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Wake Forest University
1.
Marquez-Lara, Alejandro J.
INFLAMMATION AND FRACTURE HEALING: A NEW PARADIGM.
Degree: 2019, Wake Forest University
URL: http://hdl.handle.net/10339/94326 
► Inflammation plays a fundamental role in bone healing. This complex process is regulated by a myriad of cells and inflammatory mediators that create an adequate…
(more)
▼ Inflammation plays a fundamental role in bone healing. This complex process is regulated by a myriad of cells and inflammatory mediators that create an adequate environment for subsequent stages of the bone healing cascade. Despite this awareness, most of our understanding of the bone healing process derives from experimental animal models that fail to take into consideration the impact of surgical fixation on fracture healing. The ability to apply pre-clinical findings to clinical practice depends on the translational characteristics of a specific model. As such the first part of this body of work is focused on developing and describing a novel translational fracture model that accounts for surgical fixation as a separate and independent event in the fracture healing process.
Subjects/Keywords: Animal model
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APA (6th Edition):
Marquez-Lara, A. J. (2019). INFLAMMATION AND FRACTURE HEALING: A NEW PARADIGM. (Thesis). Wake Forest University. Retrieved from http://hdl.handle.net/10339/94326
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Marquez-Lara, Alejandro J. “INFLAMMATION AND FRACTURE HEALING: A NEW PARADIGM.” 2019. Thesis, Wake Forest University. Accessed October 19, 2019.
http://hdl.handle.net/10339/94326.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Marquez-Lara, Alejandro J. “INFLAMMATION AND FRACTURE HEALING: A NEW PARADIGM.” 2019. Web. 19 Oct 2019.
Vancouver:
Marquez-Lara AJ. INFLAMMATION AND FRACTURE HEALING: A NEW PARADIGM. [Internet] [Thesis]. Wake Forest University; 2019. [cited 2019 Oct 19].
Available from: http://hdl.handle.net/10339/94326.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Marquez-Lara AJ. INFLAMMATION AND FRACTURE HEALING: A NEW PARADIGM. [Thesis]. Wake Forest University; 2019. Available from: http://hdl.handle.net/10339/94326
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Alberta
2.
Alrobaiea, Saad Mohammad.
A Novel Nude Mouse Model of Hypertrophic Scarring Using
Scratched Full-Thickness Human Skin Grafts.
Degree: MS, Department of Surgery, 2015, University of Alberta
URL: https://era.library.ualberta.ca/files/c4q77fr539
► Hypertrophic scar (HTS) is a dermal form of fibroproliferative disorder that develops following deep skin injury. This dermal fibrosis can cause deformities, functional disabilities, and…
(more)
▼ Hypertrophic scar (HTS) is a dermal form of
fibroproliferative disorder that develops following deep skin
injury. This dermal fibrosis can cause deformities, functional
disabilities, and aesthetic disfigurements. The pathophysiology of
HTS is not understood due in part, to the lack of an ideal animal
model. We hypothesize that human skin with dermal wounds of a depth
known to reproducibly cause HTS once grafted onto athymic nude mice
will develop a raised elevated scar similar to HTS seen in humans.
Our aim is to develop a representative animal model of human HTS
and to explore the cellular origin of the fibrosis either locally
derived from the deep dermal human fibroblasts or from the bone
marrow derived monocytes of the mouse. Thirty-six nude mice were
grafted with full thickness human skin with deep dermal scratch
wound before or 2 weeks after grafting. The scratch on the human
skin grafts was made using a specially designed jig creates a wound
> 0.6 mm in depth which has been demonstrated to be the
depth of injury in human skin volunteers beyond which HTS
consistently develops. Deep dermal wounds in the human skin grafts
transplanted on to the dorsal surface of athymic mice were
morphologically analyzed by digital photography. Mice were
euthanized at one, two, and three months postoperatively before
histological analysis of scar thickness, collagen synthesis and
fiber orientation, mast cells, macrophages, human leukocyte
antigen-ABC, and myofibroblasts was performed. Morphologic
persistence of human fibroblasts in the raised elevated scar was
documented up to one-year post engraftment using human anti-ABC
antibodies. The mice developed red, raised, and firm scars in the
scratched xenografts with more contraction, increased recruitment
of macrophages and myofibroblasts as compared to the xenografts
without deep dermal scratch wound. Scar thickness and collagen
bundle orientation and morphology were resembled that seen in human
HTS in the deep dermal wounds within the engrafted human skin on
the dorsum of the mice. The fibrotic scars in the wounded human
skin were morphologically and histologically similar to human HTS
and human skin epithelial cells and fibroblasts persisted in the
remodelling tissues for at least one year post-engraftment. Thus,
deep dermal injury in human skin retains its profibrotic nature
after transplantation, affording a novel model for the assessment
of therapies for the treatment of human fibroproliferative
disorders of the skin.
Subjects/Keywords: Hypertrophic Scars; Animal model; Scars
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APA (6th Edition):
Alrobaiea, S. M. (2015). A Novel Nude Mouse Model of Hypertrophic Scarring Using
Scratched Full-Thickness Human Skin Grafts. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/c4q77fr539
Chicago Manual of Style (16th Edition):
Alrobaiea, Saad Mohammad. “A Novel Nude Mouse Model of Hypertrophic Scarring Using
Scratched Full-Thickness Human Skin Grafts.” 2015. Masters Thesis, University of Alberta. Accessed October 19, 2019.
https://era.library.ualberta.ca/files/c4q77fr539.
MLA Handbook (7th Edition):
Alrobaiea, Saad Mohammad. “A Novel Nude Mouse Model of Hypertrophic Scarring Using
Scratched Full-Thickness Human Skin Grafts.” 2015. Web. 19 Oct 2019.
Vancouver:
Alrobaiea SM. A Novel Nude Mouse Model of Hypertrophic Scarring Using
Scratched Full-Thickness Human Skin Grafts. [Internet] [Masters thesis]. University of Alberta; 2015. [cited 2019 Oct 19].
Available from: https://era.library.ualberta.ca/files/c4q77fr539.
Council of Science Editors:
Alrobaiea SM. A Novel Nude Mouse Model of Hypertrophic Scarring Using
Scratched Full-Thickness Human Skin Grafts. [Masters Thesis]. University of Alberta; 2015. Available from: https://era.library.ualberta.ca/files/c4q77fr539
3.
Monga, Jitender.
Antiproliferative and chemopreventive potential of acacia
catechu willd against multiorgan carcinoma.
Degree: Pharmaceutical Sciences, 2013, Jaypee University of Information Technology, Solan
URL: http://shodhganga.inflibnet.ac.in/handle/10603/14082
► Cancer or the malignancies of the cells has been considered as one of the most dreadly disease. Tissue invasiveness and metastatic spread of cancer cells…
(more)
▼ Cancer or the malignancies of the cells has been
considered as one of the most dreadly disease. Tissue invasiveness
and metastatic spread of cancer cells are liable for most of the
morbidity and mortality allied with the disease. Agents inhibit the
proliferation of cancer cells by increasing apoptosis may provide a
useful mechanistic approach to both cancer chemoprevention and
chemotherapy. However, adverse effects and resistance of many of
the anticancer agents are serious problems. In recent years, number
of natural products has gained tremendous attention because of
their ability to induce apoptosis in cancer cells. Thus, there is
sprouting interest in the use of plant based compounds to develop
safe and efficient therapeutic agents for information for their
possible application in cancer therapy. Flavonoids are a diverse
group of low molecular weight polyphenolic compounds that are
widely distributed in nature and renewed interest has been observed
in recent years in the novel and multiple activities of flavonoids.
Acacia catechu Willd. (Fabaceae) also known as ‘Khadira’ has been
used extensively as traditional medicine in India/Asia over a long
period of time. (+)-Catechin [3',4',5,7-tetrahydroxyflavan-3-ol] is
the most abundant polyphenolic flavonoid in the Acacia catechu
heartwood.
References p. 206-226
Advisors/Committee Members: Sharma, Manu.
Subjects/Keywords: Acacia Catechu; Animal Model; Carcinoma
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APA (6th Edition):
Monga, J. (2013). Antiproliferative and chemopreventive potential of acacia
catechu willd against multiorgan carcinoma. (Thesis). Jaypee University of Information Technology, Solan. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/14082
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Monga, Jitender. “Antiproliferative and chemopreventive potential of acacia
catechu willd against multiorgan carcinoma.” 2013. Thesis, Jaypee University of Information Technology, Solan. Accessed October 19, 2019.
http://shodhganga.inflibnet.ac.in/handle/10603/14082.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Monga, Jitender. “Antiproliferative and chemopreventive potential of acacia
catechu willd against multiorgan carcinoma.” 2013. Web. 19 Oct 2019.
Vancouver:
Monga J. Antiproliferative and chemopreventive potential of acacia
catechu willd against multiorgan carcinoma. [Internet] [Thesis]. Jaypee University of Information Technology, Solan; 2013. [cited 2019 Oct 19].
Available from: http://shodhganga.inflibnet.ac.in/handle/10603/14082.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Monga J. Antiproliferative and chemopreventive potential of acacia
catechu willd against multiorgan carcinoma. [Thesis]. Jaypee University of Information Technology, Solan; 2013. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/14082
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Otago
4.
Grant, Mark Wayne.
Anatomical and physiological characterization of a novel porcine model for varicose veins
.
Degree: 2012, University of Otago
URL: http://hdl.handle.net/10523/2235
► Varicose veins constitute a significant financial and social burden. Despite being well documented since Hippocrates, there is still a lack of understanding concerning both the…
(more)
▼ Varicose veins constitute a significant financial and social burden. Despite being well documented since Hippocrates, there is still a lack of understanding concerning both the underlying pathogenesis and the rationale of treatments of varicose veins. The management of varicose veins is marked by confusion and debate, which could benefit from well-designed experiments in a suitable
animal model. Especially as the current available therapies for the treatment of varicose veins is limited by their high recurrence rates.
While studying neointimal hyperplasia in arterial ends of common femoral AVF created in pig models we, at the Department of Surgery in Dunedin Hospital, observed that the pigs also developed progressive enlargement and tortuosity of the superficial veins over the medial aspect the thigh and groin. These changes in superficial veins developed into what appeared to be an extensive network of varicose veins. This novel finding has not been described to the same extent in other
animal models of venous disease. Consequently, the aim of this thesis is to further characterize a porcine
model of varicose veins.
Eleven female domesticated large white Duroc cross pigs, aged 13-14 weeks and weights 25.1- 35 kg, were used in this research project (control pigs [n=2], surgery animals [n=9]). The first
animal was used to assist in the characterisation the normal anatomy of pigs’ hind limb, the nominal saphenous vein and its relations and the sapheno- femoral junction. Each of the remaining animals had a right common femoral side to side arteriovenous fistula (AVF) fashioned by a vascular surgeon. Post-operatively the animals were assessed to document of macroscopic changes of venous vasculature, characterise the physiological changes that occur within the superficial venous system and to document any histological changes in the vessel wall.
Venous hypertension was demonstrated within the superficial varicosities, 23±11.4 mmHg at the mid point of the study, and 20±8.3 mmHg at termination, while in the control it was 4.5± 3.5 mmHg. In all but one pig with an AVF there was variation in pressure, associated with the cardiac cycle. The flow velocities also demonstrated a degree of pulsatility.
Overall there was both an intra-vessel and inter-
animal heterogeneity to the vessel walls changes seen in the veins sampled. Finding which were consistently seen included: variable neointimal formation, medial hypertrophy, fragmentation of the medial and adventitial elastic tissue, and medial and mural atrophy. Areas of greatest intimal thickness were associated with disruption of the internal elastic lamina. A variety of valvular defects were also observed with the specimens including bilateral and unilateral elongation of cusps, and valve cusp tearing.
In conclusion we describe a stable and chronic porcine AVF
model of venous insufficiency, which is simple to create and closely replicates the human condition of venous insufficiency and superficial varicose veins. The formation of an AVF between the femoral vessels…
Advisors/Committee Members: Jones, Gregory (advisor).
Subjects/Keywords: varicose;
animal;
veins;
model
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Manager
APA (6th Edition):
Grant, M. W. (2012). Anatomical and physiological characterization of a novel porcine model for varicose veins
. (Masters Thesis). University of Otago. Retrieved from http://hdl.handle.net/10523/2235
Chicago Manual of Style (16th Edition):
Grant, Mark Wayne. “Anatomical and physiological characterization of a novel porcine model for varicose veins
.” 2012. Masters Thesis, University of Otago. Accessed October 19, 2019.
http://hdl.handle.net/10523/2235.
MLA Handbook (7th Edition):
Grant, Mark Wayne. “Anatomical and physiological characterization of a novel porcine model for varicose veins
.” 2012. Web. 19 Oct 2019.
Vancouver:
Grant MW. Anatomical and physiological characterization of a novel porcine model for varicose veins
. [Internet] [Masters thesis]. University of Otago; 2012. [cited 2019 Oct 19].
Available from: http://hdl.handle.net/10523/2235.
Council of Science Editors:
Grant MW. Anatomical and physiological characterization of a novel porcine model for varicose veins
. [Masters Thesis]. University of Otago; 2012. Available from: http://hdl.handle.net/10523/2235
University of Southern California
5.
Liu, Ying.
Insights from mouse models on the origin of ovarian cancer
and its predisposing mechanisms.
Degree: PhD, Pathobiology, 2014, University of Southern California
URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/247625/rec/3508
► Ovarian cancers are the leading cause of death from gynecological cancer in the U.S. and more than 70% of the patients are diagnosed with disseminated…
(more)
▼ Ovarian cancers are the leading cause of death from
gynecological cancer in the U.S. and more than 70% of the patients
are diagnosed with disseminated disease. Thus, the ability to
detect ovarian cancer precursor lesions before they develop into
fully mature cancers would have a profound impact on the morbidity
and mortality of the disease. However, the exact site of origin of
ovarian cancer is not fully understood. The purpose of my thesis is
to develop heritable mouse models for epithelial ovarian tumors to
answer key questions regarding ovarian cancer origin and address
the underlying predisposing mechanisms. ❧ Dr. Dubeau has argued for
many years, that the currently favoured hypothesis that tumors
lesions that are currently classified ovarian epithelial tumors do
not arise from the coelomic epithelium that covers the ovary, but
from derivatives of the müllerian ducts. In order to test our
hypothesis, we generated transgenic constructs where the Müllerian
inhibiting substance type 2 receptor (Mis2r) promoter drives
expression of either β-galactosidase (Mis2r-β–Gal) or Cre
recombinase (Mis2r-Cre), we found no evidence of an embryological
link between the müllerian ducts and coelomic epithelium, however,
a segment of the renal tubules specific for the female gender might
suggest an embryological link between the müllerian ducts and renal
development. This is important not only to a development point of
view, but also helped us understand histogenesis of clear cell
ovarian carcinomas. ❧ We also created a mouse
model by
superimposing p53 knockout targeted specifically to müllerian tract
on the Brca1 mutation already present in Fshr-Cre; Brca1 flox/flox
mice. Tumors possibly from mammary glands were observed in 60% of
mice with double knockout, and they were epithelial in nature. This
model would be a useful tool to study the role of loss of function
of p53 and Brca1 in cancers relevant to ovary and mammary glands in
origin, which will further augment our understanding on human
BRCA1-mutated related cancer. ❧ The gene profiling changes between
wide type and mutant mice with Brca1 inactivation in ovarian
granulosa cells showed the gene family that was most frequently
influenced was that of olfactory receptor. We validated the
presence of olfactory receptors in mouse and human granulosa cells
and further hypothesized those olfactory receptors may play a role
in signal transduction in granulosa cells and contribute to ovarian
tumor predisposition by regulating mice estrous cycle. ❧ Our
previous work has been using homozygous Brca1 mutation in ovarian
granulosa cells to maximize the effects of Brca1 inactivation, we
also want to test our hypothesis that the effects of a heterozygous
mutation is similar due to the gene dosage effect, such as present
in human BRCA1 mutation carriers.
Advisors/Committee Members: Dubeau, Louis (Committee Chair), Taylor, Clive R. (Committee Member), Chuong, Cheng-Ming (Committee Member), Maxson, Robert E., Jr. (Committee Member).
Subjects/Keywords: ovarian cancer; animal model
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APA ·
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Manager
APA (6th Edition):
Liu, Y. (2014). Insights from mouse models on the origin of ovarian cancer
and its predisposing mechanisms. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/247625/rec/3508
Chicago Manual of Style (16th Edition):
Liu, Ying. “Insights from mouse models on the origin of ovarian cancer
and its predisposing mechanisms.” 2014. Doctoral Dissertation, University of Southern California. Accessed October 19, 2019.
http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/247625/rec/3508.
MLA Handbook (7th Edition):
Liu, Ying. “Insights from mouse models on the origin of ovarian cancer
and its predisposing mechanisms.” 2014. Web. 19 Oct 2019.
Vancouver:
Liu Y. Insights from mouse models on the origin of ovarian cancer
and its predisposing mechanisms. [Internet] [Doctoral dissertation]. University of Southern California; 2014. [cited 2019 Oct 19].
Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/247625/rec/3508.
Council of Science Editors:
Liu Y. Insights from mouse models on the origin of ovarian cancer
and its predisposing mechanisms. [Doctoral Dissertation]. University of Southern California; 2014. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/247625/rec/3508
University of Alberta
6.
Hong, Mandy.
The Effects of Docosahexaenoic Acid (DHA) Dietary
Supplementation in a Mouse Model of Stargardt-like Macular
Dystrophy (STGD3).
Degree: MS, Centre for Neuroscience, 2013, University of Alberta
URL: https://era.library.ualberta.ca/files/h702q689j
► Underlying mechanisms of how docosahexaenoic acid (DHA) might impact the progression of macular degeneration are unknown. We relied on the ELOVL4 mouse model of juvenile…
(more)
▼ Underlying mechanisms of how docosahexaenoic acid
(DHA) might impact the progression of macular degeneration are
unknown. We relied on the ELOVL4 mouse model of juvenile macular
degeneration, STGD3, to test the hypothesis that antenatal DHA
dietary supplementation (2% w/w of total fatty acid) would slow
down the progression of retinal degeneration as evidenced by
preserved function, anatomy, and DHA levels. DHA+, DHA-, and chow
diets commenced antenatally. Retina function was assessed by
electroretinogram at 1 and 3 months, while anatomical integrity and
fatty acid profiles were assessed with cross-sectional staining and
UPLC/MS/MS, respectively, at 3 months. Results showed a negative
ELOVL4 genotype effect on rod function, photoreceptor numbers, and
DHA/AA levels. Surprisingly, in transgenic retinas DHA
supplementation resulted in lower DHA levels compared to
non-supplemented. Although beneficial effects of DHA have been
reported, antenatal and 3 month postnatal supplementation is not
sufficient to elicit these effects in mice with
STGD3.
Subjects/Keywords: Docasahexaenoic Acid (DHA); Animal Model; Retinal Degeneration
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APA ·
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Manager
APA (6th Edition):
Hong, M. (2013). The Effects of Docosahexaenoic Acid (DHA) Dietary
Supplementation in a Mouse Model of Stargardt-like Macular
Dystrophy (STGD3). (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/h702q689j
Chicago Manual of Style (16th Edition):
Hong, Mandy. “The Effects of Docosahexaenoic Acid (DHA) Dietary
Supplementation in a Mouse Model of Stargardt-like Macular
Dystrophy (STGD3).” 2013. Masters Thesis, University of Alberta. Accessed October 19, 2019.
https://era.library.ualberta.ca/files/h702q689j.
MLA Handbook (7th Edition):
Hong, Mandy. “The Effects of Docosahexaenoic Acid (DHA) Dietary
Supplementation in a Mouse Model of Stargardt-like Macular
Dystrophy (STGD3).” 2013. Web. 19 Oct 2019.
Vancouver:
Hong M. The Effects of Docosahexaenoic Acid (DHA) Dietary
Supplementation in a Mouse Model of Stargardt-like Macular
Dystrophy (STGD3). [Internet] [Masters thesis]. University of Alberta; 2013. [cited 2019 Oct 19].
Available from: https://era.library.ualberta.ca/files/h702q689j.
Council of Science Editors:
Hong M. The Effects of Docosahexaenoic Acid (DHA) Dietary
Supplementation in a Mouse Model of Stargardt-like Macular
Dystrophy (STGD3). [Masters Thesis]. University of Alberta; 2013. Available from: https://era.library.ualberta.ca/files/h702q689j
University of Kansas
7.
Furness, Amanda Marie.
Neurochemical Investigation of Locally Induced Epilepsy and Subsequent Oxidative Damage Using Microdialysis Sampling.
Degree: PhD, Chemistry, 2017, University of Kansas
URL: http://hdl.handle.net/1808/26936
► The goal of this research was to develop and understand an anesthetized, multiple-seizure rat model for local epilepsy. Local seizures are not as well understood…
(more)
▼ The goal of this research was to develop and understand an anesthetized, multiple-seizure rat
model for local epilepsy. Local seizures are not as well understood as global seizures due to their specificity and unpredictability. Furthermore, patients are diagnosed with epilepsy after experiencing two or more unprovoked seizures. In this
model, two separate seizure episodes were induced by locally administering the epileptic agent 3-mercaptopropionic acid through a microdialysis probe to the CA1 region of the hippocampus. Upon development of the
model, attenuation in glutamate release was observed in the second seizure stimulation. To investigate neurochemical and biochemical pathways which may be responsible for the glutamate diminution, the perfusion fluid was spiked with either glucose, lactate, or dihydrokainic acid. Additionally, as it is well known that high levels of extracellular glutamate can result in excitotoxicity, neuronal staining was performed to determine the neuronal viability after the induction of the first seizure. It was determined that the attenuation in glutamate release in the second seizure episode was primarily due to a combination of mitochondrial starvation and cell damage. The local seizure
model was then used to correlate local seizure induction to oxidative damage. Glutathione (GSH) and malondialdehyde (MDA) were selected as biomarkers of oxidative stress. Intracellular levels GSH were up regulated and down regulated in hopes of modifying the amount of seizure induced oxidative damage. There was no statistically significant change in MDA formation with changing GSH levels; however, GSH did appear to serve as a release modifier of the redox cycle. Extracellular GSH increased significantly during the seizure induction and returned to basal after the seizure ended. This increase in extracellular GSH concentration can be accounted for by astrocytes and glial cells releasing GSH to counteract reactive oxygen species produced during the seizure. Additional experiments need to be done in order to make further conclusions; however, it is evident that there is a correlation between seizures and oxidative stress. Finally, Appendix I describes a small in vitro pharmacokinetic project using microdialysis sampling to measure plasma protein binding values of commercially available drugs with the ultimate goal of applying the technique for in vivo studies.
Advisors/Committee Members: Lunte, Susan M (advisor), Michaelis, Elias K (cmtemember), Dunn, Robert (cmtemember), Johnson, Michael (cmtemember), Rivera, Mario (cmtemember).
Subjects/Keywords: Analytical chemistry; Neurosciences; animal model; epilepsy; microdialysis
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Manager
APA (6th Edition):
Furness, A. M. (2017). Neurochemical Investigation of Locally Induced Epilepsy and Subsequent Oxidative Damage Using Microdialysis Sampling. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/26936
Chicago Manual of Style (16th Edition):
Furness, Amanda Marie. “Neurochemical Investigation of Locally Induced Epilepsy and Subsequent Oxidative Damage Using Microdialysis Sampling.” 2017. Doctoral Dissertation, University of Kansas. Accessed October 19, 2019.
http://hdl.handle.net/1808/26936.
MLA Handbook (7th Edition):
Furness, Amanda Marie. “Neurochemical Investigation of Locally Induced Epilepsy and Subsequent Oxidative Damage Using Microdialysis Sampling.” 2017. Web. 19 Oct 2019.
Vancouver:
Furness AM. Neurochemical Investigation of Locally Induced Epilepsy and Subsequent Oxidative Damage Using Microdialysis Sampling. [Internet] [Doctoral dissertation]. University of Kansas; 2017. [cited 2019 Oct 19].
Available from: http://hdl.handle.net/1808/26936.
Council of Science Editors:
Furness AM. Neurochemical Investigation of Locally Induced Epilepsy and Subsequent Oxidative Damage Using Microdialysis Sampling. [Doctoral Dissertation]. University of Kansas; 2017. Available from: http://hdl.handle.net/1808/26936
The Ohio State University
8.
Brooks, Julie Marie.
Transient Inactivation of the Neonatal Ventral Hippocampus
as a Novel Animal Model of Schizophrenia.
Degree: PhD, Psychology, 2011, The Ohio State University
URL: http://rave.ohiolink.edu/etdc/view?acc_num=osu1303918697
► Cognitive deficits are core symptoms in schizophrenia (SZ). These symptoms reflect developmental dysregulations within a distributed neural system involving the ventral hippocampus (VH), nucleus accumbens…
(more)
▼ Cognitive deficits are core symptoms in schizophrenia
(SZ). These symptoms reflect developmental dysregulations within a
distributed neural system involving the ventral hippocampus (VH),
nucleus accumbens (NAC), basal forebrain (BF), and prefrontal
cortex (PFC). We have reported that activation of NMDA receptors in
NAC results in increased acetylcholine (ACh) release in PFC but not
in other cortical regions in intact rats. This NAC-mediated
cholinergic activation may facilitate top-down regulation of
attentional processing when motivation is heightened following
increased demands. Given the importance of VH input to NAC and PFC
development, we determined the neurochemical and cognitive effects
of transiently inactivating VH projections, during development. The
first experiments determined the ability of intra-NAC NMDA
administration to increase cortical ACh release in adult rats
sustaining VH infusions of tetrodotoxin (TTX) or saline on
postnatal day 7 (PD7) or 32 (PD32). In saline control animals,
intra-NAC perfusions of NMDA (250 µM) increased ACh in the PFC.
This effect was absent in PD7 TTX infusion rats. Conversely, PD32
TTX infusion rats exhibited an NMDA-evoked increase in PFC ACh that
did not differ from controls. These data suggest an age-dependent
period during which VH inactivation impacts the maturational
development of the NAC-BFCS-PFC circuit. Moreover, identical PD7
TTX inactivation of the dorsal hippocampus or basolateral amygdala
did not affect NMDA-evoked cortical cholinergic transmission
demonstrating the necessity of developmental VH outflow in the
development of the NAC-BFCS-PFC circuit. The second set of
experiments examined the functional consequences of VH inactivation
in an attentional set-shifting task. In this task, rats are
required to solve a two-pot discrimination in order to secure a
cereal reward. Following acquisition of the discrimination, animals
are tested for several reversals, an intra-dimensional shift (IDS)
and an extra-dimensional shift (EDS). Previous studies have
demonstrated that performance is dependent upon PFC function and
patients with SZ exhibit deficits in the reversal and EDS stages of
such tasks. TTX infusions did not affect the initial acquisition or
IDS. However, TTX rats exhibited significant deficits (greater
trials to criterion) during the first reversal and EDS shift stages
when compared to control animals. These cognitive deficits were
also age-specific as rats sustaining VH infusion of TTX or saline
at PD32 exhibited comparable performance at all discrimination
stages of the task. Finally, the third set of experiments
investigated potential neurochemical correlates underlying the
cognitive flexibility impairments seen following VH inactivation
during early neonatal development. Prefrontal glutamatergic and
cholinergic neurotransmission have previously shown to contribute
to different forms of cognitive flexibility. Prefrontal cortical
infusion of the NMDA receptor antagonist MK801 in intact rats
produced TTX-like deficits in the EDS stage of the task.…
Advisors/Committee Members: Bruno, John (Advisor).
Subjects/Keywords: Behavioral Psychology; Neurosciences; schizophrenia; cognition; animal model
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APA (6th Edition):
Brooks, J. M. (2011). Transient Inactivation of the Neonatal Ventral Hippocampus
as a Novel Animal Model of Schizophrenia. (Doctoral Dissertation). The Ohio State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=osu1303918697
Chicago Manual of Style (16th Edition):
Brooks, Julie Marie. “Transient Inactivation of the Neonatal Ventral Hippocampus
as a Novel Animal Model of Schizophrenia.” 2011. Doctoral Dissertation, The Ohio State University. Accessed October 19, 2019.
http://rave.ohiolink.edu/etdc/view?acc_num=osu1303918697.
MLA Handbook (7th Edition):
Brooks, Julie Marie. “Transient Inactivation of the Neonatal Ventral Hippocampus
as a Novel Animal Model of Schizophrenia.” 2011. Web. 19 Oct 2019.
Vancouver:
Brooks JM. Transient Inactivation of the Neonatal Ventral Hippocampus
as a Novel Animal Model of Schizophrenia. [Internet] [Doctoral dissertation]. The Ohio State University; 2011. [cited 2019 Oct 19].
Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1303918697.
Council of Science Editors:
Brooks JM. Transient Inactivation of the Neonatal Ventral Hippocampus
as a Novel Animal Model of Schizophrenia. [Doctoral Dissertation]. The Ohio State University; 2011. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1303918697
9.
鮫島, 直樹.
The values of wall shear stress, turbulence kinetic energy and blood pressure gradient are associated with atherosclerotic plaque erosion in rabbits : 動脈硬化巣におけるびらん性傷害に関与する血行力学的因子の検討 : 家兎動脈硬化モデルでのコンピューターシュミレーション解析.
Degree: 博士(医学), 2014, University of Miyazaki / 宮崎大学
URL: http://hdl.handle.net/10458/4966
► 以下に掲載:Journal of Atherosclerosis and Thrombosis. 2014, 21, 8, p.831-838, doi: 10.5551/jat.23093.
Aim: To clarify the contribution of hemodynamic factors to the onset of plaque erosion…
(more)
▼ 以下に掲載:Journal of Atherosclerosis and Thrombosis. 2014, 21, 8, p.831-838, doi: 10.5551/jat.23093.
Aim: To clarify the contribution of hemodynamic factors to the onset of plaque erosion in smooth muscle cell (SMC)-rich atherosclerotic plaque.###Methods: We developed a rabbit model of SMC-rich atherosclerotic plaque with various degree of stenosis induced by incomplete ligation and generated three-dimensional models of five rabbit femoral arteries based on 130-162 serial histological cross-sections at 100-μm intervals per artery. We performed a computational blood flow simulation using the Reynolds-averaged Navier-Stokes model and calculated the wall shear stress (WSS), turbulence kinetic energy (TKE), blood pressure (BP) and blood pressure gradients (BPG) in eight sections (the inlet, the stenotic portion and areas 1, 2 and 5mm from the stenotic portion) in each rabbit. We also investigated whether the magnitude of WSS or TKE was related to the presence or absence of erosive injury by evaluating six points (the locally highest, median and lowest of WSS or TKE) in each section.###Results: The magnitudes of WSS, TKE and BPG, but not BP, correlated significantly with the extent of histologically-defined plaque erosion (WSS, r=0.55, p<0.001; TKE, r=0.53, p<0.001; BPG, r=0.61, p<0.0001, n=40). The values for WSS and TKE were significantly larger at sites with, compared to without, erosive injury (n=107 and n=119 points, respectively; both p<0.0001).###Conclusions: These results suggest that increased values of WSS, TKE and BPG considerably contribute to the onset of plaque erosion.
本論文の著作権は日本動脈硬化学会が保持しています。
Subjects/Keywords: Plaque erosion; Animal model; Computational fluid dynamics
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APA (6th Edition):
鮫島, . (2014). The values of wall shear stress, turbulence kinetic energy and blood pressure gradient are associated with atherosclerotic plaque erosion in rabbits : 動脈硬化巣におけるびらん性傷害に関与する血行力学的因子の検討 : 家兎動脈硬化モデルでのコンピューターシュミレーション解析. (Thesis). University of Miyazaki / 宮崎大学. Retrieved from http://hdl.handle.net/10458/4966
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
鮫島, 直樹. “The values of wall shear stress, turbulence kinetic energy and blood pressure gradient are associated with atherosclerotic plaque erosion in rabbits : 動脈硬化巣におけるびらん性傷害に関与する血行力学的因子の検討 : 家兎動脈硬化モデルでのコンピューターシュミレーション解析.” 2014. Thesis, University of Miyazaki / 宮崎大学. Accessed October 19, 2019.
http://hdl.handle.net/10458/4966.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
鮫島, 直樹. “The values of wall shear stress, turbulence kinetic energy and blood pressure gradient are associated with atherosclerotic plaque erosion in rabbits : 動脈硬化巣におけるびらん性傷害に関与する血行力学的因子の検討 : 家兎動脈硬化モデルでのコンピューターシュミレーション解析.” 2014. Web. 19 Oct 2019.
Vancouver:
鮫島 . The values of wall shear stress, turbulence kinetic energy and blood pressure gradient are associated with atherosclerotic plaque erosion in rabbits : 動脈硬化巣におけるびらん性傷害に関与する血行力学的因子の検討 : 家兎動脈硬化モデルでのコンピューターシュミレーション解析. [Internet] [Thesis]. University of Miyazaki / 宮崎大学; 2014. [cited 2019 Oct 19].
Available from: http://hdl.handle.net/10458/4966.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
鮫島 . The values of wall shear stress, turbulence kinetic energy and blood pressure gradient are associated with atherosclerotic plaque erosion in rabbits : 動脈硬化巣におけるびらん性傷害に関与する血行力学的因子の検討 : 家兎動脈硬化モデルでのコンピューターシュミレーション解析. [Thesis]. University of Miyazaki / 宮崎大学; 2014. Available from: http://hdl.handle.net/10458/4966
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Gothenburg / Göteborgs Universitet
10.
Bian, Li.
The role of S100A4 protein as a regulator of inflammation and bone metabolism in experimental arthritis.
Degree: 2011, University of Gothenburg / Göteborgs Universitet
URL: http://hdl.handle.net/2077/26277
► S100A4 belongs to the family of calcium-binding S100 proteins and modulates cell proliferation, cytoskeletal rearrangement, cell motility, and angiogenesis. Increased levels of S100A4 expression correlate…
(more)
▼ S100A4 belongs to the family of calcium-binding S100 proteins and modulates cell proliferation,
cytoskeletal rearrangement, cell motility, and angiogenesis. Increased levels of S100A4 expression
correlate with high incidence of metastasis of cancers. Up-regulation of S100A4 protein is
demonstrated in synovial tissue and in plasma of rheumatoid arthritis (RA) patients compared with
osteoarthritis, and the elevated expression of S100A4 is associated with increased disease activity in
patients with RA. Dichloroacetate (DCA) was shown to have a potent anti-tumour effect by
facilitating apoptosis and inhibiting proliferation. The aims of this thesis are to investigate
contributions of S100A4 in experimental models of septic arthritis and antigen-induced arthritis, and
in bone formation using S100A4KO mice. In addition, we also aim to find out the impact of DCA on
collagen type II-induced arthritis.
Our studies showed that S100A4 deficiency resulted in reduced joint inflammation and
cartilage/bone destruction in both septic and antigen-induced arthritis in mice. Additionally, in
septic arthritis, S100A4KO mice had less bone loss and showed a lower bacterial load in the kidneys.
S100A4 deficiency resulted in changed pattern of adhesion molecules. In antigen-induced arthritis,
S100A4 deficiency resulted in reduced intensity of arthritis and significantly lower frequency of bone
destruction, supported by fewer numbers of CD4+ T cells and CD19+CD5+ B cells accumulated in
synovia and spleen compared with WT mice. Smaller populations of CD4+ and CD8+ T cells in
spleen of S100A4 deficient mice were accompanied by reduced productions of INF-γ and IL-17A,
and lower expression of Th17 transcription factor RORγt. Difference in the severity of arthritis was
observed in female mice in septic arthritis and in male mice in antigen-induced arthritis. To assess the
role of sex hormone on bone, we analysed BMD in S100A4KO and WT mice. S100A4KO mice had
higher total BMD and female mice displayed more cortical bone content compared with WT mice.
Following ovariectomy (OVX), both S100A4KO and WT mice lost BMD. However, cortical bone loss
was more pronounced in S100A4KO mice than in WT supported by high CTX-I level. The loss of
trabecular bone was similar in S100A4KO and WT mice. DHEA treatment resulted in a significant
increase in the trabecular and cortical BMD both in WT and S100A4KO mice. This increase of BMD
was lower in S100A4KO mice. The collagen-type II arthritis model was employed to study the
potential effect of dichloroacetate (DCA) treatment on experimental arthritis. Our results showed
that mice treated with DCA had a slower onset of CIA, and significantly lower severity and frequency
of joint inflammation and cartilage/bone destruction compared with water-treated controls.
Moreover, DCA prevented arthritis-induced loss of cortical mineral density. The beneficial effect of
DCA was present only in female DBA/1 mice. DCA treatment on the OVX mice did not protect from
the development of arthritis, indicating that effect of DCA is…
Subjects/Keywords: S100A4; arthritis; animal model; bone; inflammation
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APA (6th Edition):
Bian, L. (2011). The role of S100A4 protein as a regulator of inflammation and bone metabolism in experimental arthritis. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/26277
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Bian, Li. “The role of S100A4 protein as a regulator of inflammation and bone metabolism in experimental arthritis.” 2011. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed October 19, 2019.
http://hdl.handle.net/2077/26277.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Bian, Li. “The role of S100A4 protein as a regulator of inflammation and bone metabolism in experimental arthritis.” 2011. Web. 19 Oct 2019.
Vancouver:
Bian L. The role of S100A4 protein as a regulator of inflammation and bone metabolism in experimental arthritis. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2011. [cited 2019 Oct 19].
Available from: http://hdl.handle.net/2077/26277.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Bian L. The role of S100A4 protein as a regulator of inflammation and bone metabolism in experimental arthritis. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2011. Available from: http://hdl.handle.net/2077/26277
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Hawaii – Manoa
11.
Ciraolo, Margeaux Faye.
A computational investigation of relational reasoning in nonhuman animals.
Degree: 2016, University of Hawaii – Manoa
URL: http://hdl.handle.net/10125/101253
► M.A. University of Hawaii at Manoa 2012.
Since Darwin (1859) suggested that all animals share a common ancestry, researchers have attempted to assess how the…
(more)
▼ M.A. University of Hawaii at Manoa 2012.
Since Darwin (1859) suggested that all animals share a common ancestry, researchers have attempted to assess how the divergence between human and nonhuman animal biology and cognition came about. Animals have a large repertoire of physical and behavioral adaptations that have afforded them the ability to overcome myriad obstacles to their existence. On the behavioral level, these adaptations are as diverse as the species that exhibit them. One merely has to select an animal species at random and do a cursory investigation in order to find many complex behaviors which make that animal a perfect fit for the environment that it inhabits. However, it is possible that the high degree to which an animal is adapted to its environment may limit that animal's ability to employ flexible behavior. For example, the digger wasp has a highly stereotypical set of behavioral steps for readying a nest. If any one of these steps is disrupted in the process of nest creation, the digger wasp will not alter its behavioral program, even if doing so would ensure the life of its offspring (Fabre, 1919). In short, the digger wasp lacks flexibility in its behavioral routine. Indeed, many animal species display rigidity in their behavior. Humans, on the other hand, appear to have much more control of their behavior as well as a flexibility that has allowed them to manipulate and change their environment. The mechanism that underlies this ability may be at the heart of what makes human and nonhuman animal cognition so qualitatively different.
Subjects/Keywords: cognition; animal cognition; computational model; relational reasoning
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Manager
APA (6th Edition):
Ciraolo, M. F. (2016). A computational investigation of relational reasoning in nonhuman animals. (Thesis). University of Hawaii – Manoa. Retrieved from http://hdl.handle.net/10125/101253
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Ciraolo, Margeaux Faye. “A computational investigation of relational reasoning in nonhuman animals.” 2016. Thesis, University of Hawaii – Manoa. Accessed October 19, 2019.
http://hdl.handle.net/10125/101253.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Ciraolo, Margeaux Faye. “A computational investigation of relational reasoning in nonhuman animals.” 2016. Web. 19 Oct 2019.
Vancouver:
Ciraolo MF. A computational investigation of relational reasoning in nonhuman animals. [Internet] [Thesis]. University of Hawaii – Manoa; 2016. [cited 2019 Oct 19].
Available from: http://hdl.handle.net/10125/101253.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Ciraolo MF. A computational investigation of relational reasoning in nonhuman animals. [Thesis]. University of Hawaii – Manoa; 2016. Available from: http://hdl.handle.net/10125/101253
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
McMaster University
12.
Nicolini, Chiara.
DEFECTIVE TrkB SIGNALING PATHWAYS IN IDIOPATHIC AUTISM.
Degree: PhD, 2016, McMaster University
URL: http://hdl.handle.net/11375/20034
► Autism is a neurodevelopmental disorder characterized by impairments in social communication and interaction and by repetitive patterns of behaviour, interests and activities. It is perhaps…
(more)
▼ Autism is a neurodevelopmental disorder characterized by impairments in social communication and interaction and by repetitive patterns of behaviour, interests and activities. It is perhaps the most common and handicapping neurological disorder of childhood and as such represents a significant public health problem and a huge burden for education and social service systems. Currently there is no diagnostic test or cure available for autism and the molecular mechanisms underlying autistic behaviour remain to be elucidated. Mutations in genes linked to autism adversely affect molecules involved in synapse development and plasticity including brain-derived neurotrophic factor receptor (TrkB) and its downstream effector mammalian target of rapamycin (mTOR), which is increased in several forms of syndromic autism.
Here, we investigated whether TrkB, mTOR and their signaling pathways are disrupted in postmortem brain tissue from subjects with idiopathic autism, that is, cases of autism without a known genetic cause and thought to be of environmental/epigenetic origin. We next further examined the contribution of defective TrkB signaling to autistic behaviour in mice exposed to the histone deacetylase inhibitor valproic acid (VPA), a well-established model of environmental/epigenetic origin of autism.
We found that TrkB signaling pathways were reduced in idiopathic autism and that these disruptions were associated with decreased excitatory postsynaptic marker PSD-95, suggesting fewer excitatory synapses. Moreover, we showed that similar molecular deficits were present in VPA-exposed mice that lacked sociability and displayed increased repetitive, stereotyped behaviour. We also determined that behavioural deficits in these mice were rescued by administration of the partial TrkB agonist LM22A-4 but not by treatment with the active tripeptide fragment of the insulin-like growth factor-1, (1-3)IGF-1. Lastly, reduced TrkB signaling in VPA-exposed mice was normalized by LM22A-4 administration combined with behavioural enrichment.
The present work provides a better understanding of the molecular mechanisms that contribute to autistic behaviour and implicates TrkB signaling in autism pathogenesis. Furthermore, these data demonstrate that molecular changes observed in brains of patients with idiopathic autism differ from syndromic forms and highlight that both too much and too little signaling can be equally disruptive. The present work also shows that maternal challenge with VPA resulted in social deficits, increased repetitive, restrictive behaviour and reduced TrkB signaling in mice, pointing to epigenetic modifications as a potential underlying mechanism of molecular and behavioural disruptions in autism. Lastly, these findings suggest that pharmacological activation of TrkB using compounds such as the partial TrkB agonist LM22A-4 might play a role in treating sociability and repetitive, perseverative behaviour in autism.
Thesis
Doctor of Philosophy (PhD)
Advisors/Committee Members: Fahnestock, Margaret, Medical Sciences (Division of Physiology/Pharmacology).
Subjects/Keywords: Autism; LM22A-4; TrkB; VPA; Animal Model
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APA (6th Edition):
Nicolini, C. (2016). DEFECTIVE TrkB SIGNALING PATHWAYS IN IDIOPATHIC AUTISM. (Doctoral Dissertation). McMaster University. Retrieved from http://hdl.handle.net/11375/20034
Chicago Manual of Style (16th Edition):
Nicolini, Chiara. “DEFECTIVE TrkB SIGNALING PATHWAYS IN IDIOPATHIC AUTISM.” 2016. Doctoral Dissertation, McMaster University. Accessed October 19, 2019.
http://hdl.handle.net/11375/20034.
MLA Handbook (7th Edition):
Nicolini, Chiara. “DEFECTIVE TrkB SIGNALING PATHWAYS IN IDIOPATHIC AUTISM.” 2016. Web. 19 Oct 2019.
Vancouver:
Nicolini C. DEFECTIVE TrkB SIGNALING PATHWAYS IN IDIOPATHIC AUTISM. [Internet] [Doctoral dissertation]. McMaster University; 2016. [cited 2019 Oct 19].
Available from: http://hdl.handle.net/11375/20034.
Council of Science Editors:
Nicolini C. DEFECTIVE TrkB SIGNALING PATHWAYS IN IDIOPATHIC AUTISM. [Doctoral Dissertation]. McMaster University; 2016. Available from: http://hdl.handle.net/11375/20034
University of Edinburgh
13.
Duprez, Jessica Anais Sybille.
Experimental vaccination for onchocerciasis and the identification of early markers of protective immunity.
Degree: PhD, 2018, University of Edinburgh
URL: http://hdl.handle.net/1842/28976
► Onchocerciasis, caused by Onchocerca volvulus remains a major public health and socio-economic problem across the tropics, despite years of mass drug administration (MDA) with Ivermectin…
(more)
▼ Onchocerciasis, caused by Onchocerca volvulus remains a major public health and socio-economic problem across the tropics, despite years of mass drug administration (MDA) with Ivermectin to reduce disease burden. Through modelling, it has been shown that elimination cannot be achieved with MDA alone and additional tools are needed, such as vaccination, which remains the most cost-effective tool for long-term disease control. The feasibility behind vaccination against O. volvulus can be demonstrated in the Litomosoides sigmodontis mouse model, which shows that vaccine induced protection can be achieved with immunisation using irradiated L3, the infective stage of L. sigmodontis and with microfilariae (Mf), the transmission stage of the parasite. There is further evidence of protective immunity in humans, with individuals living in endemic areas that show no signs of infection despite being exposed to the parasite (endemic normal). The protective efficacy of promising vaccine candidates were evaluated using an immunisation time course in the L. sigmodontis model, using either DNA plasmid or peptide vaccines. In immunisation experiments in L. sigmodontis, Mf numbers are used as a measure of protection and marks the end of an immunisation time course. However, when changes in gene expression were measured at the end of an immunisation time course, in attempts to identify gene signatures that could be used as markers of protection (correlates of protection) in the blood, no gene signatures were found to be associated with protection. This suggest that at the end of an immunisation time course, when protection is measured (change in Mf numbers), it is too late in infection to measure changes in immune pathways being triggered. Changes in gene expression were therefore measured in blood samples collected throughout an immunisation time course in the L. sigmodontis model, in order to identify the time point in an immunisation experiment which are the most indicative of protection. Two independent immunisation time courses were used, either using irradiated L3 or Mf as vaccine against L. sigmodontis, as these elicit the greatest protection. This generated a large high dimensional dataset, that was too large and complex for a differential fold-change analysis. Therefore, an analysis pipeline was created using machine learning algorithms, to detect changes in gene expression throughout the time courses to detect markers of protection. The 6 hour time point following immunisation showed the greatest change in gene expression, with the analysis pipeline identifying known pathways associated with vaccine-induced immunity. The pipeline was applied to gene expression data from human samples obtained from individuals living in endemic areas who were either infected with O. volvulus or endemic normal (naturally protected), this was to identify pathways associated with protective immunity in humans. When comparing vaccine induced immunity seen in mice and natural protective immunity in humans there was some overlap in pathways being…
Subjects/Keywords: onchocerciasis; river blindness; vaccination time; animal model
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APA (6th Edition):
Duprez, J. A. S. (2018). Experimental vaccination for onchocerciasis and the identification of early markers of protective immunity. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/28976
Chicago Manual of Style (16th Edition):
Duprez, Jessica Anais Sybille. “Experimental vaccination for onchocerciasis and the identification of early markers of protective immunity.” 2018. Doctoral Dissertation, University of Edinburgh. Accessed October 19, 2019.
http://hdl.handle.net/1842/28976.
MLA Handbook (7th Edition):
Duprez, Jessica Anais Sybille. “Experimental vaccination for onchocerciasis and the identification of early markers of protective immunity.” 2018. Web. 19 Oct 2019.
Vancouver:
Duprez JAS. Experimental vaccination for onchocerciasis and the identification of early markers of protective immunity. [Internet] [Doctoral dissertation]. University of Edinburgh; 2018. [cited 2019 Oct 19].
Available from: http://hdl.handle.net/1842/28976.
Council of Science Editors:
Duprez JAS. Experimental vaccination for onchocerciasis and the identification of early markers of protective immunity. [Doctoral Dissertation]. University of Edinburgh; 2018. Available from: http://hdl.handle.net/1842/28976
University of Edinburgh
14.
Siemienowicz, Katarzyna Joanna.
Fetal programming of adult disease : causes and consequences of metabolic dysregulation in an ovine model of PCOS.
Degree: PhD, 2018, University of Edinburgh
URL: http://hdl.handle.net/1842/28977
► Polycystic ovary syndrome (PCOS) is a common and complex endocrine condition with reproductive and metabolic complications, affecting up to 10% of reproductive-age women. Hyperandrogenemia, ovulatory…
(more)
▼ Polycystic ovary syndrome (PCOS) is a common and complex endocrine condition with reproductive and metabolic complications, affecting up to 10% of reproductive-age women. Hyperandrogenemia, ovulatory dysfunction, and luteinising hormone hypersecretion are characteristic traits of PCOS however, it seems that the most concerning long-term key issues are metabolic problems associated with the syndrome, such as hyperinsulinemia, insulin resistance, obesity, dyslipidaemia and non-alcoholic liver disease. Despite the numerous studies on PCOS, its origin and pathophysiology are still not fully understood. However, there is increasing evidence that the adult PCOS phenotype is programmed in fetal life by androgen excess. Exposure to increased levels of testosterone in utero in rodents, sheep and monkeys result in adult reproductive and metabolic pathologies that parallel those seen in PCOS women. Since hyperandrogenemia is a hallmark of PCOS and daughters of PCOS mothers have elevated levels of androgens at birth, it is likely that prenatal androgenisation during early life predispose to the future development of PCOS. Animal models of PCOS provide an opportunity to examine the developmental aetiology and molecular mechanisms underlying the pathogenesis of this condition. Over last 10 years our lab has successfully utilised a well-established ovine model of PCOS, where pregnant ewes were treated with testosterone propionate (TP) through mid-gestation. From this model, we had a large sample bank of fixed and frozen tissues from the fetal, lamb and adolescent prenatally androgenised animals that allowed to carry a broad range of experiments. In addition, a new cohort of prenatally androgenised adult sheep enabled additional in vivo analysis. Past research documented that prenatal androgenisation result in hyperinsulinemia with altered pancreas structure and function, and early fatty liver without difference in body weight in adolescent sheep. This thesis examines the effects and consequences of increased in utero androgen exposure on metabolic dysregulation in adolescent and adult female sheep. During puberty, but not fetal or early life, there was decreased adipogenesis in subcutaneous adipose tissue (SAT), but not visceral adipose tissue (VAT), accompanied by decreased circulating concentrations of fibroblast growth factor 21 (FGF21), leptin and adiponectin, and increased concentrations of fasting free fatty acids (FFA) in prenatally androgenised sheep. This was countered by upregulated expression of FFA transporters in liver. As adults, TP-exposed animals had increased body weight, elevated fasting insulin and FFA concentrations but normal FGF21, leptin and adiponectin levels. Histological analysis revealed that adult TP-exposed animals had SAT hypertrophy, which was associated with increased expression of inflammatory markers and correlated with increased fasting FFA. Therefore, it is likely that impaired preadipocyte differentiation in SAT during adolescence resulted in hypertrophy and inflammation of adult SAT. This…
Subjects/Keywords: polycystic ovary syndrome; PCOS; androgen; animal model
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APA (6th Edition):
Siemienowicz, K. J. (2018). Fetal programming of adult disease : causes and consequences of metabolic dysregulation in an ovine model of PCOS. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/28977
Chicago Manual of Style (16th Edition):
Siemienowicz, Katarzyna Joanna. “Fetal programming of adult disease : causes and consequences of metabolic dysregulation in an ovine model of PCOS.” 2018. Doctoral Dissertation, University of Edinburgh. Accessed October 19, 2019.
http://hdl.handle.net/1842/28977.
MLA Handbook (7th Edition):
Siemienowicz, Katarzyna Joanna. “Fetal programming of adult disease : causes and consequences of metabolic dysregulation in an ovine model of PCOS.” 2018. Web. 19 Oct 2019.
Vancouver:
Siemienowicz KJ. Fetal programming of adult disease : causes and consequences of metabolic dysregulation in an ovine model of PCOS. [Internet] [Doctoral dissertation]. University of Edinburgh; 2018. [cited 2019 Oct 19].
Available from: http://hdl.handle.net/1842/28977.
Council of Science Editors:
Siemienowicz KJ. Fetal programming of adult disease : causes and consequences of metabolic dysregulation in an ovine model of PCOS. [Doctoral Dissertation]. University of Edinburgh; 2018. Available from: http://hdl.handle.net/1842/28977
University of Edinburgh
15.
Greenhalgh, Stephen Nicholas.
Cellular and molecular mechanisms of liver regeneration.
Degree: PhD, 2017, University of Edinburgh
URL: http://hdl.handle.net/1842/28846
► Improved understanding of how the liver regenerates would be of great value, particularly given the dearth of therapies for end-stage liver disease. Currently, the only…
(more)
▼ Improved understanding of how the liver regenerates would be of great value, particularly given the dearth of therapies for end-stage liver disease. Currently, the only effective treatment for total liver failure is transplantation. Such an invasive, costly and specialised intervention is unable to address the enormous global impact from diseases of the liver. Ironically, the liver has the greatest regenerative potential of any organ in the mammalian body. However, this capacity for repair is overwhelmed in the face of massive or repeated injury. Understanding the key factors driving or inhibiting successful liver regeneration offers the potential for novel, targeted therapies to promote regeneration of a patient’s own liver. Animal models are widely used when studying complex, dynamic, multicellular processes such as liver injury and regeneration. Continued progress in transgenic modification of mice, combined with ongoing advances in microscopy techniques, means that the opportunity now exists to observe labelled cells, and subcellular structures, in real time and in vivo, with previously unobtainable resolution and fidelity. Not only does this afford the opportunity for novel insights into both normal physiology and the response to injury or disease, it can vastly expand the amount of biologically relevant information that can be obtained from each experimental animal. Hence, it is possible to advance scientific knowledge and reduce experimental animal use simultaneously. This thesis examines the role of αv integrins in liver regeneration. Integrins are expressed on the surface of cells and can perform a range of functions, including signalling and extracellular matrix adhesion. The most well-characterised role for αv integrins is activation of transforming growth factor beta, a molecule which has been shown to inhibit hepatocyte proliferation and liver regeneration. Partial hepatectomy was used as an experimental model of liver injury and regeneration. It was performed in mice, in which one or more αv integrins had been genetically depleted from specific cell types in the liver, namely hepatocytes, hepatic stellate cells or liver sinusoidal endothelial cells. These investigations revealed that depletion of integrin αvβ8 from hepatocytes led to increased hepatocyte proliferation and accelerated liver regeneration. The possible mechanisms through which hepatocyte integrin αvβ8 may exert its braking effect on liver regeneration following injury were also explored. In parallel, a novel experimental system to permit intravital multiphoton microscopy of the regenerating liver following partial hepatectomy in mice was developed and validated. Intravital imaging of mouse liver was performed with a range of cellular labels, combined with a fluorescent cell cycle reporter and label-free imaging modalities. This demonstrated the enormous potential of the system to study the dynamics of hepatocytes and non-parenchymal cells in the regenerative niche, reconstruct the sinusoidal vascular network in three dimensions during…
Subjects/Keywords: av integrins; liver regeneration; animal model
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APA (6th Edition):
Greenhalgh, S. N. (2017). Cellular and molecular mechanisms of liver regeneration. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/28846
Chicago Manual of Style (16th Edition):
Greenhalgh, Stephen Nicholas. “Cellular and molecular mechanisms of liver regeneration.” 2017. Doctoral Dissertation, University of Edinburgh. Accessed October 19, 2019.
http://hdl.handle.net/1842/28846.
MLA Handbook (7th Edition):
Greenhalgh, Stephen Nicholas. “Cellular and molecular mechanisms of liver regeneration.” 2017. Web. 19 Oct 2019.
Vancouver:
Greenhalgh SN. Cellular and molecular mechanisms of liver regeneration. [Internet] [Doctoral dissertation]. University of Edinburgh; 2017. [cited 2019 Oct 19].
Available from: http://hdl.handle.net/1842/28846.
Council of Science Editors:
Greenhalgh SN. Cellular and molecular mechanisms of liver regeneration. [Doctoral Dissertation]. University of Edinburgh; 2017. Available from: http://hdl.handle.net/1842/28846
University of Otago
16.
Hegan, William Matthew.
Gambling Behaviour in Pigeons: Toward an Animal Model of Gambling
.
Degree: 2011, University of Otago
URL: http://hdl.handle.net/10523/1646
► The gambling addiction is a destructive impulse control disorder that leaves families destitute and lives in ruins. The treatment and pathology of gambling has become…
(more)
▼ The gambling addiction is a destructive impulse control disorder that leaves families destitute and lives in ruins. The treatment and pathology of gambling has become a popular area of research, reflected in national media campaigns here in New Zealand. Studies suggest that there are prefrontal activation differences in problem gamblers compared to healthy volunteers, areas involved with decision making and reward.
Animal research has begun to investigate an
animal model of gambling, with some studies showing behavioural similarities between animals and humans when playing gambling tasks.
The current thesis sought to further investigate an
animal model of gambling, performing two experiments using a slot machine task. Experiment 1 was an investigation into the neural basis of gambling, examining the behaviour of single neurons in the avian NCL, an equivalent to the mammalian prefrontal cortex. Four pigeons (Columba livia) served as subjects and played a touch screen slot machine task, similar to a slot machine found in any casino. Pigeons were required to peck an upright arm to initiate each trial, and then peck four rolling tumblers in succession from left to right. If four identical stimuli appeared, then a wheat reward was won. During the task, activity from single NCL neurons was recorded. Four neuronal types were found to correlate with gambling related behaviour: Reward Proximity neurons, I-Won neurons, I-Lost neurons and Near Win neurons. In addition pigeons were split into two groups with one group trained for a short (one month) and long (four month) period, in an attempt to mimic naive and problem gamblers. It was hypothesised that due to prolonged training the two groups would differ in the amount and magnitude of firing of these neurons. Results showed no statistical difference between groups in either amount of gambling neurons or magnitude of firing. Behavioural data were also collected and it was hypothesised that all birds would show evidence of a post reinforcement pause, something our results confirmed.
Experiment 2 investigated whether pigeons, similar to humans, show a preference to play slot machines with higher near win ratios. Four pigeons were again tested on a touch screen slot machine task, required to play on two different ‘machines’ differentiated by different coloured backgrounds. It was hypothesised that when pigeons were given a choice, they would choose the machine that had the higher percentage of near win trials. Our results did not show evidence of any preference, and it was concluded that the near win effect may not be replicable in animals.
In conclusion, the current thesis demonstrates that neurons in the avian NCL code for gambling behaviours while pigeons play a slot machine task. Although an analogue of slot machine gambling may be found in animals, our findings suggest gambling characteristics such as the near win effect may not be replicable. The current findings provide a base for further research to investigate an
animal model of gambling.
Advisors/Committee Members: Colombo, Michael (advisor).
Subjects/Keywords: Gambling Research;
Gambling;
Avian;
Pigeon;
Animal Model
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APA (6th Edition):
Hegan, W. M. (2011). Gambling Behaviour in Pigeons: Toward an Animal Model of Gambling
. (Masters Thesis). University of Otago. Retrieved from http://hdl.handle.net/10523/1646
Chicago Manual of Style (16th Edition):
Hegan, William Matthew. “Gambling Behaviour in Pigeons: Toward an Animal Model of Gambling
.” 2011. Masters Thesis, University of Otago. Accessed October 19, 2019.
http://hdl.handle.net/10523/1646.
MLA Handbook (7th Edition):
Hegan, William Matthew. “Gambling Behaviour in Pigeons: Toward an Animal Model of Gambling
.” 2011. Web. 19 Oct 2019.
Vancouver:
Hegan WM. Gambling Behaviour in Pigeons: Toward an Animal Model of Gambling
. [Internet] [Masters thesis]. University of Otago; 2011. [cited 2019 Oct 19].
Available from: http://hdl.handle.net/10523/1646.
Council of Science Editors:
Hegan WM. Gambling Behaviour in Pigeons: Toward an Animal Model of Gambling
. [Masters Thesis]. University of Otago; 2011. Available from: http://hdl.handle.net/10523/1646
17.
Caulder, Erin.
Metabotropic glutamate receptors as targets for antiepileptic drug therapy: a behavioral and electroencephalographic analysis.
Degree: 2013, Wake Forest University
URL: http://hdl.handle.net/10339/38534
► Epilepsy is a relatively common neurological disorder that involves recurrent seizures thought to be caused by an imbalance in the excitatory and inhibitory systems in…
(more)
▼ Epilepsy is a relatively common neurological disorder that involves recurrent seizures thought to be caused by an imbalance in the excitatory and inhibitory systems in the brain, in favor of excitation. Unfortunately, some types of epilepsy have drug resistance rates of up to 40%. Classically, targets for antiepileptic drugs have included glutamatergic ion channels. However, interfering with excitatory signalling at these channels can alter normal neural communication and can have negative side effects, including cognitive dysfunction and fatigue, which are among the most common complaints from patients. Given the high rate of drug-resistant patients, and the high rate of deleterious side effects, there is an obvious need to develop novel drugs with novel targets and mechanisms of action. Compounds targeting metabotropic glutamate receptors (mGluRs; specifically mGlur2 and 3) have shown promise in other hyperexcitatory neural disorders, and some have shown efficacy in models of epilepsy as well. The goal of these studies was to demonstrate a conclusive behavioral effect of particular mGluR active compounds in reducing the severity of seizures associated with two models of epilepsy. Both models that were used are models of generalized seizure, although one is characterized by convulsive seizures (pilocarpine model) and the other is characterized by the lack of convulsive seizure, or an "absence" seizure (GBL model). Mice were given mGluR2/3 active drugs either before or after seizure onset and behavioral observations relating to seizure were measured. In some cases, the mice had been implanted with tethered EEG devices to record neural activity that coincided with behavioral observations and measures. It was demonstrated that in generalized models of seizure, mGluR2/3 active agonists had some efficacy at reducing seizure severity. The effect of modulators at mGluR2 was also investigated. One in particular, CBiPES had a modest but significant effect in reducing the behavioral severity of pilocarpine induced seizures, but not of GBL induced seizures. In conclusion, mGluR2/3 remains a valid target for antiepileptic drug development. The ideal compound would yield higher response rates for patients while boasting a minimal negative side effect profile.
Subjects/Keywords: animal model
…considered a valid model of absense:
the behavior of the epileptic animal is similar to epileptic… …seizure) has been used in animals as a model of epilepsy for decades (Racine,
1978… …involved in epileptogenesis and in seizures are
relatively well known and understood. Animal… …rodent model
systems offers many theories. Epileptic seizures can result in the excitotoxic… …support the epileptogenic process in the
human and experimental animal brain.
2. Channelopathies…
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APA (6th Edition):
Caulder, E. (2013). Metabotropic glutamate receptors as targets for antiepileptic drug therapy: a behavioral and electroencephalographic analysis. (Thesis). Wake Forest University. Retrieved from http://hdl.handle.net/10339/38534
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Caulder, Erin. “Metabotropic glutamate receptors as targets for antiepileptic drug therapy: a behavioral and electroencephalographic analysis.” 2013. Thesis, Wake Forest University. Accessed October 19, 2019.
http://hdl.handle.net/10339/38534.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Caulder, Erin. “Metabotropic glutamate receptors as targets for antiepileptic drug therapy: a behavioral and electroencephalographic analysis.” 2013. Web. 19 Oct 2019.
Vancouver:
Caulder E. Metabotropic glutamate receptors as targets for antiepileptic drug therapy: a behavioral and electroencephalographic analysis. [Internet] [Thesis]. Wake Forest University; 2013. [cited 2019 Oct 19].
Available from: http://hdl.handle.net/10339/38534.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Caulder E. Metabotropic glutamate receptors as targets for antiepileptic drug therapy: a behavioral and electroencephalographic analysis. [Thesis]. Wake Forest University; 2013. Available from: http://hdl.handle.net/10339/38534
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Manchester
18.
Oladipo, Joanna Margaret.
The development and validation of a maternal immune
activation (mIA) animal model relevant to neurodevelopmental
disorders: A focus towards Autism Spectrum Disorder
(ASD).
Degree: 2018, University of Manchester
URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:313214
► Autism spectrum disorder (ASD) is a pervasive neurodevelopmental disorder (NDD) which, despite much research, is not well understood. The heterogeneity of ASD patient cohorts supports…
(more)
▼ Autism spectrum disorder (ASD) is a pervasive
neurodevelopmental disorder (NDD) which, despite much research, is
not well understood. The heterogeneity of ASD patient cohorts
supports the hypothesis of complex interactions of genetic and
environmental mechanisms in its aetiology and severity. The
presence of gastrointestinal (GI) disturbances in ASD patients that
disrupt the bi-directional signalling of the gut-brain axis,
suggest that this may play a role in the manifestation of ASD
phenotypes. There is also accumulating evidence for the role of
neuroinflammatory processes, in both pregnant mother and affected
offspring, in the aetiology of NDDs. The increased risk of ASD
following infection during pregnancy highlights maternal immune
activation (mIA) as a key
animal model for NDDs (notably for
schizophrenia and ASD) where relevant behavioural phenotypes
manifest in the offspring of mIA dams. ASD remains a poorly managed
NDD, with no evidence-based therapies for prevention or treatment
currently available. Validating new mIA models and refining current
methods is vital to the development of new therapeutic strategies.
This thesis has explored the development of an mIA
model to test
the maternal infection hypothesis using exposure to the viral
mimetic polyinosinic-polycytidylic acid (poly (I:C)) administered
mid-way through pregnancy (gestational day (GD) 12.5) in rats.
First, the acute effects of poly (I:C) in non-pregnant female rats
were investigated, providing a validation of the experimental
methods (strain, route of administration and dose). Separate
cohorts of Wistar rats were then used in the GD12.5 mIA
model and
the physiological responses to 10 mg/kg i.p. poly (I:C) measured.
Various measures including elevation of plasma IL-6 and changes in
core body temperature were found to be variable between treated
dams. These results confirmed the need to standardise analysis of
mIA in dams, to correlate maternal inflammation with subsequent
offspring outcomes such as phenotype and neuronal development
changes. Poly (I:C) batch differences were also thought to
contribute to these variable results and refinement of mIA methods
are proposed. Longitudinal effects of mIA on offspring of both
sexes were investigated including their developmental trajectory
measuring specific gene expression, morphology at GD21 and
post-natal day (PD) 21, and behavioural phenotyping at adolescence
and adulthood. Gestational and early postnatal changes in offspring
following mIA have yet to be systematically explored. Gene
expression analysis at GD21 and PD21 in offspring shows that this
mIA
model is useful for the identification of early developmental
changes relevant to NDDs. Moreover, analysis of gene expression
changes related to synaptic function, glial cells and blood-brain
barrier integrity demonstrated that changes were dependent on both
sex and brain region of interest. This confirms the need to include
both sexes of offspring and inclusion of different brain regions
for analysis which is a common limitation of previous…
Advisors/Committee Members: MIYAN, JALEEL JA, HARTE, MICHAEL MK, Neill, Joanna, Miyan, Jaleel, Harte, Michael.
Subjects/Keywords: maternal immune activation; neurodevelopmental; animal model
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APA ·
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Export
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Manager
APA (6th Edition):
Oladipo, J. M. (2018). The development and validation of a maternal immune
activation (mIA) animal model relevant to neurodevelopmental
disorders: A focus towards Autism Spectrum Disorder
(ASD). (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:313214
Chicago Manual of Style (16th Edition):
Oladipo, Joanna Margaret. “The development and validation of a maternal immune
activation (mIA) animal model relevant to neurodevelopmental
disorders: A focus towards Autism Spectrum Disorder
(ASD).” 2018. Doctoral Dissertation, University of Manchester. Accessed October 19, 2019.
http://www.manchester.ac.uk/escholar/uk-ac-man-scw:313214.
MLA Handbook (7th Edition):
Oladipo, Joanna Margaret. “The development and validation of a maternal immune
activation (mIA) animal model relevant to neurodevelopmental
disorders: A focus towards Autism Spectrum Disorder
(ASD).” 2018. Web. 19 Oct 2019.
Vancouver:
Oladipo JM. The development and validation of a maternal immune
activation (mIA) animal model relevant to neurodevelopmental
disorders: A focus towards Autism Spectrum Disorder
(ASD). [Internet] [Doctoral dissertation]. University of Manchester; 2018. [cited 2019 Oct 19].
Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:313214.
Council of Science Editors:
Oladipo JM. The development and validation of a maternal immune
activation (mIA) animal model relevant to neurodevelopmental
disorders: A focus towards Autism Spectrum Disorder
(ASD). [Doctoral Dissertation]. University of Manchester; 2018. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:313214
Vanderbilt University
19.
Mergy, Marc Andrew.
Generation and Characterization of the First Construct-Valid Model of ADHD, the DAT Val559 Knock-In Mouse.
Degree: PhD, Neuroscience, 2013, Vanderbilt University
URL: http://etd.library.vanderbilt.edu/available/etd-11192013-140238/
;
► Attention-deficit/hyperactivity disorder (ADHD) is the most commonly diagnosed childhood neuropsychiatric disorder. More than twenty years of genetic, behavioral, and pharmacological research support the hypothesis that…
(more)
▼ Attention-deficit/hyperactivity disorder (ADHD) is the most commonly diagnosed childhood neuropsychiatric disorder. More than twenty years of genetic, behavioral, and pharmacological research support the hypothesis that compromised brain dopamine (DA) signaling impacts risk for the disorder. To date, however, evidence for this idea is indirect, and we therefore lack a construct-valid
animal model for ADHD. To gain direct evidence for changes in DA-regulatory molecules in ADHD, we screened subjects with a DSM-IV diagnosis of the disorder and identified multiple, rare DA transporter (DAT, SLC6A3) coding variants. One of these variants, DAT Val559, induces anomalous, non-vesicular DA release in transfected cells, and efflux that can be blocked by the most common ADHD medications, D-amphetamine (AMPH) and methylphenidate. To pursue the significance of these findings in vivo, we engineered DAT Val559 knock-in mice and, as with heterologous expression studies, found the variant to support expression of wild-type (WT) levels of striatal DAT and tyrosine hydroxylase (TH) protein, as well as DA and DA metabolite levels. However, DAT Val559 mice exhibited a novel, conditional hyperactivity phenotype, âdartingâ, as well as an impaired sensitivity to the locomotor-activating properties of AMPH. In vivo microdialysis studies in the striatum of DAT Val559 animals demonstrated a pronounced elevation of basal, extracellular DA levels along with a significantly blunted efflux of DA release evoked by locally infused AMPH. Together, our studies confirm a functional impact on extracellular DA homeostasis of the DAT Val559 variant in vivo and establish the first construct-valid
animal model of ADHD.
Advisors/Committee Members: Eric Delpire (chair), Randy Blakely (chair), Hassane Mchaourab (committee member), Aurelio Galli (committee member).
Subjects/Keywords: transporter; dopamine; ADHD; transgenic; mouse; animal model
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APA (6th Edition):
Mergy, M. A. (2013). Generation and Characterization of the First Construct-Valid Model of ADHD, the DAT Val559 Knock-In Mouse. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-11192013-140238/ ;
Chicago Manual of Style (16th Edition):
Mergy, Marc Andrew. “Generation and Characterization of the First Construct-Valid Model of ADHD, the DAT Val559 Knock-In Mouse.” 2013. Doctoral Dissertation, Vanderbilt University. Accessed October 19, 2019.
http://etd.library.vanderbilt.edu/available/etd-11192013-140238/ ;.
MLA Handbook (7th Edition):
Mergy, Marc Andrew. “Generation and Characterization of the First Construct-Valid Model of ADHD, the DAT Val559 Knock-In Mouse.” 2013. Web. 19 Oct 2019.
Vancouver:
Mergy MA. Generation and Characterization of the First Construct-Valid Model of ADHD, the DAT Val559 Knock-In Mouse. [Internet] [Doctoral dissertation]. Vanderbilt University; 2013. [cited 2019 Oct 19].
Available from: http://etd.library.vanderbilt.edu/available/etd-11192013-140238/ ;.
Council of Science Editors:
Mergy MA. Generation and Characterization of the First Construct-Valid Model of ADHD, the DAT Val559 Knock-In Mouse. [Doctoral Dissertation]. Vanderbilt University; 2013. Available from: http://etd.library.vanderbilt.edu/available/etd-11192013-140238/ ;
University of Toronto
20.
Zdravic, Darko.
Investigation of the Pathophysiological Mechanisms of Intracranial Hemorrhage and Miscarriage in alphaIIb Integrin Mediated Fetal and Neonatal Alloimmune Thrombocytopenia.
Degree: 2017, University of Toronto
URL: http://hdl.handle.net/1807/76676
► Investigation of the Pathophysiological Mechanisms of Intracranial Hemorrhage and Miscarriage in anti-alphaIIb Integrin Mediated Fetal and Neonatal Alloimmune Thrombocytopenia Darko Zdravic Master of Science Department…
(more)
▼ Investigation of the Pathophysiological Mechanisms of Intracranial Hemorrhage and Miscarriage in anti-alphaIIb Integrin Mediated Fetal and Neonatal Alloimmune Thrombocytopenia
Darko Zdravic
Master of Science
Department of Laboratory Medicine and Pathobiology
University of Toronto
2017
Fetal and neonatal alloimmune thrombocytopenia (FNAIT) is a life threatening bleeding disorder often leading to bleeding diatheses including intracranial hemorrhage (ICH). Miscarriages have also been reported; however the frequency of pregnancy loss has not been investigated.
Approximately 85% of FNAIT cases are anti-beta3 mediated, whereas anti-alphaIIb mediated FNAIT makes up 3-5% of cases, although their polymorphic frequencies are similar.
We hypothesized that anti-alphaIIb antibodies target trophoblasts during pregnancy, causing impaired placental perfusion and miscarriage in alphaIIb mediated FNAIT. Miscarriages were observed in the majority of immunized alphaIIb-/- mothers, and their placentae showed ischemic appearances with vascular and structural abnormalities, poor perfusion in the labyrinths, and decreased circulating fetal erythrocytes. Neonates developed severe thrombocytopenia and ICH. In vitro experiments demonstrated that anti-alphaIIb antisera significantly inhibited endothelial cell migration and invasion. The results of our studies suggest that a lower reported incidence of anti- alphaIIb mediated FNAIT may be due to miscarriage.
M.Sc.
Advisors/Committee Members: Ni, Heyu, Laboratory Medicine and Pathobiology.
Subjects/Keywords: animal model; antibody; placenta; platelets; thrombocytopenia;
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APA ·
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APA (6th Edition):
Zdravic, D. (2017). Investigation of the Pathophysiological Mechanisms of Intracranial Hemorrhage and Miscarriage in alphaIIb Integrin Mediated Fetal and Neonatal Alloimmune Thrombocytopenia. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/76676
Chicago Manual of Style (16th Edition):
Zdravic, Darko. “Investigation of the Pathophysiological Mechanisms of Intracranial Hemorrhage and Miscarriage in alphaIIb Integrin Mediated Fetal and Neonatal Alloimmune Thrombocytopenia.” 2017. Masters Thesis, University of Toronto. Accessed October 19, 2019.
http://hdl.handle.net/1807/76676.
MLA Handbook (7th Edition):
Zdravic, Darko. “Investigation of the Pathophysiological Mechanisms of Intracranial Hemorrhage and Miscarriage in alphaIIb Integrin Mediated Fetal and Neonatal Alloimmune Thrombocytopenia.” 2017. Web. 19 Oct 2019.
Vancouver:
Zdravic D. Investigation of the Pathophysiological Mechanisms of Intracranial Hemorrhage and Miscarriage in alphaIIb Integrin Mediated Fetal and Neonatal Alloimmune Thrombocytopenia. [Internet] [Masters thesis]. University of Toronto; 2017. [cited 2019 Oct 19].
Available from: http://hdl.handle.net/1807/76676.
Council of Science Editors:
Zdravic D. Investigation of the Pathophysiological Mechanisms of Intracranial Hemorrhage and Miscarriage in alphaIIb Integrin Mediated Fetal and Neonatal Alloimmune Thrombocytopenia. [Masters Thesis]. University of Toronto; 2017. Available from: http://hdl.handle.net/1807/76676
North Carolina State University
21.
Liu, Zifei.
Measurement and Modeling Ammonia Emissions from Broiler Litter.
Degree: PhD, Biological and Agricultural Engineering, 2009, North Carolina State University
URL: http://www.lib.ncsu.edu/resolver/1840.16/5458
► Ammonia is a very important atmospheric pollutant. Agricultural activities, livestock production in particular, have been reported to be the largest contributor of ammonia emissions into…
(more)
▼ Ammonia is a very important atmospheric pollutant. Agricultural activities, livestock production in particular, have been reported to be the largest contributor of ammonia emissions into the atmosphere. Accurate estimation of ammonia emission rate from individual operations or sources is important and yet a challenging task for both regulatory agencies and
animal producers. The overall research objective of this study was to develop an emission
model which can be used to estimate ammonia emission from broiler litter. In the reported
model, the ammonia flux is essentially a function of the litter's total ammoniacal nitrogen (TAN) content, moisture content, pH, and temperature, as well as the Freundlich partition coefficient (Kf), mass transfer coefficient (KG), ventilation rate (Q), and emission surface area (A). A dynamic flow-through chamber system and a wind tunnel were designed to measure ammonia fluxes from broiler litter. The dynamic flow-through chamber experiments evaluated the reported
model with various litter samples under a constant temperature and wind profile. The wind tunnel experiments evaluated the reported
model under various temperatures and wind profiles.
Model parameters such as Kf and KG were estimated. The results from the two experiments were consistent with each other. The estimated KG ranged from 1.11 to 27.64 m h-1, and the estimated Kf ranged from 0.56 to 4.48 L kg-1. Regression sub-models were developed to estimate Kf as a function of litter pH and temperature and to estimate KG as a function of air velocity and temperature. Sensitivity analysis of the
model showed that ammonia flux is very sensitive to litter pH and to a lesser extent temperature. A validation metric based on the mean and covariance in the measurement and in the
model parameters were used to validate the ammonia emission
model in the presence of measurement and
model parameter uncertainties.
Advisors/Committee Members: Peter Bloomfield, Committee Member (advisor), Sanjay Shah, Committee Member (advisor), David Beasley , Committee Co-Chair (advisor), Lingjuan Wang, Committee Chair (advisor).
Subjects/Keywords: emission; model; ammonia; animal feeding operation
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Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Liu, Z. (2009). Measurement and Modeling Ammonia Emissions from Broiler Litter. (Doctoral Dissertation). North Carolina State University. Retrieved from http://www.lib.ncsu.edu/resolver/1840.16/5458
Chicago Manual of Style (16th Edition):
Liu, Zifei. “Measurement and Modeling Ammonia Emissions from Broiler Litter.” 2009. Doctoral Dissertation, North Carolina State University. Accessed October 19, 2019.
http://www.lib.ncsu.edu/resolver/1840.16/5458.
MLA Handbook (7th Edition):
Liu, Zifei. “Measurement and Modeling Ammonia Emissions from Broiler Litter.” 2009. Web. 19 Oct 2019.
Vancouver:
Liu Z. Measurement and Modeling Ammonia Emissions from Broiler Litter. [Internet] [Doctoral dissertation]. North Carolina State University; 2009. [cited 2019 Oct 19].
Available from: http://www.lib.ncsu.edu/resolver/1840.16/5458.
Council of Science Editors:
Liu Z. Measurement and Modeling Ammonia Emissions from Broiler Litter. [Doctoral Dissertation]. North Carolina State University; 2009. Available from: http://www.lib.ncsu.edu/resolver/1840.16/5458
University of New South Wales
22.
Siegle, Jessica Sarah.
A mouse model of childhood asthma: mechanisms of development and progression following an early-life respiratory viral infection.
Degree: Medical Sciences, 2011, University of New South Wales
URL: http://handle.unsw.edu.au/1959.4/50331
;
https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9212/SOURCE02?view=true
► Background: Lower respiratory tract infections in childhood, including viruses such as respiratory syncytial virus (RSV), are strongly linked to development of allergic asthma. The aim…
(more)
▼ Background: Lower respiratory tract infections in childhood, including viruses such as respiratory syncytial virus (RSV), are strongly linked to development of allergic asthma. The aim of this project was to develop a mouse
model of the induction phase of childhood asthma, to facilitate investigation of the interaction of early-life infection with RSV, subsequent allergen exposure and development of asthma, as well as the underlying mechanisms. Methods: BALB/c mice were neonatally infected with pneumonia virus of mice (PVM, which is a mouse-specific virus of the same family and genus as RSV). Following recovery, mice were intranasally sensitised with ovalbumin and challenged with a low level of aerosolised antigen for 4 weeks, followed by a single moderate-level challenge to trigger acute allergic inflammation. To assess underlying mechanisms, antibodies against IL-4 or IL-25, which contribute to induction of a Th2 response, were administered either during the chronic challenge period or in early life alone. Results: Development of an asthmatic phenotype (allergic airway inflammation, changes of remodelling and airway hyperresponsiveness (AHR)) required both recovery from neonatal infection and subsequent allergen sensitisation/challenge. By comparison, changes of remodelling were evident in mice that received allergen challenge alone, while development of AHR was associated with PVM infection alone. Signalling via the IL-4 receptor alpha chain was crucial to the development of allergic inflammation, goblet cell change and AHR, because these were absent in receptor-deficient mice. Administration of anti-IL-4 during chronic challenge inhibited allergic airway inflammation and goblet cell hyperplasia/metaplasia, but not other changes of remodelling. In contrast, anti-IL-25 selectively suppressed recruitment of eosinophils, but not of neutrophils. Anti-IL-25 also inhibited airway remodelling, but had no effect on goblet cells. Treatment with anti-IL-25 in early life had similar effects. Both antibodies suppressed development of a Th2 response, while anti-IL-25 promoted a Th17 response. Conclusion: In this murine
model, interaction between early-life viral infection and allergen sensitisation/challenge is essential for development of changes typical of an asthmatic phenotype. Furthermore, suppressing the Th2 response, either during the neonatal period or later in childhood, prevents development of some of the key features of childhood asthma.
Advisors/Committee Members: Kumar, Rakesh, Medical Sciences, Faculty of Medicine, UNSW, Thomas, Paul, Medical Sciences, Faculty of Medicine, UNSW.
Subjects/Keywords: Animal model; Childhood asthma; Th2 response
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APA (6th Edition):
Siegle, J. S. (2011). A mouse model of childhood asthma: mechanisms of development and progression following an early-life respiratory viral infection. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/50331 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9212/SOURCE02?view=true
Chicago Manual of Style (16th Edition):
Siegle, Jessica Sarah. “A mouse model of childhood asthma: mechanisms of development and progression following an early-life respiratory viral infection.” 2011. Doctoral Dissertation, University of New South Wales. Accessed October 19, 2019.
http://handle.unsw.edu.au/1959.4/50331 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9212/SOURCE02?view=true.
MLA Handbook (7th Edition):
Siegle, Jessica Sarah. “A mouse model of childhood asthma: mechanisms of development and progression following an early-life respiratory viral infection.” 2011. Web. 19 Oct 2019.
Vancouver:
Siegle JS. A mouse model of childhood asthma: mechanisms of development and progression following an early-life respiratory viral infection. [Internet] [Doctoral dissertation]. University of New South Wales; 2011. [cited 2019 Oct 19].
Available from: http://handle.unsw.edu.au/1959.4/50331 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9212/SOURCE02?view=true.
Council of Science Editors:
Siegle JS. A mouse model of childhood asthma: mechanisms of development and progression following an early-life respiratory viral infection. [Doctoral Dissertation]. University of New South Wales; 2011. Available from: http://handle.unsw.edu.au/1959.4/50331 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9212/SOURCE02?view=true
University of Manchester
23.
Oladipo, Joanna.
The development and validation of a maternal immune activation (mIA) animal model relevant to neurodevelopmental disorders : a focus towards Autism Spectrum Disorder (ASD).
Degree: PhD, 2018, University of Manchester
URL: https://www.research.manchester.ac.uk/portal/en/theses/the-development-and-validation-of-a-maternal-immune-activation-mia-animal-model-relevant-to-neurodevelopmental-disorders-a-focus-towards-autism-spectrum-disorder-asd(aa39ca74-6972-430f-83d1-e77e0a1418c5).html
;
https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.771375
► Autism spectrum disorder (ASD) is a pervasive neurodevelopmental disorder (NDD) which, despite much research, is not well understood. The heterogeneity of ASD patient cohorts supports…
(more)
▼ Autism spectrum disorder (ASD) is a pervasive neurodevelopmental disorder (NDD) which, despite much research, is not well understood. The heterogeneity of ASD patient cohorts supports the hypothesis of complex interactions of genetic and environmental mechanisms in its aetiology and severity. The presence of gastrointestinal (GI) disturbances in ASD patients that disrupt the bi-directional signalling of the gut-brain axis, suggest that this may play a role in the manifestation of ASD phenotypes. There is also accumulating evidence for the role of neuroinflammatory processes, in both pregnant mother and affected offspring, in the aetiology of NDDs. The increased risk of ASD following infection during pregnancy highlights maternal immune activation (mIA) as a key animal model for NDDs (notably for schizophrenia and ASD) where relevant behavioural phenotypes manifest in the offspring of mIA dams. ASD remains a poorly managed NDD, with no evidence-based therapies for prevention or treatment currently available. Validating new mIA models and refining current methods is vital to the development of new therapeutic strategies. This thesis has explored the development of an mIA model to test the maternal infection hypothesis using exposure to the viral mimetic polyinosinic-polycytidylic acid (poly (I:C)) administered mid-way through pregnancy (gestational day (GD) 12.5) in rats. First, the acute effects of poly (I:C) in non-pregnant female rats were investigated, providing a validation of the experimental methods (strain, route of administration and dose). Separate cohorts of Wistar rats were then used in the GD12.5 mIA model and the physiological responses to 10 mg/kg i.p. poly (I:C) measured. Various measures including elevation of plasma IL-6 and changes in core body temperature were found to be variable between treated dams. These results confirmed the need to standardise analysis of mIA in dams, to correlate maternal inflammation with subsequent offspring outcomes such as phenotype and neuronal development changes. Poly (I:C) batch differences were also thought to contribute to these variable results and refinement of mIA methods are proposed. Longitudinal effects of mIA on offspring of both sexes were investigated including their developmental trajectory measuring specific gene expression, morphology at GD21 and post-natal day (PD) 21, and behavioural phenotyping at adolescence and adulthood. Gestational and early postnatal changes in offspring following mIA have yet to be systematically explored. Gene expression analysis at GD21 and PD21 in offspring shows that this mIA model is useful for the identification of early developmental changes relevant to NDDs. Moreover, analysis of gene expression changes related to synaptic function, glial cells and blood-brain barrier integrity demonstrated that changes were dependent on both sex and brain region of interest. This confirms the need to include both sexes of offspring and inclusion of different brain regions for analysis which is a common limitation of previous preclinical…
Subjects/Keywords: animal model; neurodevelopmental; maternal immune activation
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MLA ·
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to Zotero / EndNote / Reference
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APA (6th Edition):
Oladipo, J. (2018). The development and validation of a maternal immune activation (mIA) animal model relevant to neurodevelopmental disorders : a focus towards Autism Spectrum Disorder (ASD). (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/the-development-and-validation-of-a-maternal-immune-activation-mia-animal-model-relevant-to-neurodevelopmental-disorders-a-focus-towards-autism-spectrum-disorder-asd(aa39ca74-6972-430f-83d1-e77e0a1418c5).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.771375
Chicago Manual of Style (16th Edition):
Oladipo, Joanna. “The development and validation of a maternal immune activation (mIA) animal model relevant to neurodevelopmental disorders : a focus towards Autism Spectrum Disorder (ASD).” 2018. Doctoral Dissertation, University of Manchester. Accessed October 19, 2019.
https://www.research.manchester.ac.uk/portal/en/theses/the-development-and-validation-of-a-maternal-immune-activation-mia-animal-model-relevant-to-neurodevelopmental-disorders-a-focus-towards-autism-spectrum-disorder-asd(aa39ca74-6972-430f-83d1-e77e0a1418c5).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.771375.
MLA Handbook (7th Edition):
Oladipo, Joanna. “The development and validation of a maternal immune activation (mIA) animal model relevant to neurodevelopmental disorders : a focus towards Autism Spectrum Disorder (ASD).” 2018. Web. 19 Oct 2019.
Vancouver:
Oladipo J. The development and validation of a maternal immune activation (mIA) animal model relevant to neurodevelopmental disorders : a focus towards Autism Spectrum Disorder (ASD). [Internet] [Doctoral dissertation]. University of Manchester; 2018. [cited 2019 Oct 19].
Available from: https://www.research.manchester.ac.uk/portal/en/theses/the-development-and-validation-of-a-maternal-immune-activation-mia-animal-model-relevant-to-neurodevelopmental-disorders-a-focus-towards-autism-spectrum-disorder-asd(aa39ca74-6972-430f-83d1-e77e0a1418c5).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.771375.
Council of Science Editors:
Oladipo J. The development and validation of a maternal immune activation (mIA) animal model relevant to neurodevelopmental disorders : a focus towards Autism Spectrum Disorder (ASD). [Doctoral Dissertation]. University of Manchester; 2018. Available from: https://www.research.manchester.ac.uk/portal/en/theses/the-development-and-validation-of-a-maternal-immune-activation-mia-animal-model-relevant-to-neurodevelopmental-disorders-a-focus-towards-autism-spectrum-disorder-asd(aa39ca74-6972-430f-83d1-e77e0a1418c5).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.771375
AUT University
24.
Al-Rawi, Mohammad.
Computational fluid dynamic modelling for arterial diseases assessment
.
Degree: 2013, AUT University
URL: http://hdl.handle.net/10292/5202
► One of the leading causes of death is cardiovascular disease, being 30% of all deaths worldwide and 40% of those in New Zealand. In other…
(more)
▼ One of the leading causes of death is cardiovascular disease, being 30% of all deaths worldwide and 40% of those in New Zealand. In other words, every 90 minutes a New Zealander dies due to cardiovascular disease. Cardiovascular mortality is higher in New Zealand than Australia, but the reasons for this are not clear. Although Australia and New Zealand are similar politically, culturally, and socioeconomically, mortality from cardiovascular disease is about 25% higher in New Zealand than in Australia.
In recent years, engineers and scientists have collaborated with the medical community to find new methods and approaches for assessing and investigating the development of cardiovascular diseases such as abdominal aortic aneurysm and atherosclerosis. In this thesis, atherosclerosis and aneurysm diseases are investigated and analysed using computational fluid dynamic/finite element (CFD/FE) methods. These models are validated against the in vivo and in vitro experiments performed on animals. The experimental models are also investigated; the assessment of arterial blockages using blood pressure waveforms obtained invasively at the right femoral artery.
The
animal experiments are performed following appropriate ethical protocols (R915) on Wistar rats weighing between 250-350g. An arterial blockage is created surgically within the abdominal aorta of healthy animals to create an unhealthy condition. Blood pressure waveforms are measured by injecting catheter into the right femoral artery of the rat. These measurements are taken at the baseline (healthy condition) and at four different severities of arterial blockage of the abdominal aorta for the same specimen. In vivo and in vitro measurements of the arterial diameter and wall thickness are also taken using Magnetic Resonance Imaging (MRI) and microscopic techniques, respectively.
These data are then input onto CFD/FE models in order to develop a new, non-invasive method of assessing arterial blockage. The experimental and computational results indicate that arterial blockages occurring within the abdominal aorta could be assessed, and the development of the disease diagnosed, very clearly and non-invasively at the right femoral artery. The findings of the
animal model are then implemented in the human
model for screening atherosclerosis and aneurysm at the brachial artery. These diseases are modelled and simulated in a 3D CFD/FE aorta geometry using the fluid–structure interaction (FSI) approach on the commercial software ANSYS®14.0. Literature blood flow waveform datum is assumed at the inlet and invasive catheter pulsatile pressure waveforms data is imposed at the four outlets of the aorta (provided by Green Lane Hospital under ethic approval number NTX/09/11/109). Correlations between the stress phase angle (SPA), augmentation index (AI), lumen diameter and blood pressure waveforms for various scenarios of diseased models are made and compared to the control
model. The results show that CFD/FE models with different radii and thicknesses at the abdominal…
Advisors/Committee Members: Al-Jumaily, Ahmed (advisor), Lowe, Andrew (advisor).
Subjects/Keywords: CFD/FE;
Animal model;
Arterial diseases
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Al-Rawi, M. (2013). Computational fluid dynamic modelling for arterial diseases assessment
. (Thesis). AUT University. Retrieved from http://hdl.handle.net/10292/5202
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Al-Rawi, Mohammad. “Computational fluid dynamic modelling for arterial diseases assessment
.” 2013. Thesis, AUT University. Accessed October 19, 2019.
http://hdl.handle.net/10292/5202.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Al-Rawi, Mohammad. “Computational fluid dynamic modelling for arterial diseases assessment
.” 2013. Web. 19 Oct 2019.
Vancouver:
Al-Rawi M. Computational fluid dynamic modelling for arterial diseases assessment
. [Internet] [Thesis]. AUT University; 2013. [cited 2019 Oct 19].
Available from: http://hdl.handle.net/10292/5202.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Al-Rawi M. Computational fluid dynamic modelling for arterial diseases assessment
. [Thesis]. AUT University; 2013. Available from: http://hdl.handle.net/10292/5202
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Colorado State University
25.
Layer, Emily L.
Understanding Mycobacterium abscessus pulmonary and disseminated disease.
Degree: MS(M.S.), Microbiology, Immunology, and Pathology, 2017, Colorado State University
URL: http://hdl.handle.net/10217/183863
► Mycobacterium abscessus is an emerging human pathogen which is difficult to treat and results in increased mortality. Moreover, the cause of increasing case rates and…
(more)
▼ Mycobacterium abscessus is an emerging human pathogen which is difficult to treat and results in increased mortality. Moreover, the cause of increasing case rates and also the pathogenesis of M. abscessus are poorly understood. M. abscessus belongs to the family of nontuberculous mycobacteria (NTM) classified as members of the rapidly growing mycobacteria (RGM). These environmental pathogens are ubiquitous and found in shower heads, tap water, natural water sources, and soil. Humans contract pulmonary or disseminated infections with M. abscessus by breathing in the aerosolized bacteria or ingesting contaminated water. Immunocompromised individuals such as HIV or AIDS patients, are more susceptible to infection with M. abscessus as are those with cystic fibrosis, bronchiectasis, and individuals on tumor necrosis factor α (TNFα) inhibitors. Strangely, an increasing population of patients becoming infected with M. abscessus are immunocompetent, tall, slender, Caucasian, non-smoking women. To expand our understanding of M. abscessus pathogenesis we developed mouse models that maintain high levels of bacterial infection to study immune responses induced by clinical strains of M. abscessus. Our results support the hypothesis that this bacteria can only persist in our
animal models that possess a deficiency in macrophages and T cell function. Clustered bacterial strains obtained from Cystic Fibrosis patients are more virulent than unclustered bacterial strains obtained from Cystic Fibrosis patients. Additionally, counts of viable mycobacterial colony forming units and histological analysis in (Severe Combined Immunodeficiency) SCID mice on a beige background infected with clustered versus unclustered M. abscessus strains which were isolated from Cystic Fibrosis patients also supported the increased virulence exhibited by the clustered strains. Lastly, we show that major human M. abscessus outbreak strains, when infecting IL-3, GM-CSF deficient mice on an IL-2, Rag2 deficient background (GM/Rag-dblKO mice), result in increased bacterial replication and organ pathology and impaired protective immunity against this pathogen.
Advisors/Committee Members: Ordway, Diane (advisor), Orme, Ian (committee member), Chatterjee, Delphi (committee member), Kirby, Michael (committee member).
Subjects/Keywords: Animal; Mouse; Nontuberculous; Model; Abscessus; Mycobacteria
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APA ·
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Export
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APA (6th Edition):
Layer, E. L. (2017). Understanding Mycobacterium abscessus pulmonary and disseminated disease. (Masters Thesis). Colorado State University. Retrieved from http://hdl.handle.net/10217/183863
Chicago Manual of Style (16th Edition):
Layer, Emily L. “Understanding Mycobacterium abscessus pulmonary and disseminated disease.” 2017. Masters Thesis, Colorado State University. Accessed October 19, 2019.
http://hdl.handle.net/10217/183863.
MLA Handbook (7th Edition):
Layer, Emily L. “Understanding Mycobacterium abscessus pulmonary and disseminated disease.” 2017. Web. 19 Oct 2019.
Vancouver:
Layer EL. Understanding Mycobacterium abscessus pulmonary and disseminated disease. [Internet] [Masters thesis]. Colorado State University; 2017. [cited 2019 Oct 19].
Available from: http://hdl.handle.net/10217/183863.
Council of Science Editors:
Layer EL. Understanding Mycobacterium abscessus pulmonary and disseminated disease. [Masters Thesis]. Colorado State University; 2017. Available from: http://hdl.handle.net/10217/183863
University of Adelaide
26.
Lett, Bron Douglas.
[EMBARGOED] Mesenchymal stem cells in an ovine model of kidney transplantation.
Degree: 2018, University of Adelaide
URL: http://hdl.handle.net/2440/120861
► Mesenchymal stem cells (MSCs) have the potential to address current issues in transplantation with their immunosuppressive and regenerative abilities. MSCs as a therapy to improve…
(more)
▼ Mesenchymal stem cells (MSCs) have the potential to address current issues in transplantation with their immunosuppressive and regenerative abilities. MSCs as a therapy to improve kidney transplant outcomes have already been taken to the clinical trial stage. The results of these trials have, unfortunately, been disappointing with no significant improvements seen over current transplant outcomes. A return to basic science will help to answer many of the questions surrounding the best methods for the use of MSCs in transplantation medicine. To this end this thesis has set out to examine the application of MSCs in a sheep
model of heterotopic kidney transplantation. Chapter 3 describes the isolation, characterisation, and labelling of MSCs with a superparamagnetic iron oxide (SPIO) nano particle that can be used to track the cells using MRI and Prussian blue staining. Importantly, labelling the cells with the SPIO did not have an impact on their phenotype or function. In Chapter 5, the SPIO-MSCs then had their migration tracked when delivered systemically in a sheep kidney autotransplantation
model, the development of which is described in chapter 4. The observations indicated the cells passed through the transplanted kidney at 15 minutes post administration but had dispersed by 30 minutes. Upon histological study, significantly more cells had been found to localize to the transplanted kidney than to the native kidney. Lastly, chapter 6 details the effects of MSCs delivered into the artery of kidney allografts. Looking at the creatinine, urea, and kim-1 levels of sheep early after transplantation and later undergoing rejection, gave suggestions that MSCs could reduce kim-1 levels soon after transplantation and may reduce some aspects of rejection. Additionally, the MSCs did not negatively impact the transplanted kidney, demonstrating the safety of delivering the cells arterially.
Advisors/Committee Members: Coates, Toby (advisor), Drogemuller, Chris (advisor), Adelaide Medical School (school).
Subjects/Keywords: Stem cells; kidney transplantation; animal model
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Lett, B. D. (2018). [EMBARGOED] Mesenchymal stem cells in an ovine model of kidney transplantation. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/120861
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Lett, Bron Douglas. “[EMBARGOED] Mesenchymal stem cells in an ovine model of kidney transplantation.” 2018. Thesis, University of Adelaide. Accessed October 19, 2019.
http://hdl.handle.net/2440/120861.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Lett, Bron Douglas. “[EMBARGOED] Mesenchymal stem cells in an ovine model of kidney transplantation.” 2018. Web. 19 Oct 2019.
Vancouver:
Lett BD. [EMBARGOED] Mesenchymal stem cells in an ovine model of kidney transplantation. [Internet] [Thesis]. University of Adelaide; 2018. [cited 2019 Oct 19].
Available from: http://hdl.handle.net/2440/120861.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Lett BD. [EMBARGOED] Mesenchymal stem cells in an ovine model of kidney transplantation. [Thesis]. University of Adelaide; 2018. Available from: http://hdl.handle.net/2440/120861
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Kansas State University
27.
Endalew, Abaineh Dagne.
Development
of animal model, vaccines, and diagnostics for Schmallenberg
virus.
Degree: PhD, Department of Diagnostic
Medicine/Pathobiology, 2019, Kansas State University
URL: http://hdl.handle.net/2097/39701
► Schmallenberg virus (SBV) is a novel orthobunyavirus in the Simbu serogroup, genus Orthobunyavirus, family Peribunyaviridae, and order Bunyavirales. The virus emerged in late 2011 near…
(more)
▼ Schmallenberg virus (SBV) is a novel orthobunyavirus
in the Simbu serogroup, genus Orthobunyavirus, family
Peribunyaviridae, and order Bunyavirales. The virus emerged in late
2011 near the German/Dutch border region and was mostly associated
with a mild transient disease of sheep and cattle. It is
transmitted by biting midges (Culicoides species) and causes
abortions, stillbirths, and congenital defects in naïve pregnant
sheep and cattle. SBV has spread throughout most of Europe.
However, to date, the initial introduction route of the virus to
Europe is poorly understood. Consequently, SBV poses a threat to
other countries like the US, where competent insect vector species
and susceptible livestock populations exist and extensive trade
with Europe is conducted. To this end, research work was conducted
with the following three aims: (1) development of a large
animal
model for SBV infection; (2) subunit vaccine development for SBV;
and (3) development and evaluation of Schmallenberg disease
diagnostics. This dissertation contains four chapters. The first
chapter provides a literature review on SBV emergence, taxonomy,
replication, transmission, pathogenesis, diagnosis, and control.
The remaining three chapters contain the research conducted to
address the above-mentioned three study aims.
In chapter two, the
clinical, virological, and serological responses in two ruminant
models, i.e., cattle and sheep, are presented. Infectious serum was
shown to be the best inoculum in both species when compared to
infectious cell culture supernatant and brain homogenate. The
virological and serological responses to SBV were more apparent in
cattle than in sheep. Thus, cattle are recommended as the better
SBV infection
model for the evaluation of vaccines and diagnostics.
Chapter three presents the immunogenicity and efficacy of a
baculovirus-expressed subunit vaccine composed of SBV glycoproteins
C and N. After vaccination, SBV Gc-specific antibody response was
detected in all vaccinated animals. Neither of the vaccines
conferred protection against SBV challenge infection. Therefore,
future studies should focus on better understanding of the
difference in post-translational modifications on Gc protein in
different expression systems and subsequent conformational and
stability conditions that are crucial for its immunogenicity.
Using the different reagents (sera, recombinant proteins, and
tissues) generated in the SBV
animal model development and vaccine
experiments, we tried to develop and evaluate serological and
molecular diagnostic assays for SBV. Among the different SBV
proteins evaluated for SBV antibody detection, N and Gc were the
most reactive antigens, followed by Gn. In the indirect ELISA
experiments, the SBV-infected cell lysate was the least reactive.
Among the three commercial nucleic acid extraction kits, the
GeneReach total RNA extraction kit yielded approximately 10× more
SBV in vitro transcribed RNA than the Qiagen and Applied Biosystems
extraction kits. Multiplex RT-qPCR using in vitro transcribed SBV
RNA resulted…
Advisors/Committee Members: Juergen Richt.
Subjects/Keywords: Schmallenberg virus; Animal
model;
Ruminants;
Vaccines;
Diagnostics
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Endalew, A. D. (2019). Development
of animal model, vaccines, and diagnostics for Schmallenberg
virus. (Doctoral Dissertation). Kansas State University. Retrieved from http://hdl.handle.net/2097/39701
Chicago Manual of Style (16th Edition):
Endalew, Abaineh Dagne. “Development
of animal model, vaccines, and diagnostics for Schmallenberg
virus.” 2019. Doctoral Dissertation, Kansas State University. Accessed October 19, 2019.
http://hdl.handle.net/2097/39701.
MLA Handbook (7th Edition):
Endalew, Abaineh Dagne. “Development
of animal model, vaccines, and diagnostics for Schmallenberg
virus.” 2019. Web. 19 Oct 2019.
Vancouver:
Endalew AD. Development
of animal model, vaccines, and diagnostics for Schmallenberg
virus. [Internet] [Doctoral dissertation]. Kansas State University; 2019. [cited 2019 Oct 19].
Available from: http://hdl.handle.net/2097/39701.
Council of Science Editors:
Endalew AD. Development
of animal model, vaccines, and diagnostics for Schmallenberg
virus. [Doctoral Dissertation]. Kansas State University; 2019. Available from: http://hdl.handle.net/2097/39701
University of Oxford
28.
Coutinho, Maria Ester Freitas Barbosa Pereira.
Central nervous system autoimmunity in neuropsychiatric disorders.
Degree: PhD, 2016, University of Oxford
URL: http://ora.ox.ac.uk/objects/uuid:389fb830-4b4e-4201-9965-19acb2c63ff3
;
https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.729904
► The recent history of autoimmune neurology is marked by the discovery of many central nervous system (CNS) antibody-mediated diseases. These disorders are caused by antibodies…
(more)
▼ The recent history of autoimmune neurology is marked by the discovery of many central nervous system (CNS) antibody-mediated diseases. These disorders are caused by antibodies that target important proteins expressed in the neuronal surface, which are believed to be directly pathogenic. These antibodies are immunoglobulin G (IgG) isotype and, as such, have the potential to cross the placenta during gestation. Foetal exposure to CNS-targeting antibodies could alter developing neuronal circuits, leading to disease. However, the consequences of exposure to these antibodies during neurodevelopment has hardly been considered. To study the relationship between maternal antibodies towards neuronal surface proteins and neurodevelopmental disorders in the foetus a dual approach was undertaken. First, pregnancy serum samples from mothers of children later diagnosed with a neurodevelopmental disorder and from mothers of children with typical development were screened for the presence of neuronal surface antibodies. Next, the effects of pathogenic neuronal surface antibodies in the offspring were assessed in a maternal-to-foetal transfer mouse model. Antibodies to neuronal surface proteins in the gestational serum, particularly CASPR2 antibodies, were found to associate with an increased risk of mental retardation and disorders of psychological development in the progeny. The animal model showed that mice exposed in utero to CASPR2 antibodies have long term behavioural sequelae and histological findings suggestive of abnormalities in brain development. These findings support a model in which maternal antibodies towards foetal neuronal proteins cause long-term behavioural deficits and permanent abnormalities at the cellular and synaptic level in a subset of children with neurodevelopmental disorders.
Subjects/Keywords: 616.8; Neuroimmunology; Neurodevelopmental disorders; Autoantibodies; animal model
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APA (6th Edition):
Coutinho, M. E. F. B. P. (2016). Central nervous system autoimmunity in neuropsychiatric disorders. (Doctoral Dissertation). University of Oxford. Retrieved from http://ora.ox.ac.uk/objects/uuid:389fb830-4b4e-4201-9965-19acb2c63ff3 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.729904
Chicago Manual of Style (16th Edition):
Coutinho, Maria Ester Freitas Barbosa Pereira. “Central nervous system autoimmunity in neuropsychiatric disorders.” 2016. Doctoral Dissertation, University of Oxford. Accessed October 19, 2019.
http://ora.ox.ac.uk/objects/uuid:389fb830-4b4e-4201-9965-19acb2c63ff3 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.729904.
MLA Handbook (7th Edition):
Coutinho, Maria Ester Freitas Barbosa Pereira. “Central nervous system autoimmunity in neuropsychiatric disorders.” 2016. Web. 19 Oct 2019.
Vancouver:
Coutinho MEFBP. Central nervous system autoimmunity in neuropsychiatric disorders. [Internet] [Doctoral dissertation]. University of Oxford; 2016. [cited 2019 Oct 19].
Available from: http://ora.ox.ac.uk/objects/uuid:389fb830-4b4e-4201-9965-19acb2c63ff3 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.729904.
Council of Science Editors:
Coutinho MEFBP. Central nervous system autoimmunity in neuropsychiatric disorders. [Doctoral Dissertation]. University of Oxford; 2016. Available from: http://ora.ox.ac.uk/objects/uuid:389fb830-4b4e-4201-9965-19acb2c63ff3 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.729904
29.
Thomaz, Cassia Roberta da Cunha.
Possíveis inter-relações entre a submissão ao Chronic Mild Stree(CMS) e o desempenho operante.
Degree: PhD, Psicologia Experimental, 2009, University of São Paulo
URL: http://www.teses.usp.br/teses/disponiveis/47/47132/tde-26112009-135126/
;
► Chronic Mild Stress (CMS) é um modelo animal de depressão no qual ratos são submetidos a um protocolo de estressores moderados de forma crônica. Em…
(more)
▼ Chronic Mild Stress (CMS) é um modelo animal de depressão no qual ratos são submetidos a um protocolo de estressores moderados de forma crônica. Em função disso, o consumo e preferência por água com sacarose diminuem. Tal redução costuma ser considerada uma medida de anedonia, sintoma central da depressão em humanos. Três estudos realizados no Laboratório do Programa de Estudos Pós- Graduados em Psicologia Experimental da PUC-SP demonstraram que esse efeito é atenuado pela exposição a uma condição operante em esquema concorrente FR água FR sacarose. O presente estudo teve por objetivo investigar se a submissão a uma condição operante que envolvesse diferentes estímulos reforçadores teria o mesmo efeito. Para isso, as seguintes condições experimentais foram propostas: 1) exposição a um protocolo de estressores por seis semanas; 2) testes semanais de consumo de água e água + 2% sacarose; 3) sessões operantes. Dos nove sujeitos utilizados, quatroforam expostos também a uma condição na qual a resposta de pressão à barra foi consequenciada com acesso à roda de atividades, dois a uma condição na qual a resposta de pressão à barra foi consequenciada com uma pelota de alimento em FR6 e dois em FR12. Como resultado, observou-se que no sujeito submetido somente aos estressores (sujeito 09) foi replicado mais uma vez o efeito de redução no consumo de solução de sacarose. Esse efeito não pode ser observado em nenhum dos sujeitos submetidos às sessões operantes durante a exposição. Observou-se uma queda somente no primeiro teste após o término dessa, indicando que possivelmente a submissão a essas afetou o efeito tradicionalmente observado em decorrência da exposição ao protocolo de estressores. Tais resultados corroboram e ampliam os estudos anteriores. Nas sessões operantes, observou-se redução na taxa de respostas na quinta semana de exposição para os sujeitos em FR12 (02 e 03) e na quinta ou sexta para o sujeitos em FR6 (01 e 04). O desempenho na roda de atividades pareceu ficar sob controle da alteração no peso corporal (sujeitos 05 a 09). É possível que a exposição à condição operante tenha atenuado os efeitos do protocolo de estressores e a redução no valor reforçador dos estímulos tenha sido retardada e/ou observada em condições com maior custo de resposta.
Chronic Mild Stress (CMS) is an animal model of depression. Chronic exposure of rats to a protocol of mild stressors produces decrease in sucrose intake and reduction in the preference for sucrose over water, which is considered as a measure of anhedonia, a core symptom of depression. Three Brazilian studies from PUC-SP showed that the additional exposure of rats to operant sessions using FR water FR sucrose concurrent schedule of reinforcement attenuates this effect. The objective of this study was to investigate if the submission to operant conditions that involves other reinforcers would also attenuate the decrease in sucrose consumption. Three experimental conditions were proposed: 1) exposure to a protocol of mild stressors for six weeks; 2) weekly tests of…
Advisors/Committee Members: Silva, Maria Thereza de Araujo.
Subjects/Keywords: Anedonia; Anhedonia; Animal ethology; Animal Model; Depressão; Depression; Etologia animal; Modelos animais; Stress; Stress
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APA ·
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MLA ·
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CSE |
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APA (6th Edition):
Thomaz, C. R. d. C. (2009). Possíveis inter-relações entre a submissão ao Chronic Mild Stree(CMS) e o desempenho operante. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/47/47132/tde-26112009-135126/ ;
Chicago Manual of Style (16th Edition):
Thomaz, Cassia Roberta da Cunha. “Possíveis inter-relações entre a submissão ao Chronic Mild Stree(CMS) e o desempenho operante.” 2009. Doctoral Dissertation, University of São Paulo. Accessed October 19, 2019.
http://www.teses.usp.br/teses/disponiveis/47/47132/tde-26112009-135126/ ;.
MLA Handbook (7th Edition):
Thomaz, Cassia Roberta da Cunha. “Possíveis inter-relações entre a submissão ao Chronic Mild Stree(CMS) e o desempenho operante.” 2009. Web. 19 Oct 2019.
Vancouver:
Thomaz CRdC. Possíveis inter-relações entre a submissão ao Chronic Mild Stree(CMS) e o desempenho operante. [Internet] [Doctoral dissertation]. University of São Paulo; 2009. [cited 2019 Oct 19].
Available from: http://www.teses.usp.br/teses/disponiveis/47/47132/tde-26112009-135126/ ;.
Council of Science Editors:
Thomaz CRdC. Possíveis inter-relações entre a submissão ao Chronic Mild Stree(CMS) e o desempenho operante. [Doctoral Dissertation]. University of São Paulo; 2009. Available from: http://www.teses.usp.br/teses/disponiveis/47/47132/tde-26112009-135126/ ;
Universidade de Brasília
30.
Ana Carmen de Freitas Oliveira.
Estresse moderado crônico : efeitos sobre a atividade geral em ratos.
Degree: 2009, Universidade de Brasília
URL: http://bdtd.bce.unb.br/tedesimplificado/tde_busca/arquivo.php?codArquivo=6694
► O Chronic Mild Stress (CMS) é um modelo animal experimental de depressão induzida por meio da exposição crônica de ratos a alterações ambientais aversivas, moderadas…
(more)
▼ O Chronic Mild Stress (CMS) é um modelo animal experimental de depressão induzida por meio da exposição crônica de ratos a alterações ambientais aversivas, moderadas e incontroláveis. Este modelo é reconhecido por produzir anedonia, além de outras alterações comportamentais características da depressão. O objetivo do presente estudo foi a identificação de efeitos decorrentes da submissão ao protocolo CMS sobre a atividade geral do organismo. O delineamento foi composto de três condições experimentais: (1) exposição dos animais a um protocolo de alterações ambientais moderadamente aversivas, crônicas e incontroláveis; (2) aplicação de testes de consumo e preferência de água e sacarose antes, durante e após a exposição dos sujeitos ao protocolo e (3) submissão a sessões em uma caixa de atividades feita sob medida, contendo seis compartimentos, que possibilitaram o engajamento em diferentes atividades. Essas condições ocorreram de diferentes maneiras para os sujeitos. Os sujeitos S1, S2 e S3 foram expostos a todas as três condições. S4, S5 e S6 foram expostos às condições 2 e 3. S7 foi exposto às condições 1 e 2. As principais alterações observadas em S1, S2 e S3, durante a exposição ao protocolo, foram: (a) perda de peso corporal; (b) aumento na ingestão de sacarose e redução na preferência da sacarose sobre a água, medidos pelo teste de consumo e preferência de líquidos; (c) redução da frequência de respostas de pressão à barra que produzia alimento nas sessões na caixa de atividades múltiplas; (d) redução da ingestão de água durante as sessões na caixa de atividades; (e) aumento da quantidade de voltas corridas na roda de atividade e (f) aumento do número de alternações entre os diferentes compartimentos da caixa de atividades múltiplas. O sujeito S7 replicou os resultados comumente produzidos no modelo CMS. Os sujeitos S4, S5 e S6 não mostraram alterações nos padrões de comportamento na caixa de atividades. Foram levantadas algumas possíveis explicações para as interações encontradas entre o CMS e a atividade geral, as quais demandam uma investigação mais aprofundada.
Chronic Mild Stress (CMS) is an experimental animal model of depression induced by chronic exposure of rats to mild and uncontrollable aversive environmental changes. This model is known to produce anhedonia, and other behavioral changes characteristic of depression. The objective of this study was to identify effects of a CMS protocol on subject‟s overall activity. Three experimental conditions were designed: (1) exposure of animals to a protocol of chronic and uncontrollable mildly aversive environmental changes; (2) tests of total fluid intake and preference for sucrose over water, before, during and after exposure of subjects to the protocol and (3) sessions in a multi environment chamber with six compartments, which allowed the subjects to engage in different activities, such as bar pressing reinforced by food, water drinking, wheel running and moving across compartments. The subjects were differently exposed to the three conditions.…
Advisors/Committee Members: Roberto Alves Banaco, Antonio Pedro de Mello Cruz, Marcelo Frota Benvenuti, Maria Teresa de Araujo Silva, Lincoln da Silva Gimenes.
Subjects/Keywords: modelo animal; depressão; PSICOLOGIA; animal model; Chronic Mild Stress; depression
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APA ·
Chicago ·
MLA ·
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CSE |
Export
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APA (6th Edition):
Oliveira, A. C. d. F. (2009). Estresse moderado crônico : efeitos sobre a atividade geral em ratos. (Thesis). Universidade de Brasília. Retrieved from http://bdtd.bce.unb.br/tedesimplificado/tde_busca/arquivo.php?codArquivo=6694
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Oliveira, Ana Carmen de Freitas. “Estresse moderado crônico : efeitos sobre a atividade geral em ratos.” 2009. Thesis, Universidade de Brasília. Accessed October 19, 2019.
http://bdtd.bce.unb.br/tedesimplificado/tde_busca/arquivo.php?codArquivo=6694.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Oliveira, Ana Carmen de Freitas. “Estresse moderado crônico : efeitos sobre a atividade geral em ratos.” 2009. Web. 19 Oct 2019.
Vancouver:
Oliveira ACdF. Estresse moderado crônico : efeitos sobre a atividade geral em ratos. [Internet] [Thesis]. Universidade de Brasília; 2009. [cited 2019 Oct 19].
Available from: http://bdtd.bce.unb.br/tedesimplificado/tde_busca/arquivo.php?codArquivo=6694.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Oliveira ACdF. Estresse moderado crônico : efeitos sobre a atividade geral em ratos. [Thesis]. Universidade de Brasília; 2009. Available from: http://bdtd.bce.unb.br/tedesimplificado/tde_busca/arquivo.php?codArquivo=6694
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
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Open Access Theses and Dissertations
