methodology
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Abstract/Description
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The problem investigated in this study was to determine the significance of agreement between the perceptions of parents and speech/language pathologists toward selected social competency needs of speech/language impaired children in the personal, family, and school contexts. Preschool children exhibiting speech/language impairments are more likely to demonstrate a lack of social competency development than children with normal speech and language development. As children with speech/language...
Show moreThe problem investigated in this study was to determine the significance of agreement between the perceptions of parents and speech/language pathologists toward selected social competency needs of speech/language impaired children in the personal, family, and school contexts. Preschool children exhibiting speech/language impairments are more likely to demonstrate a lack of social competency development than children with normal speech and language development. As children with speech/language impairments receive intervention in the absence of parental support, the intervention results may be minimized. If perceptions of parents and speech/language pathologists differ significantly, parents may not reinforce carryover activities in the home, thereby reducing therapy gains. The evaluation instrument utilized in this study was a 31-item survey developed by Tunstall (1993) at the College of Education, University of South Carolina. The survey was created using a 4-point Likert-type scale. Reliability was obtained by Tunstall in 1993 and revealed good internal reliabilities. In 1996, this study included the entire sample of 100 respondents to obtain a high reliability coefficient alpha of .9189. The sample included 70 parents of preschool speech/language impaired students and 30 speech/language pathologists of the Broward County Public School System in Florida, during the fall of 1996. Surveys were distributed to parents of children exhibiting a speech/language impairment, who attended a preschool speech/language, developmental, and hearing screening provided by the Broward County Public Schools. During an annual Speech/Language Policies and Procedures meeting in August of 1996, surveys were distributed to 30 speech/language pathologists providing treatment for preschool children. Three hypotheses were developed to determine if there was a significant difference in the perceptions of the two groups surveyed. Analyses of variance were utilized to test the statistical significance of the group (parents and speech/language pathologists) differences for each factor (personal, family, and school). Descriptive statistics were included to describe the demographic characteristics of the respondents from the survey instrument. A Boneferonni type adjustment was made to the nominal alpha of .05, such that all the hypotheses were tested at the .017 level. Based on the findings of this study, there was a significant difference between the perceptions of the parents and speech/language pathologists toward selected social competency needs of preschool children with speech/language impairments within the family context, F(1,98) = 7.44, p =.0078. The results revealed the two groups were not in agreement as to the importance of family factors and the contributions of those factors to a preschool child's social competency. The mean score of the parents' responses was significantly higher than that of the speech/language pathologists.
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Date Issued
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1997
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PURL
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http://purl.flvc.org/fcla/dt/12544
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Subject Headings
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Health Sciences, Speech Pathology, Education, Early Childhood, Education, Special
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Format
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Document (PDF)
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Title
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PHOTORECEPTOR DEGENERATION AND ABNORMAL RETINAL VASCULOGENESIS.
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Creator
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Nguyen, Matthew, Shen, Wen, Florida Atlantic University, Department of Biomedical Science, Charles E. Schmidt College of Medicine
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Abstract/Description
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Abnormal vasculature in the retina, specifically tortuous blood vessels, are common to many of the most prevalent retinal degenerative diseases currently affecting millions across the world. The mechanisms of their formation and development in the context of retinal degenerative disease, however, are still poorly understood. The rd1 and rd10 mice are relatively well-studied animal models of retinal degenerative disease, however, there lacks a systematic characterization of vascular changes co...
Show moreAbnormal vasculature in the retina, specifically tortuous blood vessels, are common to many of the most prevalent retinal degenerative diseases currently affecting millions across the world. The mechanisms of their formation and development in the context of retinal degenerative disease, however, are still poorly understood. The rd1 and rd10 mice are relatively well-studied animal models of retinal degenerative disease, however, there lacks a systematic characterization of vascular changes co-related to photoreceptor degeneration in the rd1 and rd10 retina. Here, we utilize advancements in confocal microscopy, immunohistochemistry, and image analysis software in order to systematically characterize vascular changes before and after retinal development in the rd1 and rd10 mice. We show that there are plexus specific changes in the retinal vasculature that parallel photoreceptor degeneration. Such information will be of particular use to future studies investigating the role of vascular changes in retinal degenerative disease therapies.
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Date Issued
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2021
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PURL
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http://purl.flvc.org/fau/fd/FA00013818
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Subject Headings
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Retinal Degeneration, Retinal Vessels--pathology, Retina—Diseases, Photoreceptors
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Format
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Document (PDF)
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Title
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Tissue Protection and Cell Death Pathways in Myocardial Ischemia.
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Creator
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Rickaway, Zach T., Prentice, Howard, Florida Atlantic University
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Abstract/Description
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The excess generation of Reactive oxygen species (ROS) can damage cell components and disrupt cellular functions. Methionine in proteins is easily oxidized by ROS and converted to methionine sulfoxide. The enzyme peptide Methionine Sulfoxide Reductase reduces methionine sulfoxide back to methionine. We report here that MsrA over expression in rat cardiac myocytes prevents damage from ROS and increases cell viability after hypoxic/reoxygenation events. The nonsteroidal anti-inflamatory drug ...
Show moreThe excess generation of Reactive oxygen species (ROS) can damage cell components and disrupt cellular functions. Methionine in proteins is easily oxidized by ROS and converted to methionine sulfoxide. The enzyme peptide Methionine Sulfoxide Reductase reduces methionine sulfoxide back to methionine. We report here that MsrA over expression in rat cardiac myocytes prevents damage from ROS and increases cell viability after hypoxic/reoxygenation events. The nonsteroidal anti-inflamatory drug (NSAID) sulindac contains a methyl sulfoxide moiety that can scavenge ROS. Sulindac can be reduced by MsrA and contribute as an antioxidant in the cell. Our results demonstrate that 1 OOuM sulindac can reduce cell death in rat cardiac myocytes during hypoxia/reoxygenation, and ischemia/reperfusion in Langendorf[ perfusions. The BNIP proteins are pro-apoptotic members of the Bcl-2 family of apoptosis regulating proteins. Hypoxia/acidosis stabilizes BNIP-3 and increases its association with the mitochondria, causing the release of cytochrome C and cell death. We report the retrograde perfusion Langendorffmodel is inconclusive in mouse hearts.
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Date Issued
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2006
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PURL
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http://purl.flvc.org/fau/fd/FA00000820
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Subject Headings
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Mitochondrial pathology, Heart--Pathophysiology, Apoptosis, Cell differentiation
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Format
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Document (PDF)
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Title
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CHARACTERIZATION OF DIFFERENTIATED HUMAN NEUROBLASTOMA SH-SY5Y CELLS IN CULTURE.
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Creator
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Condikey, Siri, Prentice, Howard, Florida Atlantic University, Department of Biomedical Science, Charles E. Schmidt College of Medicine
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Abstract/Description
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Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases affecting an estimated 20 million worldwide. The primary pathology of AD is the progressive loss of basal forebrain cholinergic neurons, which is responsible for the cognitive decline experienced by AD patients. The mechanisms underlying this selective vulnerability have not been fully elucidated. Furthermore, oxidative stress is a key factor behind the pathology of AD leading to this neuronal loss. The current...
Show moreAlzheimer’s disease (AD) is one of the most common neurodegenerative diseases affecting an estimated 20 million worldwide. The primary pathology of AD is the progressive loss of basal forebrain cholinergic neurons, which is responsible for the cognitive decline experienced by AD patients. The mechanisms underlying this selective vulnerability have not been fully elucidated. Furthermore, oxidative stress is a key factor behind the pathology of AD leading to this neuronal loss. The current literature suggests that there are limited in-vitro models available to accurately simulate the hallmark symptoms of Alzheimer's disease (AD). The SH-SY5Y cell line has been used extensively to study neuronal stress responses but the undifferentiated cell type has been predominantly used. Undifferentiated SH-SY5Y versus differentiated SH-SY5Y have been shown to have different interaction, expression and localization with AD hallmark, amyloid-b -42. This project sought to use differentiated cholinergic cells from the line SH-SY5Y to further isolate and elucidate, in-vitro, the mechanisms behind the oxidative stress response, a key stressor in the pathology of AD. Building upon previous studies, a protocol to differentiate SH-SY5Y cells with retinoic acid (RA) and neurotrophin (BDNF) to mature neurons of the cholinergic phenotype was optimized and implemented. The results showed successful differentiation into the cholinergic phenotype as evidenced via immunofluorescence imaging of choline acetyl transferase (ChAT) expression and mature neurite morphology. To simulate oxidative stress, we exposed both undifferentiated and differentiated SH-SY5Y cells to hypoxic conditions. Results indicated a stress response to mild hypoxic conditions with higher sensitivity in cholinergic differentiated SH-SY5Y. Understanding these hallmark mechanisms behind oxidative stress is crucial to developing mechanism-based therapeutics for AD.
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Date Issued
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2023
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PURL
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http://purl.flvc.org/fau/fd/FA00014347
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Subject Headings
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Alzheimer Disease, Cholinergic Neurons, Alzheimer Disease--pathology
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Format
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Document (PDF)
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Title
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Developmental delays in methionine sulfoxide reductase mutants in Drosophila Melanogaster.
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Creator
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Hausman, William, Binninger, David, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biological Sciences
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Abstract/Description
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Aging is a biological process that has many detrimental effects due to the accumulation of oxidative damage to key biomolecules due to the action of free radicals. Methionine sulfoxide reductase (Msr) functions to repair oxidative damage to methionine residues. Msr comes in two forms, MsrA and MsrB, each form has been shown to reduce a specific enantiomer of bound and free oxidized methionine. Effects of Msr have yet to be studied in the major developmental stages of Drosophila melanogaster...
Show moreAging is a biological process that has many detrimental effects due to the accumulation of oxidative damage to key biomolecules due to the action of free radicals. Methionine sulfoxide reductase (Msr) functions to repair oxidative damage to methionine residues. Msr comes in two forms, MsrA and MsrB, each form has been shown to reduce a specific enantiomer of bound and free oxidized methionine. Effects of Msr have yet to be studied in the major developmental stages of Drosophila melanogaster despite the enzymes elevated expression during these stages. A developmental timeline was determined for MsrA mutant, MsrB mutant, and double null mutants against a wild type control. Results show that the Msr double mutant is delayed approximately 20 hours in the early/mid third instar stage while each of the single mutants showed no significant difference to the wild type. Data suggests that the reasoning of this phenomenon is due to an issue gaining mass.
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Date Issued
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2014
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PURL
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http://purl.flvc.org/fau/fd/FA00004200, http://purl.flvc.org/fau/fd/FA00004200
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Subject Headings
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Aging -- Molecular aspects, Cellular signal transduction, Drosophila melanogaster -- Genetics, Mitochondrial pathology, Mutation (Biology), Oxidative stress
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Format
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Document (PDF)
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Title
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Disordered caffeination: a biocultural analysis of adverse reactions to caffeine.
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Creator
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Porter, Carlyn M., Cameron, Mary, Florida Atlantic University, Dorothy F. Schmidt College of Arts and Letters, Department of Anthropology
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Abstract/Description
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While coffee culture has long since been positively associated with intellectual and working life, the health and safety of its primary stimulant, caffeine, has recently fallen under scrutiny by the FDA. This medical anthropology thesis provides a biocultural synthesis of caffeine culture, health effects, and biological variation in adverse effects related to pharmacodynamics and pharmacokinetics. Supporting evidence for variation in responses to caffeine was found through surveying 100...
Show moreWhile coffee culture has long since been positively associated with intellectual and working life, the health and safety of its primary stimulant, caffeine, has recently fallen under scrutiny by the FDA. This medical anthropology thesis provides a biocultural synthesis of caffeine culture, health effects, and biological variation in adverse effects related to pharmacodynamics and pharmacokinetics. Supporting evidence for variation in responses to caffeine was found through surveying 100 participants, investigating caffeine consumption levels, perceptions and health beliefs, adverse effects experienced, and medical encounters. Increased rates of adverse effects were found for students, pharmaceutical and over-the-counter drug users, and for participants reporting negative or ambivalent perceptions of caffeine, intolerance, or sensitivity to caffeine. Variation in rates of adverse effects suggests biocultural interactions account not only for patterns in pharmacological data, but are also clinically significant in constructing risk of caffeine intoxication.
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Date Issued
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2014
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PURL
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http://purl.flvc.org/fau/fd/FA00004319, http://purl.flvc.org/fau/fd/FA00004319
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Subject Headings
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Adenosine triphosphate -- Physiological effect, Caffeine -- Health aspects, Caffeine -- Physiological effect, Medical anthropology, Physiology, Pathological
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Format
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Document (PDF)
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Title
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aB- crystallin/sHSP is required for mitochondrial function in human ocular tissue.
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Creator
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McGreal, Rebecca., Charles E. Schmidt College of Science, Department of Biological Sciences
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Abstract/Description
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The central premise of this dissertation is that the small heat shock protein (sHSP), (Sa(BB-crystallin is essential for lens and retinal pigmented epithelial (RPE) cell function and oxidative stress defense. To date, the mechanism by which it confers protection is not known. We hypothesize that these functions could occur through its ability to protect mitochondrial function in lens and RPE cells. To test this hypothesis, we examined the expression of (Sa(BB-crystallin/sHSP in lens and RPE...
Show moreThe central premise of this dissertation is that the small heat shock protein (sHSP), (Sa(BB-crystallin is essential for lens and retinal pigmented epithelial (RPE) cell function and oxidative stress defense. To date, the mechanism by which it confers protection is not known. We hypothesize that these functions could occur through its ability to protect mitochondrial function in lens and RPE cells. To test this hypothesis, we examined the expression of (Sa(BB-crystallin/sHSP in lens and RPE cells, we observed its localization in the cells, we examined translocation to the mitochondria in these cells upon oxidative stress treatment, we determined its ability to form complexes with and protect cytochrome c (cyt c) against damage, and we observed its ability to preserve mitochondrial function under oxidative stress conditions in lens and RPE cells. In addition to these studies, we examined the effect of mutations of (Sa(BB-crystallin/sHSP on its cellular localization and translocation patterns under oxidative stress, its in vivo and in vitro chaperone activity, and its ability to protect cyt c against oxidation. Our data demonstrated that (Sa(BB-crystallin/sHSP is expressed at high levels in the mitochondria of lens and RPE cells and specifically translocates to the mitochondria under oxidative stress conditions. We demonstrate that (Sa(BB-crystallin/sHSP complexes with cyt c and protects it against oxidative inactivation. Finally, we demonstrate that (Sa(BB-crystallin/sHSP directly protects mitochondria against oxidative inactivation in lens and RPE cells. Since oxidative stress is a key component of lens cataract formation and age-related macular degeneration (AMD), these data provide a new paradigm for understanding the etiology of these diseases.
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Date Issued
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2012
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PURL
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http://purl.flvc.org/FAU/3342242
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Subject Headings
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Mitochondrial pathology, Chemical mutagenesis, Oxidative stress, Prevention, Cellular signal transduction, Eye, Diseases, Etiology, Molecular chaperones
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Format
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Document (PDF)
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Title
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Morbid jealousy from an evolutionary psychological perspective.
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Creator
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Easton, Judith A., Florida Atlantic University, Shackelford, Todd K.
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Abstract/Description
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Individuals diagnosed with morbid jealousy have hypersensitive jealousy mechanisms that cause them to have irrational thoughts about their partners and to exhibit extreme behaviors. Because morbid jealousy is defined as a malfunction of evolved jealousy mechanisms such that they produce increased chances of perceiving partner infidelity, research guided by an evolutionary psychological perspective can add insight to the understanding of the disorder. The present research tested eleven...
Show moreIndividuals diagnosed with morbid jealousy have hypersensitive jealousy mechanisms that cause them to have irrational thoughts about their partners and to exhibit extreme behaviors. Because morbid jealousy is defined as a malfunction of evolved jealousy mechanisms such that they produce increased chances of perceiving partner infidelity, research guided by an evolutionary psychological perspective can add insight to the understanding of the disorder. The present research tested eleven evolutionarily relevant hypotheses about jealousy, in an attempt to improve the understanding of the etiology of morbid jealousy. To investigate a large enough sample, I created a database of all the morbid jealousy case histories published in English. Chi-square analyses were used to test all eleven hypotheses. Results for seven hypotheses were significant. By illustrating that there may be an adaptive purpose for some of the associated behaviors and for jealousy, the results of this study can aid clinicians in treating morbid jealousy.
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Date Issued
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2006
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PURL
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http://purl.flvc.org/fcla/dt/13376
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Subject Headings
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Jealousy--Case studies, Psychology, Pathological, Rational emotive behavior therapy--Case studies
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Format
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Document (PDF)
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Title
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Peroxiredoxin 3 and Methionine sulfoxide reductase A are Essential for Lens Cell Viability by Preserving Lens Cell Mitochondrial Function through Repair of Cytochrome c.
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Creator
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Lee, Wanda, Florida Atlantic University, Kantorow, Marc, Charles E. Schmidt College of Science, Department of Biomedical Science
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Abstract/Description
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The central premise of this dissertation is that mitochondrial antioxidant enzymes are essential to lens cell viability by preserving lens cell mitochondria and protecting and/or repairing lens cell proteins, and two mitochondrial-specific antioxidant enzymes, Peroxiredoxin 3 (PRDX3) and Methionine sulfoxide reductase A (MsrA), are explored. In this dissertation, we will examine the expression ofPRDX3 in the human lens, its colocalization to the lens cell mitochondria, its ability to be...
Show moreThe central premise of this dissertation is that mitochondrial antioxidant enzymes are essential to lens cell viability by preserving lens cell mitochondria and protecting and/or repairing lens cell proteins, and two mitochondrial-specific antioxidant enzymes, Peroxiredoxin 3 (PRDX3) and Methionine sulfoxide reductase A (MsrA), are explored. In this dissertation, we will examine the expression ofPRDX3 in the human lens, its colocalization to the lens cell mitochondria, its ability to be induced by H20 2-oxidative stress, and speculate how PRDX3 function/sf could affect the lens. We will also examine the reduced levels of MsrA by targeted gene silencing and its effect on reactive oxygen species production and mitochondrial membrane potential in human lens cells to determine its role in mitochondrial function in the lens. Lastly, we will examine the ability of MsrA to repair and restore function to a critical mitochondrial protein, Cytochrome c. The collective evidence strongly indicates that the loss of mitochondrial-specific enzymes, such as PRDX3 and MsrA, are responsible for increased reactive oxygen species levels, decreased mitochondrial membrane potential, protein aggregation and lens cell death, and further indicates that mitochondrial repair, protective, and reducing systems play key roles in the progression of age-related cataract and other agerelated diseases.
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Date Issued
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2008
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PURL
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http://purl.flvc.org/fau/fd/FA00000868
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Subject Headings
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Genetic regulation, Proteins--Chemical modification, Cellular signal transduction, Eye--Physiology, Mitochondrial pathology
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Format
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Document (PDF)
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Title
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Methionine sulfoxide reductase (Msr) deficiency leads to a reduction of dopamine levels in Drosophila.
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Creator
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Hernandez, Caesar, Binninger, David, Weissbach, Herbert, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biological Sciences
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Abstract/Description
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Biological homeostasis relies on protective mechanisms that respond to cellular oxidation caused primarily by free radical reactions. Methionine sulfoxide reductases (Msr) are a class of enzymes that reverse oxidative damage to methionine in proteins. The focus of this study is on the relationship between Msr and dopamine levels in Drosophila. Dopaminergic neurons in Drosophila have comparable roles to those found in humans. A deficit in dopamine leads to the onset of many neurological...
Show moreBiological homeostasis relies on protective mechanisms that respond to cellular oxidation caused primarily by free radical reactions. Methionine sulfoxide reductases (Msr) are a class of enzymes that reverse oxidative damage to methionine in proteins. The focus of this study is on the relationship between Msr and dopamine levels in Drosophila. Dopaminergic neurons in Drosophila have comparable roles to those found in humans. A deficit in dopamine leads to the onset of many neurological disorders including the loss of fine motor control—a neurodegenerative condition characteristic of Parkinson’s disease (PD). We found that dopamine levels in the heads of MsrAΔ/ΔBΔ/Δ mutants are significantly reduced in comparison to MsrA ⁺/⁺ B⁺/⁺ heads. In addition, wefound protein and expression levels are markedly reduced in an Msr-deficient system. Our findings suggest an important role for the Msr system in the CNS.
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Date Issued
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2014
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PURL
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http://purl.flvc.org/fau/fd/FA00004202, http://purl.flvc.org/fau/fd/FA00004202
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Subject Headings
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Cellular signal transduction, Dopamine -- Receptors, Drosophila melanogaster -- Genetics, Mitochondrial pathology, Proteins -- Chemical modification
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Format
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Document (PDF)
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Title
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THE LIFE CYCLE OF THE GALL MIDGE CTENODACTYLOMYIA WATSONI ON ITS HOST PLANTS COCCOLOBA UVIFERA AND COCCOLOBA DIVERSIFOLIA.
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Creator
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Li, Arisa, Frazier, Evelyn, Florida Atlantic University, Department of Biological Sciences, Charles E. Schmidt College of Science
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Abstract/Description
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This thesis explores interactions between the native Florida plant Coccoloba uvifera (sea grape) and the gall-inducing midge Ctenodactylomyia watsoni. Galls are tumor-like structure that form on the surface of the leaf. Galled leaves are common on sea grape foliage, with the oviposition of C. watsoni potentially contributing to or being associated with early leaf senescence. Despite its significance, the life cycle of this galling midge remains a largely unexplored topic in the literature....
Show moreThis thesis explores interactions between the native Florida plant Coccoloba uvifera (sea grape) and the gall-inducing midge Ctenodactylomyia watsoni. Galls are tumor-like structure that form on the surface of the leaf. Galled leaves are common on sea grape foliage, with the oviposition of C. watsoni potentially contributing to or being associated with early leaf senescence. Despite its significance, the life cycle of this galling midge remains a largely unexplored topic in the literature. This research also investigates the potential oviposition and gall formation on another Florida coastal plant, Coccoloba diversifolia, commonly known as pigeon plum. Given the taxonomic proximity and potential for hybridization of the two plant congeners, it was suspected that pigeon plum may serve as a potential host for C. watsoni. This thesis aimed to expand understanding of the life cycle and population dynamics of C. watsoni. The study was successful in providing insight into the population composition, periodicity, and trait differentiation between both its host plants of the galling midge C. watsoni.
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Date Issued
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2024
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PURL
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http://purl.flvc.org/fau/fd/FA00014444
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Subject Headings
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Gall midges, Gall midges--Host plants--North America, Plant pathology, Botany
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Format
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Document (PDF)
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Title
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Hypoxia-regulated glial cell-specific gene therapy to treat retinal neovascularization.
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Creator
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Biswal, Manas Ranjan., Charles E. Schmidt College of Science, Center for Complex Systems and Brain Sciences
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Abstract/Description
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Diabetic retinopathy is an ischemic retinal neovascular disease causing vision loss among adults. The studies presented involve the design and testing of a gene therapy vector to inhibit retinal revascularization, similar to that found in diabetic retinopathy. Gene therapy has proven to be an effective method to introduce therapeutic proteins to treat retinal diseases. Targeting a specific cell type and expression of therapeutic proteins according to the tissue microenvironment should have an...
Show moreDiabetic retinopathy is an ischemic retinal neovascular disease causing vision loss among adults. The studies presented involve the design and testing of a gene therapy vector to inhibit retinal revascularization, similar to that found in diabetic retinopathy. Gene therapy has proven to be an effective method to introduce therapeutic proteins to treat retinal diseases. Targeting a specific cell type and expression of therapeutic proteins according to the tissue microenvironment should have an advantage over traditional gene therapy by avoiding unwanted transgene expression. Hypoxia plays a significant role in the pathophysiology of many retinal ischemic diseases. Retinal Mèuller cells provide structural and functional support to retinal neurons, as well as playing a significant role in retinal neovascularization. Targeting Mèuller cells may be an effective strategy to prevent retinal neovascularization under pathological conditions. ... The hypoxia regulated, glial specific vector successfully reduced the abnormal neovascularization in the periphery by 93% and reduced the central vasobliterated area by 90%. A substantial amount of exogenous endostatin was produced in the retinas of P17 OIR mice. A significant increase in human endostatin protein and reduced vascular endothelial growth factor (VEGF) were identified by Western blot and ELISA, respectively. These findings suggest hypoxia-regulated, glial cell-specific scAAV mediated gene expression may be useful to prevent blindness found in devastating retinal diseases involving neovascularization.
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Date Issued
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2012
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PURL
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http://purl.flvc.org/FAU/3359290
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Subject Headings
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Diabetic retinopathy, Research, Methodology, Gene therapy, Retinal degeneration, Treatment, Neovascularization inhibitors, Mitochondrial pathology, Retina, Cytology, Gene mapping
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Format
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Document (PDF)
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Title
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High summer.
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Creator
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Hasler Martinez, Michelle., Dorothy F. Schmidt College of Arts and Letters, Department of English
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Abstract/Description
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High Summer is a manuscript-length compilation of narrative science essays that trace the relationship the narrator has with her father. These essays focus on the ongoing presence of drugs, their historical basis, and their pharmacological effects on the body.
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Date Issued
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2012
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PURL
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http://purl.flvc.org/FAU/3358552
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Subject Headings
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Fathers and daughters, Parent and child, Symbolism in literature, Psychology, Pathological, Substance abuse, Physiological aspects, Narration (Rhetoric), Creative nonfiction
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Format
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Document (PDF)
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Title
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Mitochondrial regulation pathways in the lens: pink1/parkin- and bnip3l-mediated mechanisms.
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Creator
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Aktan, Kerem, Kantorow, Marc, Florida Atlantic University, Charles E. Schmidt College of Medicine, Department of Biomedical Science
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Abstract/Description
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The mitochondrion is the powerhouse of the cell. Therefore, it is critical to the homeostasis of the cell that populations of mitochondria that are damaged or in excess are degraded. The process of targeted elimination of damaged or excess mitochondria by autophagy is called mitophagy. In this report, analysis of the mitophagy regulators PINK1/PARKIN and BNIP3L and their roles are assessed in the lens. PARKIN, an E3 ubiquitin ligase, has been shown to play a role in directing damaged...
Show moreThe mitochondrion is the powerhouse of the cell. Therefore, it is critical to the homeostasis of the cell that populations of mitochondria that are damaged or in excess are degraded. The process of targeted elimination of damaged or excess mitochondria by autophagy is called mitophagy. In this report, analysis of the mitophagy regulators PINK1/PARKIN and BNIP3L and their roles are assessed in the lens. PARKIN, an E3 ubiquitin ligase, has been shown to play a role in directing damaged mitochondria for degradation. While BNIP3L, an outer mitochondrial membrane protein, increases in expression in response to excess mitochondria and organelle degradation during cellular differentiation. We have shown that PARKIN is both induced and translocates from the cytoplasm to the mitochondria in human epithelial lens cells upon oxidative stress exposure. In addition, our findings also show that overexpression of BNIP3L causes premature clearance of mitochondria and other organelles, while loss of BNIP3L results in lack of clearance. Prior to this work, PARKIN mediated mitophagy had not been shown to act as a protective cellular response to oxidative stress in the lens. This project also resulted in the novel finding that BNIP3L-mediated mitophagy mechanisms are required for targeted organelle degradation in the lens.
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Date Issued
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2015
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PURL
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http://purl.flvc.org/fau/fd/FA00004427, http://purl.flvc.org/fau/fd/FA00004427
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Subject Headings
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Cellular signal transduction, Eye -- Diseases -- Etiology, Mitochondrial pathology, Mitophagy, Molecular chaperones, Oxidative stress -- Prevention, Protein folding
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Format
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Document (PDF)
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Title
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Methionine sulfoxide reductase (MSR) modulates lifespan andLocomotion in drosophila melanogaster.
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Creator
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Bruce, Lindsay, Binninger, David, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biological Sciences
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Abstract/Description
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Oxidative stress is considered a major factor in the etiology of age related diseases and the aging process itself. Organisms have developed mechanisms to protect against oxidative damage resulting from increased production of reactive oxygen species during aging. One of the major antioxidant systems is the methionine sulfoxide reductase (Msr) enzyme family. The two major Msr enzymes, MsrA and MsrB, can stereospecifically reduce the S and R epimers, respectively, of methionine sulfoxide in...
Show moreOxidative stress is considered a major factor in the etiology of age related diseases and the aging process itself. Organisms have developed mechanisms to protect against oxidative damage resulting from increased production of reactive oxygen species during aging. One of the major antioxidant systems is the methionine sulfoxide reductase (Msr) enzyme family. The two major Msr enzymes, MsrA and MsrB, can stereospecifically reduce the S and R epimers, respectively, of methionine sulfoxide in proteins back to methionine. This study, using Drosophila melanogaster, decribes the first animal system lacking both MsrA and MsrB. The loss of either MsrA or MsrB had no effect on lifespan in Drosophila, but loss of MsrB results in a slight decrease in locomotor activity from middle age onward. Double mutants lacking both forms of Msr have a significantly decreased lifespan and decreased locomotor activity at all ages examined. The double Msr mutants had no detectable increase in protein oxidation or decrease in mitochondrial function and were not more sensitive to oxidative stress. These results suggested that other cellular antioxidant systems were protecting the flies against oxidative damage and the decreased life span observed in the double knockouts was not due to widespread oxidative damage. However, one cannot exclude limited oxidative damage to a specific locus or cell type. In this regard, it was observed that older animals, lacking both MsrA and MsrB, have significantly reduced levels of dopamine, suggesting there might be oxidative damage to the dopaminergic neurons. Preliminary results also suggest that the ratio of F to G actin is skewed towards G actin in all mutants. The present results could have relevance to the loss of dopaminergic neurons in Parkinson’s disease.
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Date Issued
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2015
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PURL
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http://purl.flvc.org/fau/fd/FA00004431, http://purl.flvc.org/fau/fd/FA00004431
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Subject Headings
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Aging -- Molecular aspects, Cellular signal transduction, Drosophila melanogaster -- Genetics, Mitochondrial pathology, Mutation (Biology), Oxidative stress, Proteins -- Chemical modification
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Format
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Document (PDF)
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Title
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Developmental and Protective Mechanisms of the Ocular Lens.
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Creator
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Chauss, Daniel C., Kantorow, Marc, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biomedical Science
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Abstract/Description
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The vertebrate eye lens functions to focus light onto the retina to produce vision. The lens is composed of an anterior monolayer of cuboidal epithelial cells that overlie a core of organelle free fiber cells. The lens develops and grows throughout life by the successive layering of lens fiber cells via their differentiation from lens epithelial cells. Lens developmental defect and damage to the lens are associated with cataract formation, an opacity of the lens that is a leading cause of...
Show moreThe vertebrate eye lens functions to focus light onto the retina to produce vision. The lens is composed of an anterior monolayer of cuboidal epithelial cells that overlie a core of organelle free fiber cells. The lens develops and grows throughout life by the successive layering of lens fiber cells via their differentiation from lens epithelial cells. Lens developmental defect and damage to the lens are associated with cataract formation, an opacity of the lens that is a leading cause of visual impairment worldwide. The only treatment to date for cataract is by surgery. Elucidating those molecules and mechanisms that regulate the development and lifelong protection of the lens is critical toward the development of future therapies to prevent or treat cataract. To determine those molecules and mechanisms that may be important for these lens requirements we employed high-throughput RNA sequencing of microdissected differentiation statespecific lens cells to identify an extensive range of transcripts encoding proteins expressed by these functionally distinct cell types. Using this data, we identified differentiation state-specific molecules that regulate mitochondrial populations between lens epithelial cells that require the maintenance of a functional population of mitochondria and lens fiber cells that must eliminate their mitochondria for their maturation. In addition, we discovered a novel mechanism for how lens epithelial cells clear apoptotic cell debris that could arise from damage to the lens and found that UVlight likely compromises this system. Moreover, the data herein provide a framework to determine novel lens cell differentiation state-specific mechanisms. Future studies are required to determine the requirements of the identified molecules and mechanisms during lens development, lens defense against damage, and cataract formation.
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Date Issued
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2016
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PURL
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http://purl.flvc.org/fau/fd/FA00004577
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Subject Headings
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Eye--Diseases--Etiology., Cell differentiation., Cellular signal transduction., Protein folding., Mitochondrial pathology., Cellular control mechanisms., Apoptosis., Oxidative stress--Prevention.
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Format
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Document (PDF)
Pages