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Texas A&M University
1.
Ketcham, Paulina Dean.
Using Stages to Assess the Relationship Between Osteoclasts and Cellular Proliferation During Regeneration of the Terminal Phalanx in CD1 Mice Following Amputation.
Degree: MS, Biomedical Sciences, 2018, Texas A&M University
URL: http://hdl.handle.net/1969.1/173293
► Compared to amphibians like the Axolotl, mammals display limited endogenous regenerative ability. However, the digit tips of mice, humans, and other primates possess some regenerative…
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▼ Compared to amphibians like the Axolotl, mammals display limited endogenous regenerative ability. However, the digit tips of mice, humans, and other primates possess some regenerative capabilities, providing hope that enhanced mammalian regeneration might be possible. Mouse digit tip regeneration progresses through a series of well-characterized and discrete events: histolysis, blastema formation and redifferentiation. However, the onset of these events varies between digits as well as individual mice. This variation has the potential to dilute meaningful results and hinder the development of future therapies which could improve the lives of many. To address this issue, we used micro-computed tomography (μCT) to develop a novel method for staging digits during regeneration, focusing on the histolytic phase. Features easily identifiable from a μCT scan, i.e. bone pitting and secondary amputation, were used to categorize regenerating digits. When comparing bone volumes, we found that the bone volumes of digits within the same stage were more similar than digits on the same day post amputation. We then used this method of categorization to look at the relationship between osteoclasts, a cell known for its catabolic role in bone, and cellular proliferation, an anabolic event. Although these two, catabolism and anabolism, seem to be opposing events, the role of bone degeneration and bone formation in regeneration is not known. To explore these unknowns, the digit tips of adult CD1 female mice were amputated. The digits were scanned using the μCT and were immunostained for osteoclasts (Cathepsin K) and an indicator of cellular proliferation (EdU). These scans were used to categorize digits based on stage within the degradation event. Osteoclasts and cellular proliferation were quantified by manual cell counting and compared between and across stages. We found that osteoclasts were associated with cellular proliferation, suggesting that degeneration may be important to the regenerative process. This study provides a method for staging digits and a step towards understanding the role of histolysis during regeneration.
Advisors/Committee Members: Muneoka, Ken (advisor), Welsh, Jane (committee member), Gaddy, Dana (committee member).
Subjects/Keywords: staging; regeneration; mice; osteoclasts; proliferation
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APA (6th Edition):
Ketcham, P. D. (2018). Using Stages to Assess the Relationship Between Osteoclasts and Cellular Proliferation During Regeneration of the Terminal Phalanx in CD1 Mice Following Amputation. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/173293
Chicago Manual of Style (16th Edition):
Ketcham, Paulina Dean. “Using Stages to Assess the Relationship Between Osteoclasts and Cellular Proliferation During Regeneration of the Terminal Phalanx in CD1 Mice Following Amputation.” 2018. Masters Thesis, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/173293.
MLA Handbook (7th Edition):
Ketcham, Paulina Dean. “Using Stages to Assess the Relationship Between Osteoclasts and Cellular Proliferation During Regeneration of the Terminal Phalanx in CD1 Mice Following Amputation.” 2018. Web. 03 Mar 2021.
Vancouver:
Ketcham PD. Using Stages to Assess the Relationship Between Osteoclasts and Cellular Proliferation During Regeneration of the Terminal Phalanx in CD1 Mice Following Amputation. [Internet] [Masters thesis]. Texas A&M University; 2018. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/173293.
Council of Science Editors:
Ketcham PD. Using Stages to Assess the Relationship Between Osteoclasts and Cellular Proliferation During Regeneration of the Terminal Phalanx in CD1 Mice Following Amputation. [Masters Thesis]. Texas A&M University; 2018. Available from: http://hdl.handle.net/1969.1/173293

Texas A&M University
2.
Khanshour, Anas M.
Genetic Diversity and Population Structure of the Arabian Horse Populations from Syria and other Countries.
Degree: PhD, Biomedical Sciences, 2013, Texas A&M University
URL: http://hdl.handle.net/1969.1/151156
► Humans and horses weaved together wonderful stories of adventure and generosity. As a part of human history and civilization, Arabian horses ignite imagination throughout the…
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▼ Humans and horses weaved together wonderful stories of adventure and generosity. As a part of human history and civilization, Arabian horses ignite imagination throughout the world. Populations of this breed exist in many countries. Here I explored different populations of Arabians representing Middle Eastern and Western populations. The main two aims of this study were to provide the genetic diversity description of Arabians from different origins and to examine the traditional classification system of the breed. A third aim was to tackle the distribution pattern of the genetic variability within the genome to show whether there are differences in relative variability of different types of markers.
First, I analyzed the genetic structure of 537Arabian horses from seven populations by using microsatellites. The results consistently showed higher levels of diversity within the Middle Eastern populations compared to the Western populations. All American-Arabians showed differentiation from Middle Eastern populations.
Second, I sequenced the whole mtDNA D-loop of 251 Arabian horses. The whole D-loop sequence was more informative than using just the HVR1. Native populations from the Middle East, such as Syrian, represented a hot spot of genetic diversity. Most importantly, there was no evidence that the Arabian horse breed has clear subdivisions depending on the traditional maternal based strain classification system.
Third, I tested the heterozygosity distribution pattern along the genome of 22 Peruvian Paso horses using 232 microsatellites and Single Nucleotide Polymorphisms (SNPs). The pattern of genetic diversity was completely different between these two markers where no correlation was found. Runs of homozygosity test of SNPs and associated microsatellites noticeably showed that all of associated microsatellites loci were homozygous in the matched case.
The findings of this study will help in understanding the evolutionary history and developing breeding and conservation programs of horses. This study provided databases including parentage testing system and maternal lineages that will help to recover the Syrian Arabian population after the armed conflict started in Syria in 2011. The results here can be applied not only to horses, but also to other animal species with similar criteria.
Advisors/Committee Members: Cothran, Ernest Gus (advisor), Welsh, Jane (committee member), Derr, James (committee member), Raudsepp, Terje (committee member).
Subjects/Keywords: Syrian horse population; Genetic diversity; Arabian horse strains; Populations genetics; Syrian horses; American-Arabian horses; Genetic differentiation
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APA (6th Edition):
Khanshour, A. M. (2013). Genetic Diversity and Population Structure of the Arabian Horse Populations from Syria and other Countries. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/151156
Chicago Manual of Style (16th Edition):
Khanshour, Anas M. “Genetic Diversity and Population Structure of the Arabian Horse Populations from Syria and other Countries.” 2013. Doctoral Dissertation, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/151156.
MLA Handbook (7th Edition):
Khanshour, Anas M. “Genetic Diversity and Population Structure of the Arabian Horse Populations from Syria and other Countries.” 2013. Web. 03 Mar 2021.
Vancouver:
Khanshour AM. Genetic Diversity and Population Structure of the Arabian Horse Populations from Syria and other Countries. [Internet] [Doctoral dissertation]. Texas A&M University; 2013. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/151156.
Council of Science Editors:
Khanshour AM. Genetic Diversity and Population Structure of the Arabian Horse Populations from Syria and other Countries. [Doctoral Dissertation]. Texas A&M University; 2013. Available from: http://hdl.handle.net/1969.1/151156

Texas A&M University
3.
Jones, Daniel K.
Neuroprotection Therapy for Traumatic Brain Injury.
Degree: MS, Medical Sciences, 2016, Texas A&M University
URL: http://hdl.handle.net/1969.1/157161
► The main goal of this project was to test the effectiveness of a novel combination neuroprotection therapy for traumatic brain injury (TBI). TBI affects millions…
(more)
▼ The main goal of this project was to test the effectiveness of a novel combination neuroprotection therapy for traumatic brain injury (TBI). TBI affects millions of people worldwide every year. Neuroinflammation, excitotoxicity and neuronal death as well as related mechanisms contribute to the development of acute and complex neurological deficits, including post-traumatic seizures and cognitive dysfunction. Neuroprotection approaches targeting acute and chronic phases of TBI are needed to limit the damage and prevent post-TBI dysfunction. A variety of neuroprotection approaches such as statins, progesterone (P), cyclosporine A and anti-inflammatory agents have been tested that either target neurons or non-neuronal cells in animal models of TBI. Herein we evaluated the neuroprotective potential of the neurosteroid Ganaxolone (GX) in a mouse TBI model. GX is a synthetic neurosteroid related to allopregnanolone that has sedative, anxiolytic, and anticonvulsant effects. To our knowledge GX has not been used as a neuroprotective agent for TBI. We utilized a controlled cortical impact (CCI) model, which simulates aspects of concussions, brain contusions, and hemorrhages seen in human TBI. Our pilot studies showed the feasibility of TBI-induced chronic epilepsy model in mice. Ganaxolone treatment had positive outcomes on motor function and additional promising disease-modifying or protective potential to reduce epileptic seizures. This pilot study will be advanced further in a larger cohort to confirm Ganaxolone’s ability to reduce or prevent PTE.
Advisors/Committee Members: Reddy, Samba (advisor), Toussaint, Leonide G (committee member), Welsh, Jane (committee member).
Subjects/Keywords: ganaxolone; traumatic brain injury; neuroprotection; epileptogenesis
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APA ·
Chicago ·
MLA ·
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APA (6th Edition):
Jones, D. K. (2016). Neuroprotection Therapy for Traumatic Brain Injury. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/157161
Chicago Manual of Style (16th Edition):
Jones, Daniel K. “Neuroprotection Therapy for Traumatic Brain Injury.” 2016. Masters Thesis, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/157161.
MLA Handbook (7th Edition):
Jones, Daniel K. “Neuroprotection Therapy for Traumatic Brain Injury.” 2016. Web. 03 Mar 2021.
Vancouver:
Jones DK. Neuroprotection Therapy for Traumatic Brain Injury. [Internet] [Masters thesis]. Texas A&M University; 2016. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/157161.
Council of Science Editors:
Jones DK. Neuroprotection Therapy for Traumatic Brain Injury. [Masters Thesis]. Texas A&M University; 2016. Available from: http://hdl.handle.net/1969.1/157161

Texas A&M University
4.
Whitaker, Dustin Thad.
Molecular Determinants of Photoreceptor Presynaptic Terminal Morphology.
Degree: PhD, Neuroscience, 2018, Texas A&M University
URL: http://hdl.handle.net/1969.1/173283
► Rod and cone photoreceptors are light-receptive cells in the visual system that convert photons into an electrochemical signal to be processed through the retina and…
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▼ Rod and cone photoreceptors are light-receptive cells in the visual system that convert photons into an electrochemical signal to be processed through the retina and transmitted into the brain. From the first visual synapse, from photoreceptor to interneurons, rod spherules and cone pedicles diverge in morphology and connectivity patterns. It is known that the transcription factor Nrl is sufficient to drive the cone-to-rod cell fate conversion and morphological change. To dissect the source of the spherule versus pedicle differences, we performed a directed RNAi screen using in vivo electroporation to knock down a select portion of the Nrl regulome to identify genes associated with morphological features.
We systematically characterized four distinct features of rod spherules and S-cone pedicles: spherule width, terminal position in the outer plexiform layer, ribbon number, and presence or absence of telodendrites. Using previously published next-generation sequencing data of the transcriptome of developing rod and cone-like photoreceptors as well as key transcription factor binding profiles, we defined a set of genes potentially associated with restricting spherule morphology from that of the default pedicle state. By knocking down genes individually, we were able to dissect the effects each gene has to restrict spherules. Our screen identified twenty-seven genes that control one or two independent features of rod photoreceptor spherule morphology, terminal width or outer plexiform layer position. Many of these were confirmed either through rescue experiments or examination of loss of function of mouse strains.
Lastly, we generated a protein interaction network to connect the seemingly random sets of genes that controlled spherule morphology. Clustering of genes in this network did not show enrichment of our positive screen targets into communities. When we created shortest network pathways between all pairs of positive targets, we discovered that there was an enrichment of pathways that utilized Ncoa2, and this gene has a direct path to Nrl. We hypothesize that we have discovered a more directly involved gene regulatory network associated with the restriction of rod photoreceptor spherules. This knowledge should help in blinding disease treatment strategies to improve proper integration into the native retinal circuitry after loss of photoreceptors.
Advisors/Committee Members: Smotherman, Michael (advisor), Ko, Gladys (committee member), Riley, Bruce (committee member), Welsh, Jane (committee member).
Subjects/Keywords: rod; spherule; retina; network; synapse
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
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APA (6th Edition):
Whitaker, D. T. (2018). Molecular Determinants of Photoreceptor Presynaptic Terminal Morphology. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/173283
Chicago Manual of Style (16th Edition):
Whitaker, Dustin Thad. “Molecular Determinants of Photoreceptor Presynaptic Terminal Morphology.” 2018. Doctoral Dissertation, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/173283.
MLA Handbook (7th Edition):
Whitaker, Dustin Thad. “Molecular Determinants of Photoreceptor Presynaptic Terminal Morphology.” 2018. Web. 03 Mar 2021.
Vancouver:
Whitaker DT. Molecular Determinants of Photoreceptor Presynaptic Terminal Morphology. [Internet] [Doctoral dissertation]. Texas A&M University; 2018. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/173283.
Council of Science Editors:
Whitaker DT. Molecular Determinants of Photoreceptor Presynaptic Terminal Morphology. [Doctoral Dissertation]. Texas A&M University; 2018. Available from: http://hdl.handle.net/1969.1/173283

Texas A&M University
5.
Hameed, Samer Sadeq.
Avian Bornavirus: Recombinant N Protein Vaccine and Pathogenesis.
Degree: PhD, Veterinary Pathobiology, 2017, Texas A&M University
URL: http://hdl.handle.net/1969.1/173078
► Proventricular dilatation disease (PDD) is a fatal viral disease that affects mainly psittacine birds, although some non-psittacine species can be affected. Gastrointestinal and/or neurological signs…
(more)
▼ Proventricular dilatation disease (PDD) is a fatal viral disease that affects mainly psittacine birds, although some non-psittacine species can be affected. Gastrointestinal and/or neurological signs can be seen in PDD-affected birds. These signs are likely a result of non-suppurative inflammation of the central, peripheral and autonomic nervous systems. Parrot bornavirus (PaBV) was discovered as a causative agent of PDD in 2008. The prognosis of PDD is very poor once clinical signs have developed and no specific treatments or commercial vaccines are available to date.
In order to investigate methods of protection, we vaccinated cockatiels using inactivated whole PaBV and/or recombinant PaBV N protein vaccines followed by challenge with virulent PaBV-2. In the first experiment, inactivated PaBV-2-infected cells were administrated via intramuscular (IM) inoculation, three times, followed by one IM injection of recombinant N protein vaccine. In a second experiment, the recombinant N protein vaccine was administered alone, two times, via the IM route. Over 28 weeks post challenge, cloacal swabs were collected and body weights and any clinical signs were noted. Using tissues collected at necropsy, histopathologic examination was used to detect the presence of microscopic lesions characteristic of PDD. Quantitative RealTime PCR (qRT-PCR) and immunohistochemistry (IHC) were used to detect PaBVRNA and antigen respectively. Using western blots assays, we were not able to detect a humoral response after vaccination with the inactivated vaccine. Conversely, the recombinant N protein vaccine stimulated production of anti-N antibodies.
The results of both vaccine studies indicated that the recombinant N protein vaccine was able to protect subsequently challenged birds from lesions associated with PDD. Further, the vaccine protected birds from PDD-related morbidity and mortality. However, the vaccine did not protect "efficiently" against infection, as PaBV- RNA and antigen were detected in organs and cloacal swabs of vaccinated and unvaccinated birds. Moreover, there was no evidence that vaccination, either before or after challenge, increased the severity of the infection. We hypothesized that this protective response was a result of a switch from a type 1 cell-mediated immune response to a type 2 humoral immune response. This hypothesis was supported by a third study which revealed that treatment of cockatiels with cyclosporine A, an immunosuppressant, at the time of challenge with virulent PaBV-2, also conferred complete protection against PDD at the expense of increasing the viral load. This experiment showed that PDD might be an immunologically mediated disease, similar to Borna disease in mammals.
Advisors/Committee Members: Payne, Susan (advisor), Tizard, Ian (committee member), Wilson, Van (committee member), Welsh, Jane (committee member).
Subjects/Keywords: Bornavirus; Avian Bornavirus; Vaccine; Recombinant N protein; Proventricular dilatation disease; PDD; Pathogenesis; Cyclosporine; Cockatiel
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Hameed, S. S. (2017). Avian Bornavirus: Recombinant N Protein Vaccine and Pathogenesis. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/173078
Chicago Manual of Style (16th Edition):
Hameed, Samer Sadeq. “Avian Bornavirus: Recombinant N Protein Vaccine and Pathogenesis.” 2017. Doctoral Dissertation, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/173078.
MLA Handbook (7th Edition):
Hameed, Samer Sadeq. “Avian Bornavirus: Recombinant N Protein Vaccine and Pathogenesis.” 2017. Web. 03 Mar 2021.
Vancouver:
Hameed SS. Avian Bornavirus: Recombinant N Protein Vaccine and Pathogenesis. [Internet] [Doctoral dissertation]. Texas A&M University; 2017. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/173078.
Council of Science Editors:
Hameed SS. Avian Bornavirus: Recombinant N Protein Vaccine and Pathogenesis. [Doctoral Dissertation]. Texas A&M University; 2017. Available from: http://hdl.handle.net/1969.1/173078

Texas A&M University
6.
McGruder, Brenna Mariechen.
Potential Genetic Contributions to a Pneumopathogenic MHV-1 Virus: Analysis by Targeted Recombination and Whole Genome Sequencing in the MHV-1 Model of SARS-COV Lung Disease.
Degree: PhD, Medical Sciences, 2014, Texas A&M University
URL: http://hdl.handle.net/1969.1/152630
► A targeted recombination system was developed for MHV-1 by generation of a Donor plasmid that consisted of sequences consisting of the first 448 nucleotides of…
(more)
▼ A targeted recombination system was developed for MHV-1 by generation of a
Donor plasmid that consisted of sequences consisting of the first 448 nucleotides of the
MHV-1 genome fused to sequences from codon 28 in the HE gene through the 3’UTR to
the poly(A) tail. The Donor plasmid was transcribed in vitro and transfected into FCWF
cells that had been infected with a felinized MHV-1 recombinant virus. Recombinant
viruses were selected by overlaying infected/transfected FCWF cells onto murine DBT
cells and monitoring for syncytia formation and cell death. Recombinant viruses were
plaque purified and expanded in murine cells. Several recombinant viruses that were not
significantly different from MHV-1 in tissue culture were isolated, but none were
pneumopathogenic in the A/J mouse. During the generation of multiple wild type
MHV-1 stocks for mouse studies we discovered that MHV-1 rapidly lost
pnuemopathogenicity during passage in DBT cells. This finding demonstrated that
targeted recombination may not be a viable method of genetic manipulation of MHV-1
because the multiple passages in cell culture required to generate viruses by targeted
recombination may cause loss of virulence. Using Next-Generation sequencing
technology a virulent and non-virulent MHV-1 passage were sequenced, and two
potential mutations that are present in the subpopulation of virulent viruses were
identified that may contribute to pneumopathogenicity: nsp13 C17015A and ns4
G28454A.
We are developing an infectious cDNA clone using in vitro assembly of MHV-1
cDNA fragments. The fragments are flanked by type II restriction enzymes which, when
digested liberate cDNA fragments that only contain MHV-1 genetic sequence and can be
ligated together. By housing portions of the MHV-1 genome in low-copy plasmids we
were able to create a system that is easily maintained in bacteria and easily manipulated
by restriction digestion or site-directed mutagenesis. This infectious clone will be used
to determine if the mutations that were discovered during the sequencing of the MHV-1
pneumovirulent virus are sufficient and able to generate a pnueumopathogenic virus.
The infectious clone will also be used to determine the role, if any, of ns2 in an MHV-1
infection of lungs.
Advisors/Committee Members: Leibowitz, Julian (advisor), Payne, Susan (committee member), Tesh, Vernon (committee member), Welsh, Jane (committee member).
Subjects/Keywords: MHV-1; lung pathogenesis, SARS-CoV; mouse hepatitis virus strain 1; reverse genetic; whole genome
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
McGruder, B. M. (2014). Potential Genetic Contributions to a Pneumopathogenic MHV-1 Virus: Analysis by Targeted Recombination and Whole Genome Sequencing in the MHV-1 Model of SARS-COV Lung Disease. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/152630
Chicago Manual of Style (16th Edition):
McGruder, Brenna Mariechen. “Potential Genetic Contributions to a Pneumopathogenic MHV-1 Virus: Analysis by Targeted Recombination and Whole Genome Sequencing in the MHV-1 Model of SARS-COV Lung Disease.” 2014. Doctoral Dissertation, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/152630.
MLA Handbook (7th Edition):
McGruder, Brenna Mariechen. “Potential Genetic Contributions to a Pneumopathogenic MHV-1 Virus: Analysis by Targeted Recombination and Whole Genome Sequencing in the MHV-1 Model of SARS-COV Lung Disease.” 2014. Web. 03 Mar 2021.
Vancouver:
McGruder BM. Potential Genetic Contributions to a Pneumopathogenic MHV-1 Virus: Analysis by Targeted Recombination and Whole Genome Sequencing in the MHV-1 Model of SARS-COV Lung Disease. [Internet] [Doctoral dissertation]. Texas A&M University; 2014. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/152630.
Council of Science Editors:
McGruder BM. Potential Genetic Contributions to a Pneumopathogenic MHV-1 Virus: Analysis by Targeted Recombination and Whole Genome Sequencing in the MHV-1 Model of SARS-COV Lung Disease. [Doctoral Dissertation]. Texas A&M University; 2014. Available from: http://hdl.handle.net/1969.1/152630

Texas A&M University
7.
Tsai, Pai Chi.
miR-153 and miR-335, Ethanol Sensitive MicroRNAs, Control NSC/NPC Maturation during Fetal Brain Development.
Degree: PhD, Medical Sciences, 2014, Texas A&M University
URL: http://hdl.handle.net/1969.1/152634
► Maternal alcohol consumption during pregnancy, especially during the first and second trimester, can cause the wide range of severe birth defects classified as fetal alcohol…
(more)
▼ Maternal alcohol consumption during pregnancy, especially during the first and second trimester, can cause the wide range of severe birth defects classified as fetal alcohol spectrum disorder (FASD). FASD is a wide spectrum disease characterized by delayed fetal growth, facial abnormalities, and cognitive and behavioral deficits of the central nervous system. The cost of FASD to the U.S. healthcare system is estimated at more than $6 billion annually, suggesting the problem of maternal consumption is increasing through years.
Previous research by Sathyan and his colleague has shown that only few miRNAs, miR-9, miR-21, miR-153, and miR-335, were able to mediate ethanol’s teratogenic effects through regulation neural stem/progenitor cell (NSC/NPC). However, the mechanisms whereby miRNAs mediate fetal neural stem cell (NSC) vulnerability and contribute to ethanol’s teratology are complex and still unclear. Therefore, the goal of my dissertation is to discover novel pathways of two miRNAs, miR-153 and miR-335, as key modulators of ethanol. Data from the miR-153 study identified NFIA (nuclear factor-1A) and its paralog, NFIB, as direct targets of miR-153 ex vivo as well as in vivo, and miR-153 overexpression prevented neuronal differentiation. MiR-153 functional analysis in neurospheres suggested that overexpression of this microRNA prevented, and partly reversed ethanol’s teratogenic
effects on miR-153 target transcripts. This antagonistic effect was also found in the pharmacology studies using varenicline, a FDA-approved drug as a partial nicotinic acetylcholine receptor agonist, which increased miR-153 expression. These data collectively suggested a role for miR-153 in preventing NSCs/NPCs differentiation, and showed that direct or pharmacological manipulation of miRNAs in an ex vivo model have the potential capability to prevent or even reverse ethanol’s effects on fetal brain development. Data from miR-335 research presented show that miR-335 regulates NSCs/NPCs markers DCX, NeuroD1, and c-Kit, and that miR-335 dysregulation results in neuronal premature-maturation via increasing asymmetric cell divisions, driving neuronal early differentiation through inducing stem cell genes DCX and NeuroD1 in the ventricular zone (VZ) of the developing cortex.
In sum, my data conclude that miR-335 and miR-153 act as molecular brakes to prevent NSCs/NPCs early maturation by regulating cell differentiation genes during the second trimester, and ethanol leads to organizational defects in the developing cerebral cortex through driving premature-maturation. In addition, preliminary data from miRNA functional studies indicate that misregulation of miRNA-regulated genes by ethanol exposure can be prevented or reversed in the presence of microRNAs or specific pharmaceuticals. This evidence explores the application of candidate miRNAs, as well as other medical drugs, as potential therapeutics to overcome ethanol’s teratology.
Advisors/Committee Members: Miranda, Rajesh (advisor), Sohrabji, Farida (committee member), Chapkin, Robert (committee member), Welsh, Jane (committee member).
Subjects/Keywords: miR-153; miR-335
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Tsai, P. C. (2014). miR-153 and miR-335, Ethanol Sensitive MicroRNAs, Control NSC/NPC Maturation during Fetal Brain Development. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/152634
Chicago Manual of Style (16th Edition):
Tsai, Pai Chi. “miR-153 and miR-335, Ethanol Sensitive MicroRNAs, Control NSC/NPC Maturation during Fetal Brain Development.” 2014. Doctoral Dissertation, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/152634.
MLA Handbook (7th Edition):
Tsai, Pai Chi. “miR-153 and miR-335, Ethanol Sensitive MicroRNAs, Control NSC/NPC Maturation during Fetal Brain Development.” 2014. Web. 03 Mar 2021.
Vancouver:
Tsai PC. miR-153 and miR-335, Ethanol Sensitive MicroRNAs, Control NSC/NPC Maturation during Fetal Brain Development. [Internet] [Doctoral dissertation]. Texas A&M University; 2014. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/152634.
Council of Science Editors:
Tsai PC. miR-153 and miR-335, Ethanol Sensitive MicroRNAs, Control NSC/NPC Maturation during Fetal Brain Development. [Doctoral Dissertation]. Texas A&M University; 2014. Available from: http://hdl.handle.net/1969.1/152634

Texas A&M University
8.
Allen, Marilyn Jean.
N-3 Polyunsaturated Fatty Acids Reduce Th17 Differentiation by Decreasing Responsiveness to Interleukin-6 in Mice.
Degree: MS, Nutrition, 2014, Texas A&M University
URL: http://hdl.handle.net/1969.1/153215
► CD4^(+) effector T cell subsets (e.g., Th1, Th17) are implicated in autoimmune and inflammatory disorders such as multiple sclerosis, psoriasis and rheumatoid arthritis. For optimal…
(more)
▼ CD4^(+) effector T cell subsets (e.g., Th1, Th17) are implicated in autoimmune and inflammatory disorders such as multiple sclerosis, psoriasis and rheumatoid arthritis. For optimal activation, IL-6 induces Th17 polarization and signals through the membrane-bound signal transducer, gp130. Previously, we have demonstrated that n-3 polyunsaturated fatty acids (PUFA), when supplied in the diet or in fat-1 transgenic mice which generate n-3 PUFA de novo, suppress CD4^(+) T cell activation and differentiation into pathogenic Th17 cells. Here we report that n-3 PUFA alter the response of CD4^(+) T cells to IL-6 in a lipid raft membrane-dependent fashion. Naïve splenic CD4^(+) T cells from fat-1 mice exhibited significantly lower surface expression of the IL-6 receptor (IL-6R). This membrane bound receptor is known to be shed upon cellular activation in response to antigen; however, the release of soluble IL-6R after treatment with anti-CD3 and anti-CD28 was not changed in fat-1 mice suggesting that the decrease in surface expression is not due to ectodomain release. We observed a significant decrease in the association of gp130 with lipid rafts in activated fat-1 CD4^(+) T cells and a 35% reduction in gp130 homodimerization, an obligate requirement for downstream signaling. The phosphorylation of STAT3, a downstream target of IL-6-dependent signaling, was also decreased in response to exogenous IL-6 in fat-1 CD4^(+) T cells. Our results suggest that n-3 PUFA suppress Th17 cell differentiation, in part, by reducing membrane raft-dependent responsiveness to IL-6, an essential polarizing cytokine.
Advisors/Committee Members: Chapkin, Robert S (advisor), McMurray, David N (committee member), Welsh, Jane (committee member).
Subjects/Keywords: n-3 PUFA; lipid rafts; Th17; IL-6-gp130-STAT3
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APA (6th Edition):
Allen, M. J. (2014). N-3 Polyunsaturated Fatty Acids Reduce Th17 Differentiation by Decreasing Responsiveness to Interleukin-6 in Mice. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/153215
Chicago Manual of Style (16th Edition):
Allen, Marilyn Jean. “N-3 Polyunsaturated Fatty Acids Reduce Th17 Differentiation by Decreasing Responsiveness to Interleukin-6 in Mice.” 2014. Masters Thesis, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/153215.
MLA Handbook (7th Edition):
Allen, Marilyn Jean. “N-3 Polyunsaturated Fatty Acids Reduce Th17 Differentiation by Decreasing Responsiveness to Interleukin-6 in Mice.” 2014. Web. 03 Mar 2021.
Vancouver:
Allen MJ. N-3 Polyunsaturated Fatty Acids Reduce Th17 Differentiation by Decreasing Responsiveness to Interleukin-6 in Mice. [Internet] [Masters thesis]. Texas A&M University; 2014. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/153215.
Council of Science Editors:
Allen MJ. N-3 Polyunsaturated Fatty Acids Reduce Th17 Differentiation by Decreasing Responsiveness to Interleukin-6 in Mice. [Masters Thesis]. Texas A&M University; 2014. Available from: http://hdl.handle.net/1969.1/153215

Texas A&M University
9.
Chamoun Emanuelli, Ana M.
Characterization of Viral Entry Inhibitors.
Degree: PhD, Chemical Engineering, 2014, Texas A&M University
URL: http://hdl.handle.net/1969.1/153447
► Hepatitis C virus (HCV), Human Immunodeficiency virus (HIV) and Herpes Simplex virus (HSV) are pathogenic viruses known to cause liver disorder, acquired immunodeficiency and skin…
(more)
▼ Hepatitis C virus (HCV), Human Immunodeficiency virus (HIV) and Herpes Simplex virus (HSV) are pathogenic viruses known to cause liver disorder, acquired immunodeficiency and skin lesions, respectively. Although current therapies have played substantial roles in the fight against these pathogens, their use is limited and for the most part does not result in viral eradication. Moreover, most antivirals target viral encoded structures which overtime foster the development of resistant strains. Hence, antivirals aimed at preventing initial infection represent a promising strategy for viral combat.
This dissertation focuses on the characterization of viral entry inhibitors and their potential use. The first compounds evaluated come from the phenothiazines family, widely used as antipsychotic drugs. Phenothiazines were shown to suppress HCV entry by intercalating into cholesterol-rich membrane domains of target cells thus reducing viral-host fusion.
The second candidates studied are two members of the H1-anthistamines currently used for allergy treatment. Both compounds strongly reduce HCV entry, likely at the fusion step, and its inhibition was associated with cholesterol content in the virion and host cells, pointing to the use of an NPC1L1-receptor dependent mechanism.
Lastly, we evaluated the antiviral activity of PD 404,182 (PD) as an alternate treatment for HCV-HIV coinfected patients as well as its potential use as an anti-HIV microbicide. PD is able to reduce viral entry of the three pathogens through physical disruption of virions releasing the nucleic acids into the surrounding medium. Moreover, PD possesses several qualities pointing to its use as a potential microbicide.
Advisors/Committee Members: Chen, Zhilei (advisor), Jayaraman, Arul (committee member), Kao, Katy (committee member), Welsh, Jane (committee member).
Subjects/Keywords: HCV; HSV; HIV; entry inhibitors
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MLA ·
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APA (6th Edition):
Chamoun Emanuelli, A. M. (2014). Characterization of Viral Entry Inhibitors. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/153447
Chicago Manual of Style (16th Edition):
Chamoun Emanuelli, Ana M. “Characterization of Viral Entry Inhibitors.” 2014. Doctoral Dissertation, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/153447.
MLA Handbook (7th Edition):
Chamoun Emanuelli, Ana M. “Characterization of Viral Entry Inhibitors.” 2014. Web. 03 Mar 2021.
Vancouver:
Chamoun Emanuelli AM. Characterization of Viral Entry Inhibitors. [Internet] [Doctoral dissertation]. Texas A&M University; 2014. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/153447.
Council of Science Editors:
Chamoun Emanuelli AM. Characterization of Viral Entry Inhibitors. [Doctoral Dissertation]. Texas A&M University; 2014. Available from: http://hdl.handle.net/1969.1/153447

Texas A&M University
10.
Kim, Janice J.
Reversible Inactivation of the Bed Nucleus of the Stria Terminalis Blocks Reinstatement But Not Renewal of Extinguished Fear.
Degree: MS, Psychology, 2014, Texas A&M University
URL: http://hdl.handle.net/1969.1/154180
► The bed nucleus of the stria terminalis (BNST) is thought to be involved in the expression of fear to shock-associated contexts, but not to discrete…
(more)
▼ The bed nucleus of the stria terminalis (BNST) is thought to be involved in the expression of fear to shock-associated contexts, but not to discrete conditional stimuli (CSs) paired with shock. Because context plays an important role in the extinction and relapse of fear, we sought to examine the contribution of the BNST to two different relapse phenomena: renewal and reinstatement. In the renewal experiment, male Long-Evans rats received 5 tone-shock trials for conditioning in “context A”; 24 hours later they received 45 tone–alone (extinction) trials in either “context B” or “context C”. Ten minutes prior to a retrieval test (5 tone-alone trials), rats were infused with either selective agonist for GABAA receptors, muscimol or vehicle in the BNST. In the reinstatement experiment, rats underwent a similar procedure, but were presented with an unsignaled ‘reminder’ shock in the extinction context to reinstate fear. As before, we examined the influence of muscimol inactivation of the BNST during a retrieval testing 24-hours after the reinstatement shock. In the reinstatement test, rats with muscimol infusion showed significantly less freezing than did rats with vehicle infusion. In contrast, BNST inactivation did not attenuate the renewal of fear to an extinguished CS outside the extinction context. These data indicate that the BNST is involved in forms of fear relapse that depend on direct associations of the test context with an aversive US.
Advisors/Committee Members: Maren, Stephen (advisor), Packard, Mark (committee member), Wellman, Paul (committee member), Welsh, Jane (committee member).
Subjects/Keywords: BNST; context; extinction; fear conditioning; rat; reinstatement; relapse; renewal
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Kim, J. J. (2014). Reversible Inactivation of the Bed Nucleus of the Stria Terminalis Blocks Reinstatement But Not Renewal of Extinguished Fear. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/154180
Chicago Manual of Style (16th Edition):
Kim, Janice J. “Reversible Inactivation of the Bed Nucleus of the Stria Terminalis Blocks Reinstatement But Not Renewal of Extinguished Fear.” 2014. Masters Thesis, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/154180.
MLA Handbook (7th Edition):
Kim, Janice J. “Reversible Inactivation of the Bed Nucleus of the Stria Terminalis Blocks Reinstatement But Not Renewal of Extinguished Fear.” 2014. Web. 03 Mar 2021.
Vancouver:
Kim JJ. Reversible Inactivation of the Bed Nucleus of the Stria Terminalis Blocks Reinstatement But Not Renewal of Extinguished Fear. [Internet] [Masters thesis]. Texas A&M University; 2014. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/154180.
Council of Science Editors:
Kim JJ. Reversible Inactivation of the Bed Nucleus of the Stria Terminalis Blocks Reinstatement But Not Renewal of Extinguished Fear. [Masters Thesis]. Texas A&M University; 2014. Available from: http://hdl.handle.net/1969.1/154180

Texas A&M University
11.
Thompson, Jeffrey.
The Role of Caspase-8 in Oligodendrocyte Development and Mechanisms of Oxidative Injury in Neurons and Glia.
Degree: MS, Biomedical Sciences, 2012, Texas A&M University
URL: http://hdl.handle.net/1969.1/148320
► Apoptosis is essential not only to the normal development of a multicellular organism but also for the maintenance of tissue homeostasis. This proposal seeks to…
(more)
▼ Apoptosis is essential not only to the normal development of a multicellular organism but also for the maintenance of tissue homeostasis. This proposal seeks to investigate, in part, the role of oligodendrocyte (OL) apoptosis in myelination. We used an OL-specific conditional knockout animal to study caspase-8 function in OL development; analyzing histological differences in myelination at postnatal day 10 and alterations to OL proliferation, differentiation, and cell death in culture. Our preliminary data suggests that deletion of caspase-8 did not alter OL proliferation or differentiation in culture, but reduced the percentage of apoptotic cells following nutrient deprivation. In vivo, we found an increase in myelinated axons in the spinal cord of caspase-8 deficient mice, indicating a role for caspase-8 in the myelination process.
This study also seeks to investigate mechanisms of cell death in OLs, astrocytes, and neurons following oxidative injury. Exposure of primary OLs, astrocytes, and neurons to arachidonic acid (AA) resulted in oxidative stress and cell death. Necrostation-1, the specific inhibitor of receptor interacting protein kinase 1 (RIP-1), markedly prevented AA-induced oxidative death in OLs and astrocytes, but not in neurons. Similarly, we found that blockade of 12-lipoxygenase (LOX) and c-Jun N-terminal kinase (JNK) protected OLs and astrocytes but not neurons against AA toxicity. Consistent with the inability of necrostatin-1 to rescue neurons, we found very low expression of RIP-1 as well as RIP-3 in neurons. Finally, the zinc chelator TPEN effectively abolished AA-induced oxidative death in all three cell types, suggesting zinc release as a common mechanism. Taken together, our findings indicate differences in cell death mechanisms following oxidative injury in astrocytes, OLs, and neurons.
Advisors/Committee Members: Li, Jianrong (advisor), Welsh, Jane (committee member), Abbott, Louise (committee member), Wellman, Paul (committee member).
Subjects/Keywords: Necroptosis; RIP-1; Oxidative Stress; Oligodendrocytes; Apoptosis
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
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APA (6th Edition):
Thompson, J. (2012). The Role of Caspase-8 in Oligodendrocyte Development and Mechanisms of Oxidative Injury in Neurons and Glia. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/148320
Chicago Manual of Style (16th Edition):
Thompson, Jeffrey. “The Role of Caspase-8 in Oligodendrocyte Development and Mechanisms of Oxidative Injury in Neurons and Glia.” 2012. Masters Thesis, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/148320.
MLA Handbook (7th Edition):
Thompson, Jeffrey. “The Role of Caspase-8 in Oligodendrocyte Development and Mechanisms of Oxidative Injury in Neurons and Glia.” 2012. Web. 03 Mar 2021.
Vancouver:
Thompson J. The Role of Caspase-8 in Oligodendrocyte Development and Mechanisms of Oxidative Injury in Neurons and Glia. [Internet] [Masters thesis]. Texas A&M University; 2012. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/148320.
Council of Science Editors:
Thompson J. The Role of Caspase-8 in Oligodendrocyte Development and Mechanisms of Oxidative Injury in Neurons and Glia. [Masters Thesis]. Texas A&M University; 2012. Available from: http://hdl.handle.net/1969.1/148320

Texas A&M University
12.
Mitchell, Nicole Jean.
Human Exposure to Foodborne Toxins in Ghana: Intervention Strategy for Reduction of Aflatoxin and Fumonisin Bioavailability.
Degree: PhD, Toxicology, 2013, Texas A&M University
URL: http://hdl.handle.net/1969.1/151665
► International health has typically focused on remediation of infectious diseases in developing countries. However, recent reports from the International Agency for Research on Cancer (IARC)…
(more)
▼ International health has typically focused on remediation of infectious diseases in developing countries. However, recent reports from the International Agency for Research on Cancer (IARC) have highlighted the importance of cancer incidence/ mortality in the developing world. Foodborne mycotoxins produced by fungi, called aflatoxin (AF) and fumonisin (FB), have been associated with hepatocellular and esophageal carcinomas among other deleterious effects, such as growth faltering and immune dysfunction. Exposure to these toxins in Ghana is particularly high due to food insecurity, climate, and lack of regulatory infrastructures. Work to alleviate AF and FB contamination in Africa has focused on instituting good agricultural and storage practices however, exposures remain inextricable in many communities. Utilization of a calcium montmorillonite clay, UPSN, shows promise of tightly binding both AF and FB in the gastrointestinal tract, thereby reducing their bioavailability. The objectives of this research were to determine exposure susceptibility in Ghana and to assess efficacy and safety of UPSN treatment within vulnerable populations.
Cross-sectional data from six different regions of Ghana indicated that AF exposure is associated with maize consumption and region of residence. However, food preparation practices were not correlated to AF levels in the present study. Therefore, future intervention strategies were focused on the end point of the food consumption chain by reducing AF exposure from maize immediately prior to ingestion (i.e. UPSN treatment). In a three-month trial an encapsulated montmorillonite clay was efficacious in reducing AF exposure. However, concern for sustainability and its applicability for children led to an effort to alter the dose dissemination form. Inclusion of UPSN in common Ghanaian foods retained the efficacy of the clay, reducing a short-term biomarker (AFM_(1)) by 55%, and was determined to be safe in children (ages 3-9). Importantly, daily assessment of AFM_(1) levels was successful in providing statistical significance of intervention effects within only five days of treatment. Initial results indicate that UPSN could efficiently to bind both AF and FB in the gastrointestinal tract, reducing biomarkers for both toxins in animal models. Thus, UPSN could positively impact health in developing communities at risk for AF and FB exposure.
Advisors/Committee Members: Phillips, Timothy D (advisor), Porter, Weston W (committee member), Safe, Stephen H (committee member), Welsh, Jane C (committee member).
Subjects/Keywords: Aflatoxin; Fumonisin; Bioavailability; NovaSil clay; Enterosorption
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Mitchell, N. J. (2013). Human Exposure to Foodborne Toxins in Ghana: Intervention Strategy for Reduction of Aflatoxin and Fumonisin Bioavailability. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/151665
Chicago Manual of Style (16th Edition):
Mitchell, Nicole Jean. “Human Exposure to Foodborne Toxins in Ghana: Intervention Strategy for Reduction of Aflatoxin and Fumonisin Bioavailability.” 2013. Doctoral Dissertation, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/151665.
MLA Handbook (7th Edition):
Mitchell, Nicole Jean. “Human Exposure to Foodborne Toxins in Ghana: Intervention Strategy for Reduction of Aflatoxin and Fumonisin Bioavailability.” 2013. Web. 03 Mar 2021.
Vancouver:
Mitchell NJ. Human Exposure to Foodborne Toxins in Ghana: Intervention Strategy for Reduction of Aflatoxin and Fumonisin Bioavailability. [Internet] [Doctoral dissertation]. Texas A&M University; 2013. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/151665.
Council of Science Editors:
Mitchell NJ. Human Exposure to Foodborne Toxins in Ghana: Intervention Strategy for Reduction of Aflatoxin and Fumonisin Bioavailability. [Doctoral Dissertation]. Texas A&M University; 2013. Available from: http://hdl.handle.net/1969.1/151665

Texas A&M University
13.
Martin, Cameron Lee.
Characterization of a Broadly Reactive Anti-CD40 Agonistic Monoclonal Antibody for Potential Use as an Adjuvant.
Degree: MS, Biomedical Sciences, 2017, Texas A&M University
URL: http://hdl.handle.net/1969.1/161578
► Lack of safe and effective adjuvants is a major hindrance to the development of efficacious vaccines. Signaling via CD40 pathway leads to enhanced antigen processing…
(more)
▼ Lack of safe and effective adjuvants is a major hindrance to the development of efficacious vaccines. Signaling via CD40 pathway leads to enhanced antigen processing and presentation, nitric oxide expression, pro-inflammatory cytokine expression by antigen presenting cells, and stimulation of B-cells to undergo somatic hypermutation, immunoglobulin class switching, and proliferation. Agonistic anti-CD40 antibodies have shown promising adjuvant qualities in human and mouse vaccine studies. An antiCD40 monoclonal antibody (mAb), designated 2E4E4, was identified and shown to have strong agonistic effects on primary cells from multiple livestock species. The mAb recognize swine, bovine, caprine, and ovine CD40, and evoked 25 fold or greater proliferation of peripheral blood mononuclear cells (PBMCs) from these species relative to cells incubated with an isotype control (p<0.001). In addition, the mAb induced significant nitric oxide (p<0.0001) release by bovine macrophages. Furthermore, the mAb upregulated the expression of MHC-II by PBMCs, and stimulated significant p<0.0001) IL-1α, IL-6, IL- 8, and TNF-α expression by PBMCs. These results suggest that the mAb 2E4E4 can target and stimulate cells from multiple livestock species and thus, it is a potential candidate for adjuvant development. This the first study to report an anti-swine CD40 agonistic mAb that is also broadly reactive against multiple species.
Advisors/Committee Members: Mwangi, Waithaka (advisor), Waghela, Suryakant (committee member), Criscitiello, Michael (committee member), Welsh, Jane (committee member), Rathore, Keerti (committee member).
Subjects/Keywords: Agonistic anti-CD40 mAb; Ovine; Caprine; Bovine; Vaccines; Adjuvant
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
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APA (6th Edition):
Martin, C. L. (2017). Characterization of a Broadly Reactive Anti-CD40 Agonistic Monoclonal Antibody for Potential Use as an Adjuvant. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/161578
Chicago Manual of Style (16th Edition):
Martin, Cameron Lee. “Characterization of a Broadly Reactive Anti-CD40 Agonistic Monoclonal Antibody for Potential Use as an Adjuvant.” 2017. Masters Thesis, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/161578.
MLA Handbook (7th Edition):
Martin, Cameron Lee. “Characterization of a Broadly Reactive Anti-CD40 Agonistic Monoclonal Antibody for Potential Use as an Adjuvant.” 2017. Web. 03 Mar 2021.
Vancouver:
Martin CL. Characterization of a Broadly Reactive Anti-CD40 Agonistic Monoclonal Antibody for Potential Use as an Adjuvant. [Internet] [Masters thesis]. Texas A&M University; 2017. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/161578.
Council of Science Editors:
Martin CL. Characterization of a Broadly Reactive Anti-CD40 Agonistic Monoclonal Antibody for Potential Use as an Adjuvant. [Masters Thesis]. Texas A&M University; 2017. Available from: http://hdl.handle.net/1969.1/161578

Texas A&M University
14.
Emery, Michael A.
Drug-Specific Differences Among the Opioid Analgesics Hydrocodone, Oxycodone and Morphine.
Degree: PhD, Neuroscience, 2018, Texas A&M University
URL: http://hdl.handle.net/1969.1/173631
► Opioids have been utilized for millennia for analgesia, but are accompanied by numerous adverse effects in addition to their pain relief abilities. These include tolerance,…
(more)
▼ Opioids have been utilized for millennia for analgesia, but are accompanied by numerous adverse effects in addition to their pain relief abilities. These include tolerance, opioid-induced hyperalgesia, the propensity for abuse, and discrepancies regarding their ability to treat chronic pain. Despite efforts to find non-opioid alternatives, opioids remain the gold standard in spite of their drawbacks. Historically, both prescription and research of opioids have been guided by the assumption that analgesic properties and adverse associated effects are mediated by the same mechanisms and therefore are inseparable. Relatively recent discoveries regarding ligand-directed signaling at the opioid receptors have called this assumption into question, indicating that similar opioid analgesics may exhibit drug-specific differences in antinociceptive function and adverse effects. The current work investigated this hypothesis by examining three commonly prescribed and abused opioids, oxycodone, hydrocodone and morphine, for drug-specific differences in their antinociceptive potency and ability to prevent injury-induced hyperalgesia, their behavioral effects on the reward-related D2 signaling system, and molecular & gene expression changes.
First, a mouse burn-injury model was developed that produced significant nociception which worsened across 28 days. Then, using this model, opioids were examined for drug-specific differences in their antinociceptive potency to treat burn pain, their ability to prevent/treat injury-induced long-term hyperalgesia, and correlations between antinociceptive potency and hyperalgesia prevention.
iii
It was found that burn injury pain per se reduced the antinociceptive potency of opioids, but no drug-specific differences existed in potency. However, drug-specific differences did exist in the ability to prevent hyperalgesia development. When examined on the individual level, it was found that greater early pain relief led to reduced long-term pain outcomes.
In addition, drug-specific differences were shown to exist in the ability to increase behavioral sensitivity of the D2DR system in both the absence and presence of burn pain, to alter intracellular signaling in both the absence and presence of D2DR agonism, and to alter gene expression levels.
These findings provide evidence of wide-spread drug-specific differences between common opioid analgesics that can carry clinically relevant implications for pain treatment, chronic pain outcomes, addiction, and other long-term outcomes resulting from opioid exposure.
Advisors/Committee Members: Eitan, Shoshana (advisor), Hook, Michelle A (committee member), Welsh, Jane (committee member), Wellman, Paul J (committee member).
Subjects/Keywords: Opioids; Drug-Specific; Ligand-directed signaling; Pain; Addiction
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Emery, M. A. (2018). Drug-Specific Differences Among the Opioid Analgesics Hydrocodone, Oxycodone and Morphine. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/173631
Chicago Manual of Style (16th Edition):
Emery, Michael A. “Drug-Specific Differences Among the Opioid Analgesics Hydrocodone, Oxycodone and Morphine.” 2018. Doctoral Dissertation, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/173631.
MLA Handbook (7th Edition):
Emery, Michael A. “Drug-Specific Differences Among the Opioid Analgesics Hydrocodone, Oxycodone and Morphine.” 2018. Web. 03 Mar 2021.
Vancouver:
Emery MA. Drug-Specific Differences Among the Opioid Analgesics Hydrocodone, Oxycodone and Morphine. [Internet] [Doctoral dissertation]. Texas A&M University; 2018. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/173631.
Council of Science Editors:
Emery MA. Drug-Specific Differences Among the Opioid Analgesics Hydrocodone, Oxycodone and Morphine. [Doctoral Dissertation]. Texas A&M University; 2018. Available from: http://hdl.handle.net/1969.1/173631

Texas A&M University
15.
Johnson, Margarete.
Development and Characterization of an In-Vitro Tissue Culture Model for Equine Laminitis.
Degree: MS, Biomedical Sciences, 2014, Texas A&M University
URL: http://hdl.handle.net/1969.1/153612
► Equine laminitis, a disease affecting the laminar tissue in the hoof, is a common and debilitating disease in horses with a significant impact on the…
(more)
▼ Equine laminitis, a disease affecting the laminar tissue in the hoof, is a common and debilitating disease in horses with a significant impact on the equine industry. Currently nearly all laminitis studies are conducted in live horses, a process that is both expensive and limited in biological replicates. Thus the development of an in vitro model for the disease is an important step in advancing laminitis research. Recent evidence suggests that apolipoprotein A-IV (apoA-IV) may be involved in the chronic form of the disease but little is known about this protein in the horse, and its effects on the laminar tissue are unknown. The primary goal of this project was to produce a model for inducing inflammation in slices of laminar tissue in culture. We tested two inflammatory agents: interleukin 6 (IL-6) and lipopolysaccharide (LPS) and measured their effect on the expression of inflammatory cytokines and seven laminitis-associated genes found to be differentially expressed in horses with induced laminitis. The second goal of the project was to test the effects of apoA-IV on
laminar tissue inflammation in our model in the presence and absence of the two inflammatory agents, and to further characterize the protein in horses by determining its sequence and expression pattern in this animal.
The laminar tissue remained alive and contamination-free over the course of the experiment, showing the viability of our culture. IL-6 did not induce changes in gene expression consistent with those found in horses with laminitis. However, the addition of LPS led to changes in cytokine expression mimicking those seen in horses with induced laminitis and increased two of the seven laminitis-associated genes. The addition of apoA-IV had no effect on laminar tissue inflammation by itself or in the presence of IL-6 or LPS. We found the highest expression of APOA4 in the liver followed by the small intestine, a pattern unique in its high hepatic contribution. A better understanding of how apoA-IV is produced and functions in horses may shed light on its role in laminitis. In the future our tissue culture model could be used in testing agents suspected of causing laminar tissue inflammation and eventually in the development and testing of potential treatments for laminitis.
Advisors/Committee Members: Chowdhary, Bhanu P (advisor), Welsh, Jane C (advisor), Janecka, Jan E (committee member), Smith, Stephen B (committee member).
Subjects/Keywords: laminitis; in vitro; culture; lps; il-6; apoa-iv
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Johnson, M. (2014). Development and Characterization of an In-Vitro Tissue Culture Model for Equine Laminitis. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/153612
Chicago Manual of Style (16th Edition):
Johnson, Margarete. “Development and Characterization of an In-Vitro Tissue Culture Model for Equine Laminitis.” 2014. Masters Thesis, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/153612.
MLA Handbook (7th Edition):
Johnson, Margarete. “Development and Characterization of an In-Vitro Tissue Culture Model for Equine Laminitis.” 2014. Web. 03 Mar 2021.
Vancouver:
Johnson M. Development and Characterization of an In-Vitro Tissue Culture Model for Equine Laminitis. [Internet] [Masters thesis]. Texas A&M University; 2014. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/153612.
Council of Science Editors:
Johnson M. Development and Characterization of an In-Vitro Tissue Culture Model for Equine Laminitis. [Masters Thesis]. Texas A&M University; 2014. Available from: http://hdl.handle.net/1969.1/153612

Texas A&M University
16.
Maldonado, Sioui.
Psychological Well-Being and Spinal Cord Injury Recovery: A Two-Way Street?.
Degree: PhD, Neuroscience, 2014, Texas A&M University
URL: http://hdl.handle.net/1969.1/153842
► Spinal cord injury (SCI) leads to increased anxiety and depression in as many as 60% of patients. Yet despite extensive clinical research focused on understanding…
(more)
▼ Spinal cord injury (SCI) leads to increased anxiety and depression in as many as 60% of patients. Yet despite extensive clinical research focused on understanding the variables influencing psychological well-being following SCI, risk factors that decrease psychological well-being remain unclear. We hypothesized that excitation of the immune system, inherent to SCI, may contribute to the decrease in well-being.
We used a battery of established behavioral tests to assess depression and anxiety in contused rats and (1) characterized psychological well-being as a function of SCI severity, (2) examined peripheral (serum) and central (hippocampi and spinal cord) inflammation in relation to psychological well-being post SCI, and (3) explored whether social enrichment, as a modulator of psychological well-being, could improve overall recovery post SCI, by housing contused animals either alone, or with an injured or an intact cagemate.
Following SCI, the contused subjects showed one of three profiles: depression-like, depression- and anxiety-like, or no signs of decreased psychological well-being. Subjects exhibiting a purely depression-like profile showed higher levels of pro-inflammatory cytokines peripherally, whereas subjects exhibiting a depression- and anxiety-like profile showed higher levels of pro-inflammatory cytokines centrally (hippocampi and spinal cord). These changes in inflammation were not associated with injury severity; suggesting that the association between inflammation and the expression of behaviors characteristic of decreased psychological well-being was not confounded by differential impairments in motor ability.
Social enrichment, in the form of group housing, did not improve psychological well-being post SCI. Depression- and anxiety-like signs were found in all group housing conditions. Unexpectedly, we found that the intact animals housed with contused subjects showed depression- and anxiety-like signs similar to those of contused subjects, indicating that their psychological well-being was affected by the presence of an injured cagemate. This is reminiscent of the caregiver effect in humans, specifically the manifestation of symptoms of depression in individuals who care for patients suffering with a chronic illness, such as SCI.
These experiments demonstrate that the depression and anxiety patients experience following spinal cord injury is not due solely to psychosocial factors, but may also, in part, result from increased immune activation following the injury.
Advisors/Committee Members: Hook, Michelle A (advisor), Meagher, Mary W (committee member), Grau, James W (committee member), Miranda, Rajesh (committee member), Welsh, Jane (committee member).
Subjects/Keywords: spinal cord injury; inflammation; HPA axis; stress; depression; anxiety; cytokines; social enrichment; caregiving
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APA (6th Edition):
Maldonado, S. (2014). Psychological Well-Being and Spinal Cord Injury Recovery: A Two-Way Street?. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/153842
Chicago Manual of Style (16th Edition):
Maldonado, Sioui. “Psychological Well-Being and Spinal Cord Injury Recovery: A Two-Way Street?.” 2014. Doctoral Dissertation, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/153842.
MLA Handbook (7th Edition):
Maldonado, Sioui. “Psychological Well-Being and Spinal Cord Injury Recovery: A Two-Way Street?.” 2014. Web. 03 Mar 2021.
Vancouver:
Maldonado S. Psychological Well-Being and Spinal Cord Injury Recovery: A Two-Way Street?. [Internet] [Doctoral dissertation]. Texas A&M University; 2014. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/153842.
Council of Science Editors:
Maldonado S. Psychological Well-Being and Spinal Cord Injury Recovery: A Two-Way Street?. [Doctoral Dissertation]. Texas A&M University; 2014. Available from: http://hdl.handle.net/1969.1/153842

Texas A&M University
17.
Gautam, Raju.
Epidemiology of Bacterial Food-borne Pathogens: Linking Intermittent Pathogen Shedding and Transmission in Their Animal Hosts.
Degree: PhD, Biomedical Sciences, 2013, Texas A&M University
URL: http://hdl.handle.net/1969.1/149510
► Most bacterial foodborne pathogens are shed intermittently from their animal hosts and are able to grow and persist in the environment. Cattle and pigs constitute…
(more)
▼ Most bacterial foodborne pathogens are shed intermittently from their animal hosts and are able to grow and persist in the environment. Cattle and pigs constitute the major animal reservoirs for these pathogens. The overall objective of this dissertation research was to improve understanding of the role of intermittent shedding and environmental persistence in the transmission and maintenance of Escherichia coli O157:H7 and Salmonella Typhimurium in their animal host populations. This objective was addressed through five interdepended studies.
The study in Chapter II, describes the transmission of E. coli O157:H7 in a dairy herd using mathematical modeling that includes indirect transmission from the contaminated environment. The model predicts that the elevated ambient temperature during summer, together with the availability of large amount of drinking water per cattle, are the major factors for increased pathogen load in water and high prevalence of E. coli O157:H7 in cattle populations. The second study, in Chapter III, determined the variation in water-to-cattle ratios among feedlot pens and evaluated the association with the pen level management and environmental factors. Water-to-cattle ratio was found to vary greatly between feedlots and pens with lower water-to-cattle ratios on average had cooler drinking water. The study in Chapter IV, used a compartmental mathematical model of infection transmission, to evaluate the effect of cleaning on Salmonella Typhimurium control in a grower-finisher pig herd. Cleaning alone was not found to be an effective measure of control unless combined with other measures to reduce the level of bacterial shedding. The study in Chapter V, developed the multi-state Markov chain model to describe the fecal shedding pattern of three E. coli O157:H7 strains in cattle. One strain was not detected to shed, while the other two strains had on average different durations of host colonization, albeit not at the statistically significant level. The study in Chapter VI, used an experimental infection transmission approach to estimate and compare transmission rates for three different strains of E. coli O157:H7 in steers. The results revealed that the transmission rate of E. coli O157:H7 increases significantly with increasing levels of environmental contamination.
Collectively, the five studies have highlighted the role of these pathogen characteristics in their transmission. The improved understanding of these characteristics will allow for better design of control measure to ensure food safety.
Advisors/Committee Members: Ivanek-Miojevic, Renata (advisor), Carroll, Raymond J (committee member), Grant, William (committee member), Welsh, Jane (committee member).
Subjects/Keywords: Intermittent shedding; environmental persistence; Escherichia coli O157:H7; Salmonella Typhimurium
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APA ·
Chicago ·
MLA ·
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Export
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APA (6th Edition):
Gautam, R. (2013). Epidemiology of Bacterial Food-borne Pathogens: Linking Intermittent Pathogen Shedding and Transmission in Their Animal Hosts. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/149510
Chicago Manual of Style (16th Edition):
Gautam, Raju. “Epidemiology of Bacterial Food-borne Pathogens: Linking Intermittent Pathogen Shedding and Transmission in Their Animal Hosts.” 2013. Doctoral Dissertation, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/149510.
MLA Handbook (7th Edition):
Gautam, Raju. “Epidemiology of Bacterial Food-borne Pathogens: Linking Intermittent Pathogen Shedding and Transmission in Their Animal Hosts.” 2013. Web. 03 Mar 2021.
Vancouver:
Gautam R. Epidemiology of Bacterial Food-borne Pathogens: Linking Intermittent Pathogen Shedding and Transmission in Their Animal Hosts. [Internet] [Doctoral dissertation]. Texas A&M University; 2013. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/149510.
Council of Science Editors:
Gautam R. Epidemiology of Bacterial Food-borne Pathogens: Linking Intermittent Pathogen Shedding and Transmission in Their Animal Hosts. [Doctoral Dissertation]. Texas A&M University; 2013. Available from: http://hdl.handle.net/1969.1/149510

Texas A&M University
18.
Jia, Qian 1980-.
n-3 PUFA and Curcumin Modulate the Resolution of Murine Intestinal Inflammtion.
Degree: PhD, Nutrition, 2011, Texas A&M University
URL: http://hdl.handle.net/1969.1/150942
► Bioactive food components containing n-3 polyunsaturated fatty acids (PUFA) and curcumin modulate multiple determinants that link inflammation to cancer initiation and progression. In this dissertation,…
(more)
▼ Bioactive food components containing n-3 polyunsaturated fatty acids (PUFA) and curcumin modulate multiple determinants that link inflammation to cancer initiation and progression. In this dissertation, both transgenic and dietary mouse models were used to elucidate the effect of n-3 PUFA and curcumin treatment on murine intestinal inflammation.
Specifically, fat-1 transgenic mice, which convert endogenous n-6 PUFA to n-3 PUFA in multiple tissues, exhibited a reduced number of colonic adenocarcinomas per mouse (1.05 plus/minus 0.29 versus 2.12 plus/minus 0.51, P = 0.033), elevated apoptosis (P = 0.03), and a decrease in n-6 PUFA–derived eicosanoids compared with wild-type (wt) mice in an azoxymethane (AOM) - dextran sodium sulfate (DSS) model.
Following a 2-week recovery period after 5 days of DSS exposure, colonic inflammation and ulceration scores returned to pretreatment levels only in fat-1 mice. In addition, fat-1 vs wt mice exhibited decreased (P < 0.05) levels of CD3 , CD4 T helper, and macrophage cell numbers in the colon. The ability of n-3 PUFA to favorably modulate the resolution of intestinal inflammation in fat-1 mice was linked to an enhancement (P < 0.05) in the percentage of colonic lamina propria (cLP) CD4 FoxP3 cells and a decrease in both splenic and cLP Th17 cells (0.8 vs 1.2 percent in spleen, 1.4 vs 1.7 percent in colon) (P < 0.05) in fat-1 mice compared to wt. These results suggest that the antitumorigenic effect of n-3 PUFA may be mediated via its anti-inflammatory properties.
The combined effect of n-3 PUFA and curcumin on DSS induced colitis was assessed in C57BL/6 mice. Addition of fish oil (FO) and/or curcumin to a corn oil (CO) based diet increased animal mortality compared to CO alone (P < 0.05). Consistently, following 1 or 2 cycles of DSS treatment, both dietary FO and curcumin promoted mucosal injury/ulceration compared to CO. However, compared to other diets, FO and curcumin combined feeding enhanced the resolution of chronic inflammation and suppressed (p < 0.05) a key inflammatory mediator, NF-kB, in colon mucosa. Mucosal microarray analysis revealed that dietary FO and curcumin differentially modulated the expression of genes induced by DSS treatment. These results suggest that dietary lipids and curcumin interact to regulate mucosal homeostasis and the resolution of chronic inflammation in the colon.
Advisors/Committee Members: Chapkin, Robert S (advisor), McMurray, David N (committee member), Tian, Yanan (committee member), Welsh, Jane (committee member).
Subjects/Keywords: Resolution; Intestinal inflammation; Curcumin; n-3 PUFA
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Export
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APA (6th Edition):
Jia, Q. 1. (2011). n-3 PUFA and Curcumin Modulate the Resolution of Murine Intestinal Inflammtion. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/150942
Chicago Manual of Style (16th Edition):
Jia, Qian 1980-. “n-3 PUFA and Curcumin Modulate the Resolution of Murine Intestinal Inflammtion.” 2011. Doctoral Dissertation, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/150942.
MLA Handbook (7th Edition):
Jia, Qian 1980-. “n-3 PUFA and Curcumin Modulate the Resolution of Murine Intestinal Inflammtion.” 2011. Web. 03 Mar 2021.
Vancouver:
Jia Q1. n-3 PUFA and Curcumin Modulate the Resolution of Murine Intestinal Inflammtion. [Internet] [Doctoral dissertation]. Texas A&M University; 2011. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/150942.
Council of Science Editors:
Jia Q1. n-3 PUFA and Curcumin Modulate the Resolution of Murine Intestinal Inflammtion. [Doctoral Dissertation]. Texas A&M University; 2011. Available from: http://hdl.handle.net/1969.1/150942

Texas A&M University
19.
Busch, Catherine Michelle.
Mapping a Gene Responsible for Natural Resistance to Rift Valley Fever Virus in Inbred Rats.
Degree: PhD, Genetics, 2015, Texas A&M University
URL: http://hdl.handle.net/1969.1/155679
► The Rift Valley Fever virus (RVFV) presents an epidemic and epizootic threat in sub-Saharan Africa, Egypt, and the Arabian Peninsula, and has recently gained attention…
(more)
▼ The Rift Valley Fever virus (RVFV) presents an epidemic and epizootic threat in sub-Saharan Africa, Egypt, and the Arabian Peninsula, and has recently gained attention as a potential weapon of bioterrorism due to its ability to infect both livestock and humans. Inbred rat strains show similar characteristic responses to the disease as humans and livestock, making them a suitable model species. Previous studies had shown differences among various inbred rat strains in susceptibility to RVFV hepatic disease, including a higher susceptibility of Wistar-Furth (WF) rats compared to a more resistant Lewis (LEW) strain. Further study revealed that this resistance trait follows the pattern of a dominant gene inherited in Mendelian fashion. A congenic WF.LEW strain resistant to infection with RVFV was derived from the susceptible WF and resistant LEW strains, and a subsequent genome scan revealed two prospective regions for the location of the gene, one on chromosome 3 and the other on chromosome 9. Subsequently, this study employed the methods of backcrossing, genotyping, viral challenges, gene expression studies, and sequencing to define a practicable region of interest and to further identify a viable candidate gene and prospective mechanism by which resistance is conferred.
A program of backcrossing WF.LEW rats to WF rats, genotyping offspring using SNPs and microsatellites, and subsequently challenging N1 litters with RVFV was used to determine that the ~2Mb region on the distal end of chromosome 3 contains the gene conferring resistance. The use of genetic markers to detect recombination in further backcross generations resulted in the identification of two recombinants in this newly established region of interest. Through RVFV challenges, the recombinants narrowed the prospective region of chromosome 3 to ~500Kb containing 20 genes. Comparative qPCR analysis of all 20 genes combined with comparative sequencing studies of the entire region between susceptible WF/NHsd rats and resistant WF.LEW rats facilitated the identification of candidate gene Rtel1 and a proposed mechanism by which resistance is conferred, which will potentially become the basis for developing new preventive measures against the virus.
Advisors/Committee Members: Womack, James E (advisor), Kraemer, Duane C (committee member), Skow, Loren C (committee member), Welsh, Jane (committee member).
Subjects/Keywords: Rift Valley Fever Virus; rats; gene mapping
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APA ·
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MLA ·
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Export
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APA (6th Edition):
Busch, C. M. (2015). Mapping a Gene Responsible for Natural Resistance to Rift Valley Fever Virus in Inbred Rats. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/155679
Chicago Manual of Style (16th Edition):
Busch, Catherine Michelle. “Mapping a Gene Responsible for Natural Resistance to Rift Valley Fever Virus in Inbred Rats.” 2015. Doctoral Dissertation, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/155679.
MLA Handbook (7th Edition):
Busch, Catherine Michelle. “Mapping a Gene Responsible for Natural Resistance to Rift Valley Fever Virus in Inbred Rats.” 2015. Web. 03 Mar 2021.
Vancouver:
Busch CM. Mapping a Gene Responsible for Natural Resistance to Rift Valley Fever Virus in Inbred Rats. [Internet] [Doctoral dissertation]. Texas A&M University; 2015. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/155679.
Council of Science Editors:
Busch CM. Mapping a Gene Responsible for Natural Resistance to Rift Valley Fever Virus in Inbred Rats. [Doctoral Dissertation]. Texas A&M University; 2015. Available from: http://hdl.handle.net/1969.1/155679
20.
Johnson, Andre.
IGF-1-Mediated Reinforcement of the Blood Brain Barrier During Ischemia-Reperfusion in Middle-Aged Female Rats.
Degree: PhD, Medical Sciences, 2019, Texas A&M University
URL: http://hdl.handle.net/1969.1/187162
► Nearly three quarters of all strokes occur in people over 65, and within this older group, strokes are more common and more severe in women…
(more)
▼ Nearly three quarters of all strokes occur in people over 65, and within this older group, strokes are more common and more severe in women than men. Added to this disease burden, is the lack of suitable therapies for stroke patients. My research focused on identifying a stroke therapy that is effective for older female stroke patients. Middle-aged female rats were used as a model system to understand disparities in stroke outcomes in middle-aged postmenopausal women. Our laboratory has shown previously that post-stroke Insulin like growth factor (IGF)-I treatment reduces blood brain barrier permeability and decreases infarct volumes in middle aged female rats. In three major experiments, this dissertation tested the hypothesis that IGF-1 acts on the endothelium to reduce neuroinflammation and improve recovery. Through Experiment 1, we found that IGF-1 treatment provided by intracerebroventricular injection, decreased extravasation of CD4+ cells into the ischemic hemisphere. Similarly, IGF-1 reduced protein transfer across a monolayer of brain microvessel endothelial cells derived from middle aged females, further implicating this cell type as the locus of IGF-1 action. Experiment 2 showed that IGF-1 stabilized the actin cytoskeleleton and adhesion of endothelial cells exposed to OGD and preserved microvessel diameter and length in vivo after stroke. Both in vivo and in vitro, IGF-1’s effects were reversed with concurrent exposure to the IGFR antagonist JB-1. Additionally, while IGF-1 treatment improved microvessel morphology in early acute phase of stroke, sensory-motor behavior was improved during both the early and late acute phase of stroke. Experiment 3 tested the novel hypothesis that IGF-1 secreted by astrocytes is neuroprotective. With age, astrocyte derived IGF-1 decreases, and by using IGF-1 gene transfer targeted to astrocytes, we found reduced stroke-induced sensory motor impairment and decreased blood brain barrier permeability, without affecting infarct volumes. Collectively, these data support and suggest that the aging endothelium and astrocyte interaction may be critical for post stroke recovery.
Advisors/Committee Members: Sohrabji, Farida (advisor), White , Brad (committee member), Welsh, Jane (committee member), Li, Jianrong (committee member).
Subjects/Keywords: Stroke; insulin-like growth factor-1
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
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APA (6th Edition):
Johnson, A. (2019). IGF-1-Mediated Reinforcement of the Blood Brain Barrier During Ischemia-Reperfusion in Middle-Aged Female Rats. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/187162
Chicago Manual of Style (16th Edition):
Johnson, Andre. “IGF-1-Mediated Reinforcement of the Blood Brain Barrier During Ischemia-Reperfusion in Middle-Aged Female Rats.” 2019. Doctoral Dissertation, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/187162.
MLA Handbook (7th Edition):
Johnson, Andre. “IGF-1-Mediated Reinforcement of the Blood Brain Barrier During Ischemia-Reperfusion in Middle-Aged Female Rats.” 2019. Web. 03 Mar 2021.
Vancouver:
Johnson A. IGF-1-Mediated Reinforcement of the Blood Brain Barrier During Ischemia-Reperfusion in Middle-Aged Female Rats. [Internet] [Doctoral dissertation]. Texas A&M University; 2019. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/187162.
Council of Science Editors:
Johnson A. IGF-1-Mediated Reinforcement of the Blood Brain Barrier During Ischemia-Reperfusion in Middle-Aged Female Rats. [Doctoral Dissertation]. Texas A&M University; 2019. Available from: http://hdl.handle.net/1969.1/187162
21.
Huie, John Russell.
The Role of Tumor Necrosis Factor-Alpha in Maladaptive Spinal Plasticity.
Degree: PhD, Psychology, 2012, Texas A&M University
URL: http://hdl.handle.net/1969.1/ETD-TAMU-2010-12-8594
► Previous work has shown that the spinal cord is capable of supporting a simple form of instrumental learning. Subjects that receive controllable shock to an…
(more)
▼ Previous work has shown that the spinal cord is capable of supporting a simple
form of instrumental learning. Subjects that receive controllable shock to an extended
hind limb will increase the duration of limb flexion over time in order to reduce net
shock exposure. Exposure to as little as 6 minutes of uncontrollable stimulation prior to
instrumental testing can elicit a long-lasting learning deficit. Prior work has suggested
that this deficit may reflect an overexcitation of spinal neurons akin to central
sensitization, and that learning is inhibited by the saturation of plasticity. The
experiments in this dissertation were designed to test the role of the cytokine tumor
necrosis factor alpha (TNFa) in the induction and expression of the deficit. It is believed
that the inflammatory properties of TNFa may mediate the excitatory processes that lead
to maladaptive spinal functioning.
Experiments 1 and 2 tested the necessity of endogenous TNFa in the deficit
produced by uncontrollable shock. These experiments showed that the inhibition of
endogenous TNFa blocks both the induction and expression of the shock-induced
deficit, suggesting a necessary role for TNFa in mediating the inhibition of spinal
learning. Conversely, Experiment 3 was designed to test the sufficiency for TNFa in producing a learning deficit. I found that treatment with exogenous TNFa undermined
spinal learning in a dose-dependent fashion, whether given immediately, or 24 hours
prior to testing. Experiment 4 demonstrated that the long-term TNFa-induced deficit is
mediated by TNFa receptor activity, as a TNF inhibitor given prior to testing blocked
the expression of this deficit.
As TNFa has been shown to be predominantly of glial origin, I next assessed the
role that glia play in the TNFa-induced deficit. Experiment 5 showed that inhibiting
glial metabolism prior to TNFa treatment blocked the capacity for TNFa to produce a
long-term deficit. Experiment 6 assessed the potential for TNFa inhibition to block the
deficit induced by lipopolysaccharide (LPS), an agent known to induce TNFa. TNFa
has also been shown to drive neural excitation by increasing the trafficking of calciumpermeable
AMPA receptors to the active zone of the post-synaptic bouton. Experiment 7
showed that selectively antagonizing these receptors prior to testing blocked the TNFa-
induced deficit, suggesting a possible post-synaptic mechanism by which TNFa exerts
its effects.
Finally, histological evidence was sought to reinforce the previous behavioral
findings. Experiment 8 used quantitative RT-PCR to assess the differential expression of
TNFa mRNA in uncontrollably shocked subjects as compared to those receiving
controllable shock and no shock. To determine concentrations of TNFa protein, an
ELISA was run in Experiment 9 comparing uncontrollably shocked subjects to
unshocked controls.
Advisors/Committee Members: Grau, James (advisor), Hook (Schapiro), Michelle (committee member), Setlow, Barry (committee member), Welsh, Jane (committee member).
Subjects/Keywords: spinal cord; instrumental learning; plasticity; cytokine
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APA ·
Chicago ·
MLA ·
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CSE |
Export
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APA (6th Edition):
Huie, J. R. (2012). The Role of Tumor Necrosis Factor-Alpha in Maladaptive Spinal Plasticity. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-2010-12-8594
Chicago Manual of Style (16th Edition):
Huie, John Russell. “The Role of Tumor Necrosis Factor-Alpha in Maladaptive Spinal Plasticity.” 2012. Doctoral Dissertation, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/ETD-TAMU-2010-12-8594.
MLA Handbook (7th Edition):
Huie, John Russell. “The Role of Tumor Necrosis Factor-Alpha in Maladaptive Spinal Plasticity.” 2012. Web. 03 Mar 2021.
Vancouver:
Huie JR. The Role of Tumor Necrosis Factor-Alpha in Maladaptive Spinal Plasticity. [Internet] [Doctoral dissertation]. Texas A&M University; 2012. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2010-12-8594.
Council of Science Editors:
Huie JR. The Role of Tumor Necrosis Factor-Alpha in Maladaptive Spinal Plasticity. [Doctoral Dissertation]. Texas A&M University; 2012. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2010-12-8594
22.
Frazier, Mallory Ann.
Social Stress Sensitizes Theiler's Virus-induced Cytokine Expresssion.
Degree: MS, Psychology, 2011, Texas A&M University
URL: http://hdl.handle.net/1969.1/ETD-TAMU-2010-08-8224
► Our laboratory has previously shown that exposure to social disruption (SDR) the week prior to Theiler’s murine encephalomyelitis virus (TMEV) infection exacerbates disease course, resulting…
(more)
▼ Our laboratory has previously shown that exposure to social disruption (SDR) the week prior to Theiler’s murine encephalomyelitis virus (TMEV) infection exacerbates disease course, resulting in increased infection-related sickness behaviors, motor impairment, CNS viral titers, and CNS inflammation. These adverse effects of SDR were prevented by ICV infusion of a neutralizing antibody to IL-6 during the stress exposure period. These findings suggest that stress-induced increases in IL-6 are necessary to exacerbate acute TMEV infection, but the exact mechanism remains unknown. This thesis tested the hypotheses that SDR up-regulates central cytokine expression, exacerbates TMEV infection through cross-sensitization of virus-induced cytokine expression, and that social rank modulates the effect of SDR.
In Experiment 1, Balb/cJ mice underwent the 0, 1, or 6 SDR sessions and were then sacrificed 0, 2, or 12 hours post SDR. Experiment 2 subjects received ICV infusions of either IL-6 neutralizing antibody or its vehicle before each of six 2 h SDR sessions or the control condition, the week prior to infection.
In Experiment 3 mice were tested for pre-existing social rank prior to SDR and infection. Results indicate that (1) SDR increases virus-induced IL-6, IL-1B, and CD11b mRNA expression in brain,that these SDR-induced increases and acute TMEV exacerbation are prevented by ICV infusion of the IL-6 neutralizing antibody during the stress exposure period, and that (2) social rank does not modulate affects of SDR but baseline anxiety does. These findings suggest that SDR exacerbates acute TMEV infection through cross-sensitization of virus-induced cytokine expression and that baseline anxiety is a significant modulator of SDR.
Advisors/Committee Members: Meagher, Mary (advisor), Welsh, Jane (committee member), Hook, Michelle (committee member).
Subjects/Keywords: Social Stress; Theiler's Virus; individual differences in stress reactivity; SDR
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MLA ·
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Export
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APA (6th Edition):
Frazier, M. A. (2011). Social Stress Sensitizes Theiler's Virus-induced Cytokine Expresssion. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-2010-08-8224
Chicago Manual of Style (16th Edition):
Frazier, Mallory Ann. “Social Stress Sensitizes Theiler's Virus-induced Cytokine Expresssion.” 2011. Masters Thesis, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/ETD-TAMU-2010-08-8224.
MLA Handbook (7th Edition):
Frazier, Mallory Ann. “Social Stress Sensitizes Theiler's Virus-induced Cytokine Expresssion.” 2011. Web. 03 Mar 2021.
Vancouver:
Frazier MA. Social Stress Sensitizes Theiler's Virus-induced Cytokine Expresssion. [Internet] [Masters thesis]. Texas A&M University; 2011. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2010-08-8224.
Council of Science Editors:
Frazier MA. Social Stress Sensitizes Theiler's Virus-induced Cytokine Expresssion. [Masters Thesis]. Texas A&M University; 2011. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2010-08-8224
23.
Holgate, Rhonda Renay.
Ethanol Targeting nELAVs: Implications for Neural Stem Cell Maturation.
Degree: PhD, Medical Sciences, 2015, Texas A&M University
URL: http://hdl.handle.net/1969.1/155025
► Neurological deficits caused by fetal exposure to ethanol remains prevalent and are recognized as a serious public health issue. The effects of fetal alcohol exposure…
(more)
▼ Neurological deficits caused by fetal exposure to ethanol remains prevalent and are recognized as a serious public health issue. The effects of fetal alcohol exposure are multifaceted and is characterized by multiple structural malformations and cognitive deficiencies, however the basic molecular mechanisms central to these defects are not thoroughly understood. A central factor in embryonic development is posttranscriptional gene regulation. Post-transcriptional regulation governs all aspects of development and is an area of vulnerability that is targeted by ethanol. nELAVs RNA binding proteins are important post transcriptional regulators involved in RNA translocation and stability. Elucidating ethanol's effects as a teratogen on these regulators their target transcripts and binding partners will enable us to implement strategies to diminish several long-term effects of fetal ethanol exposure.
Advisors/Committee Members: Miranda, Rajesh (advisor), Sohrabji, Farida (committee member), Welsh, Jane (committee member), Wilson, Emily (committee member).
Subjects/Keywords: nELAVs
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APA (6th Edition):
Holgate, R. R. (2015). Ethanol Targeting nELAVs: Implications for Neural Stem Cell Maturation. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/155025
Chicago Manual of Style (16th Edition):
Holgate, Rhonda Renay. “Ethanol Targeting nELAVs: Implications for Neural Stem Cell Maturation.” 2015. Doctoral Dissertation, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/155025.
MLA Handbook (7th Edition):
Holgate, Rhonda Renay. “Ethanol Targeting nELAVs: Implications for Neural Stem Cell Maturation.” 2015. Web. 03 Mar 2021.
Vancouver:
Holgate RR. Ethanol Targeting nELAVs: Implications for Neural Stem Cell Maturation. [Internet] [Doctoral dissertation]. Texas A&M University; 2015. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/155025.
Council of Science Editors:
Holgate RR. Ethanol Targeting nELAVs: Implications for Neural Stem Cell Maturation. [Doctoral Dissertation]. Texas A&M University; 2015. Available from: http://hdl.handle.net/1969.1/155025
24.
Guo, Fengguang.
Long Chain Fatty Acyl-Coenzyme A Synthetase as Novel Drug Targets in Cryptosporidium parvum.
Degree: PhD, Veterinary Microbiology, 2014, Texas A&M University
URL: http://hdl.handle.net/1969.1/153424
► Cryptosporidium parvum infects both humans and animals, and continues to be a significant opportunistic pathogen among AIDS patients and one of the leading diarrheal pathogens…
(more)
▼ Cryptosporidium parvum infects both humans and animals, and continues to be a significant opportunistic pathogen among AIDS patients and one of the leading diarrheal pathogens in children. Despite decades of research on cryptosporidiosis including screening hundreds of compounds in vitro and in vivo, fully effective therapeutic agents are still unavailable. The major goal of this study is to explore three long-chain fatty acyl-CoA synthetase (CpACSs) of the parasite as novel drug targets. The molecular and biological data showed that the three CpACSs genes are differently expressed in the parasite different life cycle stages and their proteins display different subcellular
distribution patterns in the parasite, suggesting that the those genes may play different biological roles in the parasite. Using recombinant proteins, we have determined detailed enzyme kinetics for CpACS1 and CpACS2, and observed that the inhibitor triacsin C could inhibit their enzyme activities with Ki in the nanomolar range. Triacsin C also effectively inhibited the growth of C. parvum parasites in vitro (IC_(50) = 136 nM). Most importantly, triacsin C effectively reduced parasite oocyst production up to 88.1% with no apparent toxicity when administered to Cryptosporidium-infected IL-12 knock-out mice at 15 mg/kg/d for one week. These observations not only validate CpACSs as a pharmacological target, but also indicate that triacsin C and analogs may be explored as potential new therapeutics against cryptosporidiosis.
Advisors/Committee Members: Zhu, Guan (advisor), Welsh, Jane (committee member), Tian, Yanan (committee member), Reddy, Sanjay (committee member).
Subjects/Keywords: Cryptosporidium parvum; cryptosporidiosis; long-chain fatty acyl-CoA synthetase; drug target; triacsin C
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APA ·
Chicago ·
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Export
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APA (6th Edition):
Guo, F. (2014). Long Chain Fatty Acyl-Coenzyme A Synthetase as Novel Drug Targets in Cryptosporidium parvum. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/153424
Chicago Manual of Style (16th Edition):
Guo, Fengguang. “Long Chain Fatty Acyl-Coenzyme A Synthetase as Novel Drug Targets in Cryptosporidium parvum.” 2014. Doctoral Dissertation, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/153424.
MLA Handbook (7th Edition):
Guo, Fengguang. “Long Chain Fatty Acyl-Coenzyme A Synthetase as Novel Drug Targets in Cryptosporidium parvum.” 2014. Web. 03 Mar 2021.
Vancouver:
Guo F. Long Chain Fatty Acyl-Coenzyme A Synthetase as Novel Drug Targets in Cryptosporidium parvum. [Internet] [Doctoral dissertation]. Texas A&M University; 2014. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/153424.
Council of Science Editors:
Guo F. Long Chain Fatty Acyl-Coenzyme A Synthetase as Novel Drug Targets in Cryptosporidium parvum. [Doctoral Dissertation]. Texas A&M University; 2014. Available from: http://hdl.handle.net/1969.1/153424
25.
Burckhardt, Heather Ann.
Incorporation of analgesics into rodent embryo transfer protocols: assessing the effects on reproductive outcomes.
Degree: MS, Laboratory Animal Medicine, 2009, Texas A&M University
URL: http://hdl.handle.net/1969.1/ETD-TAMU-1140
► Surgical embryo transfer in rodents is a common procedure in today’s research laboratory, although little is known of the effect analgesics may have on not…
(more)
▼ Surgical embryo transfer in rodents is a common procedure in today’s research
laboratory, although little is known of the effect analgesics may have on not only the
recipient female but also the embryos. Two perioperative analgesics, ketoprofen and
buprenorphine, were evaluated against a saline control in terms of number of pups born,
number of pups weaned, and whether or not a litter was born. Both a uterine approach
and an oviduct approach were evaluated. Post-surgical behavior was compared among
the three surgical animals in each group, and between the non-surgical analgesic control
and its surgical counterpart. Results indicated that ketoprofen and buprenorphine have
no effect on the number of pups born, weaned, or litters born when compared to a saline
control. Significant differences were found between the non-surgical analgesic control
and its surgical counterpart in two behavioral categories; once for ketoprofen (behavior)
and once for buprenorphine (physical condition). No other differences were found.
Advisors/Committee Members: Ihrig, Melanie M. (advisor), Kier, Ann B. (committee member), Welsh, Jane C. (committee member).
Subjects/Keywords: analgesics; mice; embryo transfer; pain
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
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APA (6th Edition):
Burckhardt, H. A. (2009). Incorporation of analgesics into rodent embryo transfer protocols: assessing the effects on reproductive outcomes. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-1140
Chicago Manual of Style (16th Edition):
Burckhardt, Heather Ann. “Incorporation of analgesics into rodent embryo transfer protocols: assessing the effects on reproductive outcomes.” 2009. Masters Thesis, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/ETD-TAMU-1140.
MLA Handbook (7th Edition):
Burckhardt, Heather Ann. “Incorporation of analgesics into rodent embryo transfer protocols: assessing the effects on reproductive outcomes.” 2009. Web. 03 Mar 2021.
Vancouver:
Burckhardt HA. Incorporation of analgesics into rodent embryo transfer protocols: assessing the effects on reproductive outcomes. [Internet] [Masters thesis]. Texas A&M University; 2009. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/ETD-TAMU-1140.
Council of Science Editors:
Burckhardt HA. Incorporation of analgesics into rodent embryo transfer protocols: assessing the effects on reproductive outcomes. [Masters Thesis]. Texas A&M University; 2009. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-1140
26.
Lungu, Gina Florentina.
Role of hypoxia and hypoxia induced factors in the development of breast cancer brain metastasis.
Degree: PhD, Veterinary Microbiology, 2009, Texas A&M University
URL: http://hdl.handle.net/1969.1/ETD-TAMU-3082
► Here we studied the role of hypoxia and hypoxia-induced factors in the development of breast cancer brain metastasis by using ENU1564, a carcinogen-induced mammary adenocarcinoma…
(more)
▼ Here we studied the role of hypoxia and hypoxia-induced factors in the
development of breast cancer brain metastasis by using ENU1564, a carcinogen-induced
mammary adenocarcinoma cell line.
We detected hypoxia noninvasively by using a novel spectroscopic photoacoustic
tomography technology (SPAT). Sprague-Dawley rats inoculated intracranially with
ENU1564, a carcinogen-induced rat mammary adenocarcinoma cell line, were imaged
with SPAT three weeks post inoculation. Proteins important for tumor angiogenesis and
invasion were detected in hypoxic brain foci identified by SPAT and were elevated
compared with control brain. We showed that HIF-1α, MMP-9, VEGF-A, and VEGFR2
(Fkl-1) protein and mRNA expression levels were higher (P < 0.05) in brain tumor tissues
compared to normal brain. We also found an increased expression of HIF-1α proteins,
MMP-9, VEGF-A and VEGFR2 mRNA and proteins in hypoxic ENU1564 cells in vitro.
We also demonstrated the involvement of PI3K-Akt pathway in hypoxic regulation of
MMP-9 and VEGF but not VEGFR2 by using specific PI3K inhibitor. Using MEK1/2 inhibitor we showed that hypoxic regulation of MMP-9, VEGF-A and VEGFR2 also
involve MEK1/2-ERK pathway.
We also investigated the effect of fibroblast growth factor-1 (FGF-1), one of the
factors known to be upregulated by hypoxia, on the expression of MMP-9 in ENU1564
cell line. We observed that FGF-1 induces an increase in MMP-9 mRNA, protein, and
activity in ENU1564 cells. Next, we investigated the role of components of PI3K-Akt and
MEK1/2-ERK signaling pathways in our system. We demonstrated that FGF-1 increases
Akt phosphorylation, triggers nuclear translocation of NF-κBp65, and enhances
degradation of cytoplasmic IκBα. Pretreatment of cells with LY294002, a PI3K inhibitor,
significantly inhibited MMP-9 protein expression in FGF-1-treated cells. Conversely, our
data showed that FGF-1 increases ERK phosphorylation in ENU1564 cells, increases c-jun
and c-fos mRNA expression in a time-dependent manner, and triggers nuclear
translocation of c-jun. Pretreatment of cells with PD98059, a MEK1/2 inhibitor
significantly inhibited MMP-9 protein expression in FGF-1 treated cells. Finally, we
observed increased DNA binding of NF-κB and AP-1 in FGF-1-treated cells and that
mutation of either NF-κB or AP-1 response elements prevented MMP-9 promoter
activation by FGF-1.
Advisors/Committee Members: Stoica, Gheorghe (advisor), Abbott, Louise (committee member), Caldwell, David (committee member), Welsh, Jane (committee member).
Subjects/Keywords: metastasis; hypoxia
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Lungu, G. F. (2009). Role of hypoxia and hypoxia induced factors in the development of breast cancer brain metastasis. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-3082
Chicago Manual of Style (16th Edition):
Lungu, Gina Florentina. “Role of hypoxia and hypoxia induced factors in the development of breast cancer brain metastasis.” 2009. Doctoral Dissertation, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/ETD-TAMU-3082.
MLA Handbook (7th Edition):
Lungu, Gina Florentina. “Role of hypoxia and hypoxia induced factors in the development of breast cancer brain metastasis.” 2009. Web. 03 Mar 2021.
Vancouver:
Lungu GF. Role of hypoxia and hypoxia induced factors in the development of breast cancer brain metastasis. [Internet] [Doctoral dissertation]. Texas A&M University; 2009. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/ETD-TAMU-3082.
Council of Science Editors:
Lungu GF. Role of hypoxia and hypoxia induced factors in the development of breast cancer brain metastasis. [Doctoral Dissertation]. Texas A&M University; 2009. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-3082
27.
Du, Christina.
Investigation of Immunoglobulin Heavy Chain Isotypes in an Ancestral Mucosal Immune Model.
Degree: MS, Laboratory Animal Medicine, 2012, Texas A&M University
URL: http://hdl.handle.net/1969.1/ETD-TAMU-2011-08-10140
► The importance of gut associated lymphoid tissues has been extensively reported in higher vertebrates, but less is known in lower vertebrates. In mammals immunoglobulin (Ig)A…
(more)
▼ The importance of gut associated lymphoid tissues has been extensively reported in higher vertebrates, but less is known in lower vertebrates. In mammals immunoglobulin (Ig)A is the primary Ig of mucosal immunity. But no IgA has been identified in cold-blooded animals. In higher vertebrates, antigen must stimulate the lymphoid tissues in the intestines to elicit an IgA response, and cytokines from CD4 positive helper T cells are required for B cell switch. It is not known if this is the case in lower vertebrates, or if T cell help evolved before or after class switch recombination between functional antibody isotypes. My study will fill in these gaps in our knowledge by comparing oral antigen inoculation relative to intraperitoneal antigen inoculation in frogs (Xenopus sp.). Oral immunization is a novel approach to eliciting immune responses in Xenopus. I propose that IgX will increase with oral inoculation compared to intraperitoneal injection. This would be the first demonstration of class switch upon oral immunization to a mucosal isotype in the first vertebrates that employs higher vertebrate Ig heavy chain switch mechanism, which would shed light on the most fundamental aspects of our humoral adaptive immune system.
Using a total Ig ELISA protocol, measuring total relative levels of IgM, there was no difference between the first three groups of orally immunized frogs compared to intraperitoneally immunized frogs. However, a response to serum IgX was seen in the first group. On the other hand, the refined Ag-specific ELISA protocol did present a significant increase in serum IgM response in frogs immunized systemically over orally immunized animals, but not an overall IgX response.
Phylogenetic analysis suggests that, contrary to initial reports, IgA evolved from IgX. With consideration of entire constant region and individual constant domain analyses as well as synteny and function, we suggest new hypotheses of vertebrate antibody evolution to be tested as immunogenetic coverage of more species continues to expand.
Advisors/Committee Members: Criscitiello, Michael (advisor), Lawhon, Sara (committee member), Welsh, Jane, Gresham, Vincent (committee member).
Subjects/Keywords: IgA; IgX; Xenopus; mucosal; immunization
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Du, C. (2012). Investigation of Immunoglobulin Heavy Chain Isotypes in an Ancestral Mucosal Immune Model. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-2011-08-10140
Chicago Manual of Style (16th Edition):
Du, Christina. “Investigation of Immunoglobulin Heavy Chain Isotypes in an Ancestral Mucosal Immune Model.” 2012. Masters Thesis, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/ETD-TAMU-2011-08-10140.
MLA Handbook (7th Edition):
Du, Christina. “Investigation of Immunoglobulin Heavy Chain Isotypes in an Ancestral Mucosal Immune Model.” 2012. Web. 03 Mar 2021.
Vancouver:
Du C. Investigation of Immunoglobulin Heavy Chain Isotypes in an Ancestral Mucosal Immune Model. [Internet] [Masters thesis]. Texas A&M University; 2012. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2011-08-10140.
Council of Science Editors:
Du C. Investigation of Immunoglobulin Heavy Chain Isotypes in an Ancestral Mucosal Immune Model. [Masters Thesis]. Texas A&M University; 2012. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2011-08-10140
28.
Covaleda Salas, Lina M.
New Insights Into the Role of Equine Infectious Anemia Virus S2 Protein in Disease Expression.
Degree: PhD, Veterinary Microbiology, 2011, Texas A&M University
URL: http://hdl.handle.net/1969.1/ETD-TAMU-2010-05-7975
► Equine infectious anemia virus (EIAV) is an important animal model to study the contribution of macrophages in viral persistence during lentiviral infections. EIAV is unique…
(more)
▼ Equine infectious anemia virus (EIAV) is an important animal model to study the
contribution of macrophages in viral persistence during lentiviral infections. EIAV is
unique amongst the lentiviruses in that it causes a rapid, rather than the very slow
disease progression, characteristic of other lentiviral infections. The accessory gene, S2,
unique to EIAV, is an important determinant in viral pathogenesis. A functional S2 gene
is required to achieve high-titer viremia and the development of disease in infected
horses. Despite its essential role, the mechanisms by which S2 influences EIAV
pathogenesis remain elusive. The goal of this research was to gain insight into the role of
S2 in pathogenesis. To accomplish this goal we: (i) Examined the effects of EIAV and
its S2 protein in the regulation of the cytokine and chemokine responses in macrophages,
(ii) Assessed the influence of EIAV infection and the effect of S2 on global gene
expression in macrophages and (iii) Identified host cellular proteins that interact with S2
as a starting point for the identification of host factors implicated in S2 function.
The results from this study provide evidence for a role of S2 in enhancing a proinflammatory
cytokine and chemokine response in infected macrophages. Specifically,
S2 enhances the expression of IL-1 alpha, IL-1 beta IL-8, MCP-2, MIP-1 beta, IP-10 and a newly
discovered cytokine, IL-34. Involvement of S2 in cytokine and chemokine dysregulation
may contribute to disease development by optimizing the host cell environment to
promote viral dissemination and replication. Microarray analyses revealed an interesting
set of differentially expressed genes upon EIAV infection. Genes affected by EIAV were
involved in the immune response, transcription, translation, cell cycle and cell survival.
Finally, we used the yeast two-hybrid system to identify S2 host cellular
interacting proteins. We identified osteosarcoma amplified 9 (OS-9) and proteasome 26S
ATPase subunit 3 (PSMC3) proteins as interacting partners of S2. Additional evidence is
needed to demonstrate the physiological relevance of these interactions in vivo.
In summary, the results from this study contribute towards our understanding of
the role S2 in disease expression and allow the formulation of new hypotheses as to the
potential mechanisms of action of S2 during EIAV infection.
Advisors/Committee Members: Payne, Susan (advisor), Ball, Judith M. (committee member), Welsh, Jane (committee member), Wilson, Van G. (committee member).
Subjects/Keywords: EIAV; Cytokines; Chemokines; Macrophage; Gene expression; Dysregulation; Real-time PCR; Microarray, Yeast two-hybrid system
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Covaleda Salas, L. M. (2011). New Insights Into the Role of Equine Infectious Anemia Virus S2 Protein in Disease Expression. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-2010-05-7975
Chicago Manual of Style (16th Edition):
Covaleda Salas, Lina M. “New Insights Into the Role of Equine Infectious Anemia Virus S2 Protein in Disease Expression.” 2011. Doctoral Dissertation, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/ETD-TAMU-2010-05-7975.
MLA Handbook (7th Edition):
Covaleda Salas, Lina M. “New Insights Into the Role of Equine Infectious Anemia Virus S2 Protein in Disease Expression.” 2011. Web. 03 Mar 2021.
Vancouver:
Covaleda Salas LM. New Insights Into the Role of Equine Infectious Anemia Virus S2 Protein in Disease Expression. [Internet] [Doctoral dissertation]. Texas A&M University; 2011. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2010-05-7975.
Council of Science Editors:
Covaleda Salas LM. New Insights Into the Role of Equine Infectious Anemia Virus S2 Protein in Disease Expression. [Doctoral Dissertation]. Texas A&M University; 2011. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2010-05-7975
29.
Lokhandwala, Shehnaz Taher.
Development of Adenovirus-vectored Prototype Vaccines for African Swine Fever Virus and Bovine Viral Diarrhea Virus.
Degree: PhD, Veterinary Pathobiology, 2017, Texas A&M University
URL: http://hdl.handle.net/1969.1/161338
► The objective of this work was to develop adenovirus-vectored prototype vaccines against two pathogens, African Swine Fever Virus (ASFV) and Bovine Viral Diarrhea Virus (BVDV),…
(more)
▼ The objective of this work was to develop adenovirus-vectored prototype vaccines against two pathogens, African Swine Fever Virus (ASFV) and Bovine Viral Diarrhea Virus (BVDV), which cause disease in two major livestock species, swine and cattle respectively.
The African Swine Fever Virus is a transboundary animal pathogen that causes a lethal hemorrhagic fever in domestic pigs. Attempts to develop a vaccine for ASFV have failed thus far. This manuscript describes the use of recombinant adenovirus to deliver two unique formulations of ASFV antigens in swine (in two separate in-vivo studies) and the subsequent evaluation of the antigen-specific antibody and cellular responses induced. The robust antigen-specific immune responses observed in both studies are promising and their protective potential will be evaluated in future efficacy studies
The Bovine Viral Diarrhea Virus is a globally prevalent pathogen that can cause severe diarrhea, respiratory disease, abortions and sometimes death in calves. Killed and modified live vaccines (MLV) for BVDV have been in use since the 1960s but are not effective due to lack of cross-protection and retention of immunosuppressive characteristics. This thesis also describes the use of the recombinant adenovirus vector to deliver a cocktail of multiple mosaic BVDV antigens in calves followed by the evaluation of protection conferred upon challenge. The prototype vaccine was more immunogenic and cross-protective (based on neutralizing antibodies) than a commercial MLV BVDV vaccine. Regarding protective efficacy, all calves immunized with prototype vaccine cleared the virus within a week post-challenge, whereas one calf that received the MLV vaccine still remained viremic. Future efficacy studies with diverse BVDV strains are required to validate the cross-protective potential of this prototype vaccine.
Advisors/Committee Members: Mwangi, Waithaka (advisor), Berghman, Luc (committee member), Criscitiello, Michael (committee member), Reddy, Sanjay (committee member), Waghela, Suryakant D (committee member), Welsh, Jane (committee member).
Subjects/Keywords: Adenovirus vectors; vaccine; ASFV, BVDV; Immunology; T-cells
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Lokhandwala, S. T. (2017). Development of Adenovirus-vectored Prototype Vaccines for African Swine Fever Virus and Bovine Viral Diarrhea Virus. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/161338
Chicago Manual of Style (16th Edition):
Lokhandwala, Shehnaz Taher. “Development of Adenovirus-vectored Prototype Vaccines for African Swine Fever Virus and Bovine Viral Diarrhea Virus.” 2017. Doctoral Dissertation, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/161338.
MLA Handbook (7th Edition):
Lokhandwala, Shehnaz Taher. “Development of Adenovirus-vectored Prototype Vaccines for African Swine Fever Virus and Bovine Viral Diarrhea Virus.” 2017. Web. 03 Mar 2021.
Vancouver:
Lokhandwala ST. Development of Adenovirus-vectored Prototype Vaccines for African Swine Fever Virus and Bovine Viral Diarrhea Virus. [Internet] [Doctoral dissertation]. Texas A&M University; 2017. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/161338.
Council of Science Editors:
Lokhandwala ST. Development of Adenovirus-vectored Prototype Vaccines for African Swine Fever Virus and Bovine Viral Diarrhea Virus. [Doctoral Dissertation]. Texas A&M University; 2017. Available from: http://hdl.handle.net/1969.1/161338

Texas A&M University
30.
Mirhosseini, Negin.
Cloning and expression of equine NF-kB2.
Degree: MS, Veterinary Microbiology, 2009, Texas A&M University
URL: http://hdl.handle.net/1969.1/ETD-TAMU-2838
► Equine infectious anemia virus (EIAV) is a macrophage-tropic retrovirus that causes persistent disease in horses and ponies. In addition to its structural proteins, EIAV encodes…
(more)
▼ Equine infectious anemia virus (EIAV) is a macrophage-tropic retrovirus that
causes persistent disease in horses and ponies. In addition to its structural proteins, EIAV
encodes four regulatory/accessory genes, tat, rev, ttm, and S2. It has been documented
EIAV S2 gene expression is essential for disease expression of EIAV. Using a yeast
two-hybrid assay, it was shown that S2 protein interacts with human NF-KB2. NF-KB2
plays a key role in the alternative or non-canonical NF-KB pathway. In order to
determine if the interaction of S2 with NF-KB2 might be relevant to equine disease, a
cDNA representing full length equine NF-KB2 was generated in our laboratory using
PCR and rapid amplification of cDNA ends. To our knowledge this is the first time that
equine NF-KB2 cDNAs have been recovered and characterized. The sequence of equine
NF-KB2 was 95% homologous to human overall, however a major difference was found
in the ankyrin repeat region where protein-protein interactions occur. Two splice
variants of equine NF-KB2 were found that correspond to splice variants of human NF-
KB2. We tested the interaction of EIAV S2 and equine NF-KB2 using the yeast two
hybrid system (Y2H) and co-immunoprecipitation. Unfortunately we were not able to
detect an interaction between EIAV S2 and equine NF-KB2 in either system. Despite this result, NF-KB2 is an important component in the immune response so we examined its
expression in equine macrophages. Moreover we were interested to know if EIAV
might affect expression levels of equine NF-KB2, as NF-KB2 is a target of other viruses.
Hence, the expression level of equine NF-KB2 was measured in uninfected and infected
primary equine monocyte- derived macrophage (eMDM). Using quantitative PCR we
determined that equine NF-KB2 gene expression is decreased in eMDM after 3 days post
plating, about the time that monocytes start to differentiate into mature macrophages.
However EIAV infection of eMDM upregulated the expression level of NF-KB2.
Advisors/Committee Members: Payne, Susan (advisor), Mwangi, Waithaka (committee member), Welsh, Jane (committee member).
Subjects/Keywords: EIAV S2; NF-KB2
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Mirhosseini, N. (2009). Cloning and expression of equine NF-kB2. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-2838
Chicago Manual of Style (16th Edition):
Mirhosseini, Negin. “Cloning and expression of equine NF-kB2.” 2009. Masters Thesis, Texas A&M University. Accessed March 03, 2021.
http://hdl.handle.net/1969.1/ETD-TAMU-2838.
MLA Handbook (7th Edition):
Mirhosseini, Negin. “Cloning and expression of equine NF-kB2.” 2009. Web. 03 Mar 2021.
Vancouver:
Mirhosseini N. Cloning and expression of equine NF-kB2. [Internet] [Masters thesis]. Texas A&M University; 2009. [cited 2021 Mar 03].
Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2838.
Council of Science Editors:
Mirhosseini N. Cloning and expression of equine NF-kB2. [Masters Thesis]. Texas A&M University; 2009. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2838
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