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<title>Faculty Research Publications (Microbiology)</title>
<link>http://hdl.handle.net/1957/9973</link>
<description/>
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<rdf:li rdf:resource="http://hdl.handle.net/1957/38705"/>
<rdf:li rdf:resource="http://hdl.handle.net/1957/38587"/>
<rdf:li rdf:resource="http://hdl.handle.net/1957/38023"/>
<rdf:li rdf:resource="http://hdl.handle.net/1957/37892"/>
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<dc:date>2013-06-18T05:07:59Z</dc:date>
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<item rdf:about="http://hdl.handle.net/1957/38705">
<title>Disturbance Driven Colony Fragmentation as a Driver of a Coral Disease Outbreak</title>
<link>http://hdl.handle.net/1957/38705</link>
<description>Disturbance Driven Colony Fragmentation as a Driver of a Coral Disease Outbreak
Brandt, Marilyn E.; Smith, Tyler B.; Correa, Adrienne M. S.; Vega-Thurber, Rebecca
In September of 2010, Brewer's Bay reef, located in St. Thomas (U.S. Virgin Islands), was simultaneously affected by abnormally high temperatures and the passage of a hurricane that resulted in the mass bleaching and fragmentation of its coral community. An outbreak of a rapid tissue loss disease among coral colonies was associated with these two disturbances. Gross lesion signs and lesion progression rates indicated that the disease was most similar to the Caribbean coral disease white plague type 1. Experiments indicated that the disease was transmissible through direct contact between colonies, and five-meter radial transects showed a clustered spatial distribution of disease, with diseased colonies being concentrated within the first meter of other diseased colonies. Disease prevalence and the extent to which colonies were bleached were both significantly higher on unattached colony fragments than on attached colonies, and disease occurred primarily on fragments found in direct contact with sediment. In contrast to other recent studies, disease presence was not related to the extent of bleaching on colonies. The results of this study suggest that colony fragmentation and contact with sediment played primary roles in the initial appearance of disease, but that the disease was capable of spreading among colonies, which suggests secondary transmission is possible through some other, unidentified mechanism.
This is the publisher’s final pdf. The published article is copyrighted by Public Library of Science and can be found at: http://www.plos.org/.
</description>
<dc:date>2013-02-20T00:00:00Z</dc:date>
</item>
<item rdf:about="http://hdl.handle.net/1957/38587">
<title>A transgenic zebrafish liver tumor model with inducible Myc expression reveals conserved Myc signatures with mammalian liver tumors</title>
<link>http://hdl.handle.net/1957/38587</link>
<description>A transgenic zebrafish liver tumor model with inducible Myc expression reveals conserved Myc signatures with mammalian liver tumors
Li, Zhen; Zheng, Weiling; Wang, Zhengyuan; Zeng, Zhiqiang; Zhan, Huiqing; Li, Caixia; Zhou, Li; Yan, Chuan; Spitsbergen, Jan M.; Gong, Zhiyuan
Myc is a pleiotropic transcription factor that is involved in many cellular activities relevant to carcinogenesis, including hepatocarcinogenesis. The zebrafish has been increasingly used to model human diseases and it is particularly valuable in helping to identify common and conserved molecular mechanisms in vertebrates. Here we generated a liver tumor model in transgenic zebrafish by liver-specific expression of mouse Myc using a Tet-On system. Dosage-dependent induction of Myc expression specifically in the liver was observed in our Myc transgenic zebrafish, TO(Myc), and the elevated Myc expression caused liver hyperplasia, which progressed to hepatocellular adenoma and carcinoma with prolonged induction. Next generation sequencing-based transcriptomic analyses indicated that ribosome proteins were overwhelmingly upregulated in the Myc-induced liver tumors. Cross-species analyses showed that the zebrafish Myc model correlated well with Myc transgenic mouse models for liver cancers. The Myc-induced zebrafish liver tumors also possessed molecular signatures highly similar to human those of hepatocellular carcinoma. Finally, we found that a small Myc target gene set of 16 genes could be used to identify liver tumors due to Myc upregulation. Thus, our zebrafish model demonstrated the conserved role of Myc in promoting hepatocarcinogenesis in all vertebrate species.
This is the publisher’s final pdf. The published article is copyrighted by The Company of Biologists Ltd. and can be found at: http://www.biologists.com/journals.html
</description>
<dc:date>2013-03-01T00:00:00Z</dc:date>
</item>
<item rdf:about="http://hdl.handle.net/1957/38023">
<title>Microsporidiosis in zebrafish research facilities</title>
<link>http://hdl.handle.net/1957/38023</link>
<description>Microsporidiosis in zebrafish research facilities
Sanders, Justin L.; Watral, Virginia; Kent, Michael L.
Pseudoloma neurophilia (Microsporidia) is the most common pathogen detected in zebrafish (Danio rerio) from research facilities. The parasite infects the central nervous system and muscle, and may be associated with emaciation and skeletal deformities. However, many fish exhibit subclinical infections. Another microsporidium, Pleistophora hyphessobryconis, has recently been detected in a few zebrafish facilities. Here we review the methods for diagnosis and detection, modes of transmission, and approaches used to control microsporidia in zebrafish, focusing on P. neurophilia. The parasite can be readily transmitted by feeding spores or infected tissues, and we showed that cohabitation with infected fish is also an effective means of transmission. Spores are released from live fish at various points, including the urine, feces, and sex products during spawning. Indeed, P. neurophilia infects both the eggs and ovarian tissues, where we found concentrations ranging from (12,000 – 88,000 spores/ovary). Hence, various lines of evidence support the conclusion that maternal transmission is a route of infection: spores are numerous in ovaries and developing follicles in infected females, spores are present in spawned eggs and water from spawning tanks based on PCR tests, and larvae are very susceptible to the infection. Furthermore, egg surface disinfectants presently used in zebrafish laboratories are ineffective against microsporidian spores. At this time, the most effective method for prevention of these parasites is avoidance.
This is the author's peer-reviewed final manuscript, as accepted by the publisher. The article is copyrighted by the Institute for Laboratory Animal Research and published by Oxford University Press. It can be found at: http://ilarjournal.oxfordjournals.org/.
</description>
<dc:date>2012-01-01T00:00:00Z</dc:date>
</item>
<item rdf:about="http://hdl.handle.net/1957/37892">
<title>Neoplasia and Neoplasm Associated Lesions in Laboratory Colonies of Zebrafish Emphasizing Key Influences of Diet and Aquaculture System Design</title>
<link>http://hdl.handle.net/1957/37892</link>
<description>Neoplasia and Neoplasm Associated Lesions in Laboratory Colonies of Zebrafish Emphasizing Key Influences of Diet and Aquaculture System Design
Spitsbergen, Jan M.; Buhler, Donald R.; Peterson, Tracy S.
During the past decade the zebrafish has emerged as a leading model for mechanistic cancer&#13;
research due to its sophisticated genetic and genomic resources, its tractability for tissue&#13;
targeting of transgene expression, its efficiency for forward genetic approaches to cancer model&#13;
development, and its cost-effectiveness for enhancer and suppressor screens once a cancer model&#13;
is established. However, in contrast to other laboratory animal species widely used as cancer&#13;
models, much basic cancer biology information is lacking in zebrafish. As yet data are not&#13;
published regarding dietary influences on neoplasm incidences in zebrafish. Little information is&#13;
available regarding spontaneous tumor incidences or histologic types in wild-type (wt) lines of&#13;
zebrafish. So far a comprehensive database documenting the full spectrum of neoplasia in&#13;
various organ systems and tissues in not available for zebrafish as it is for other intensely studied&#13;
laboratory animal species. This manuscript confirms that as in other species diet and husbandry&#13;
can profoundly influence tumor incidences and histologic spectra in zebrafish. We show that in&#13;
many laboratory colonies wt lines of zebrafish exhibit elevated neoplasm incidences and&#13;
neoplasm associated lesions such as heptocyte megalocytosis. We present experimental evidence&#13;
showing that certain diet and water management regimens can result in high incidences of&#13;
neoplasia and neoplasm associated lesions. We document the wide array of benign and malignant&#13;
neoplasms affecting nearly every organ, tissue and cell type in zebrafish, in some cases as a&#13;
spontaneous aging change, and in other cases due to carcinogen treatment or genetic&#13;
manipulation.
This is the author's peer-reviewed final manuscript, as accepted by the publisher. The published article is copyrighted by Oxford University Press and can be found at: http://ilarjournal.oxfordjournals.org/.
</description>
<dc:date>2012-01-01T00:00:00Z</dc:date>
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