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1
Radke, James Melvin. "Studies involving somatostatin systems in the rodent central nervous system." Thesis, University of British Columbia, 1987. http://hdl.handle.net/2429/26518.
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Somatostatin is a neuropeptide found throughout the brain. Several studies have established its anatomical distribution as being quite heterogenous with relatively high concentrations appearing in the limbic and striatal systems. Presently, very little is known about the functions of somatostatin systems in the brain and how they interact with other transmitter systems. The following report is a summary of experiments undertaken to assess the functional and chemical interactions of somatostatin with other neurotransmitter systems.
Previous studies have established that the dopaminergic inputs to the basal ganglia are important for locomotor activity and reward. These systems have also been implicated in several mental and neural diseases such as schizophrenia, depression, and Parkinson’s disease.
In the first experiment, interactions between dopamine and somatostatin systems were examined using paradigms involving behavioural responses to dopamine agonists. Depletion of somatostatin levels by the drug cysteamine was found to attenuate amphetamine- and apomorphine-mediated motor behaviours but not the reinforcing aspects of amphetamine. The second experiment attempted to further characterize the nature of the dopamine-somatostatin interaction by examining the effects of haloperidol, a dopamine antagonist, on central somatostatin levels. Short term treatment with haloperidol decreased striatal somatostatin levels. Long term treatment (8 months) with haloperidol failed to alter somatostatin levels in the caudate-putamen.
Since somatostatin levels appear to be normal in Parkinsonian brains, the effects of MPTP poisoning in mice on central somatostatin levels was also studied to examine the accuracy of this animal model of Parkinson's disease and examine the effects of dopaminergic lesions on somatostatin levels. The results of this experiment indicate that MPTP causes a dose dependent increase in nigral somatostatin levels without altering striatal or cortical levels. These results are in partial disagreement with results obtained from both post-mortem Parkinsonian brains and primates given MPTP, thereby questioning the accuracy of this mouse model of Parkinson's disease.
The final experiment examined the effects of the anticonvulsant-antidepressant carbamazepine on central somatostatin levels in the rat. Although the chemical mechanisms responsible for the therapeutic effects of carbamazepine are unknown, previous studies have suggested that its efficacy in the treatment of both manic-depression and epilepsy may be associated with the ability of this drug to reduce the abnormal somatostatin levels observed in these diseases. In this experiment, neither acute, chronic, nor withdrawal from chronic treatment with carbamazepine were found to alter the levels of somatostatin in rats. The lack of effects of carbamazepine on basal somatostatin levels may indicate somatostatin cells are susceptible to carbamazepine only under pathological situations.
Together, these results are discussed in the context of recent observations of abnormal somatostatin levels in several diseases of the central nervous system and provide some insight into the interactions and functions of somatostatin systems in the normal and abnormal brain.Medicine, Faculty of
Graduate
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Stumpf, da Silva Taisa Regina. "Delivery Systems to Enhance Neural Regeneration in the Central Nervous System." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/39391.
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Hannula, M. (Manne). "Information transmission capacity of the nervous system of the arm – an information and communication engineering approach to the brachial plexus function." Doctoral thesis, University of Oulu, 2003. http://urn.fi/urn:isbn:9514272277.
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Abstract
The arm includes a large number of nerve fibres that transfer information between the central nervous system and the receptors, muscles and glands of the arm. In the nervous system there is continuous traffic. At rest, when only the receptors send information continuously towards the central nervous system, the traffic is not as intensive as during stress, e.g. during movements of the arm, when the central nervous system sends information towards the muscles, as well.
From an information and communication engineering perspective the nervous system of the arm is an information channel, the other end of which is in the central nervous system and the other end at the periphery of the arm. One principal question about such a communication system is what the maximum information transmission capacity of the channel is, e.g. how the information channel is dimensioned. The arm is a highly complex system with over sixty muscles moving it, and a huge number of sensory receptors in it. Nature has dimensioned the information channel of the arm to satisfy the requirements of the nervous system.
In this thesis a specific mathematical model is built in order to evaluate the maximum information transmission capacity of the nervous system of the arm. The model handles the nervous system of the arm as an entity in the light of information theory. The model uses the physiological and functional properties of the nervous system of the arm as the input and gives the estimate of the maximum information transmission capacity as the output.
The modelling yielded the result that the maximum information transmission capacity of the arm is about 10 Mbit/s. Hence, if a complete neural prosthesis of the arm were built, a single USB bus (12 Mbit/s) would suffice as a communication channel for each arm.
The mathematical model developed can also be applied to other parts of the peripheral nervous system. The aim of future research is to apply the developed model comprehensively to the human peripheral nervous system and to estimate the maximum information transmission capacity of the whole human peripheral nervous system.
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De, Garis Hugo. "Genetic programming. GenNets, artificial nervous systems, artificial morphogenesis." Doctoral thesis, Universite Libre de Bruxelles, 1992. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/212933.
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Alghamdi, Akram Saleh A. "Interaction between immune and nervous systems in insects." Thesis, University of Leicester, 2012. http://hdl.handle.net/2381/27682.
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In vertebrates, it has been established that interactions exist between the immune system, the nervous system, and behavior. A comparative examination of these interactions in other animals helps us understand the evolution of this interaction. It may also be possible to develop animal models of important human pathologies, which are due to the interactions between these two systems. In insects an immune-behavioral interactions similar to those seen in vertebrates has been shown to exist. This suggests that this interaction has a highly conserved function. For example, activation of immune response produces illness-induced anorexia, behavioral fever, changes in reproductive behavior, and decreased learning ability in different species. This thesis establishes further examples of this interaction between the immune and nervous system, examines the physiological basis between them and explores the evolutionary dynamics of the interaction. I establish this interaction between the immunity and memory in bumblebees in a free flying paradigm, where previously it had only been shown in artificial classical conditioning assays. Then, I checked the immunity of different bumblebee colonies of known learning ability to identify any evolutionary relationship between these two traits. I used Drosophila melanogaster to study the sleep phenomenon after activation of the immune system as a potential intermediary between immunity and memory. Finally, I checked the olfactory learning of Drosophila melanogaster after activating their immune system to see if the fruit fly would make a useful model for immune modulated memory reduction.
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Johnston, Richard Norman. "Studies on peptidergic nervous systems in triclad turbellarians." Thesis, Queen's University Belfast, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387933.
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Rubeo, Scott Edward. "Control of Simulated Cockroach Using Synthetic Nervous Systems." Case Western Reserve University School of Graduate Studies / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=case1495555770825904.
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McMinn, David. "Using evolutionary artificial neural networks to design hierarchical animat nervous systems." Thesis, Robert Gordon University, 2001. http://hdl.handle.net/10059/427.
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The research presented in this thesis examines the area of control systems for robots or animats (animal-like robots). Existing systems have problems in that they require a great deal of manual design or are limited to performing jobs of a single type. For these reasons, a better solution is desired. The system studied here is an Artificial Nervous System (ANS) which is biologically inspired; it is arranged as a hierarchy of layers containing modules operating in parallel. The ANS model has been developed to be flexible, scalable, extensible and modular. The ANS can be implemented using any suitable technology, for many different environments. The implementation focused on the two lowest layers (the reflex and action layers) of the ANS, which are concerned with control and rhythmic movement. Both layers were realised as Artificial Neural Networks (ANN) which were created using Evolutionary Algorithms (EAs). The task of the reflex layer was to control the position of an actuator (such as linear actuators or D.C. motors). The action layer performed the task of Central Pattern Generators (CPG), which produce rhythmic patterns of activity. In particular, different biped and quadruped gait patterns were created. An original neural model was specifically developed for assisting in the creation of these time-based patterns. It is shown in the thesis that Artificial Reflexes and CPGs can be configured successfully using this technique. The Artificial Reflexes were better at generalising across different actuators, without changes, than traditional controllers. Gaits such as pace, trot, gallop and pronk were successfully created using the CPGs. Experiments were conducted to determine whether modularity in the networks had an impact. It has been demonstrated that the degree of modularization in the network influences its evolvability, with more modular networks evolving more efficiently.
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Bayley, Timothy George. "Imaging calcium dynamics during motor pattern generation and sensory processing in insect nervous systems." Thesis, University of Cambridge, 2016. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709485.
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Szczecinski, Nicholas S. "Synthetic Nervous Systems and Design Tools for Legged Locomotion." Case Western Reserve University School of Graduate Studies / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=case1499122178853385.
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Espinosa, Medina Isabel. "On the development of the parasympathetic, enteric and sacral nervous systems." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066009/document.
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Les cellules de la crête neurale migrent extensivement et forment le système nerveux autonome comprenant les ganglions parasympathiques, sympathiques et entériques, qui maintiennent l'homéostasie. Dans cette étude, j'explore les migrations, interactions neuronales et dépendances moléculaires lors de la formation des circuits nerveux autonomes. Je démontre que les précurseurs des ganglions parasympathiques dérivent des précurseurs des cellules de Schwann (SCPs) qui envahissent les nerfs préganglionaires jusqu'à leur destination, proche des organes cibles (Espinosa-Medina et al., 2014). D'autre part, je montre un parallélisme entre le mécanisme de migration des précurseurs parasympathiques et celui d'une population de précurseurs du système nerveux ¿sophagien, qui migrent le long le nerve vague. Enfin, je propose un réexamen du système nerveux sacré, qui régule les fonctions urinaire, digestive et reproductrice et qui est considéré comme parasympathique depuis plus d'un siècle, sans argument moléculaire. Je présente une signature moléculaire pour distinguer les neurones parasympathiques crâniens et les neurones sympathiques thoraco-lombaires et démontre que le système nerveux sacré est en fait sympathique. En conséquence, le système nerveux autonome est composé de trois divisions contrastées par leur origine embryonnaire aussi que leur anatomie adulte: une parasympathique d'origine et de connectivité exclusivement crânienne, une sympathique spinale, allant de l'étage cervical au sacré (Espinosa-Medina et al., 2016) et une division entérique que son origine aussi bien que sa connectivité placent à l'interface des systèmes sympathique et parasympathiqueNeural crest cells migrate extensively to form the autonomic nervous system including sympathetic, parasympathetic and enteric ganglia essential for regulating bodily homeostasis. In the present work, I explore the migratory mechanisms and neuronal interactions during autonomic circuit assembly, as well as their molecular dependencies. I show that parasympathetic ganglia derive from Schwann cell precursors (SCPs) and migrate along their preganglionic nerves to locate close to their target tissues (Espinosa-Medina et al., 2014). In line with this work, I show that vagal-associated SCPs give rise to part of the oesophageal nervous system, whereas cervical sympathetic-like crest cells colonize all the gastrointestinal tract, demonstrating a dual origin and different migration mechanisms for enteric neurons. Finally, I revise the identity of the sacral autonomic outflow, whose allocation to the parasympathetic nervous system has been accepted for a century. Sacral autonomic neurons control rectal, bladder, and genital functions and analysis of their cellular phenotype was lacking. Here I present a differential molecular signature for cranial parasympathetic versus thoraco-lumbar sympathetic neurons and show that, in this light, the sacral autonomic outflow is sympathetic. Accordingly, the parasympathetic nervous system receives input from cranial nerves exclusively and the sympathetic nervous system from spinal nerves, thoracic to sacral inclusively (Espinosa-Medina et al., 2016). Interestingly the enteric nervous system, which receives input from both sympathetic and parasympathetic nerves, shares with each system aspects of its ontogeny
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Pan, Feng. "Understanding Ten-Eleven Translocation-2 in Hematological and Nervous Systems." FIU Digital Commons, 2014. http://digitalcommons.fiu.edu/etd/1925.
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I proposed the study of two distinct aspects of Ten-Eleven Translocation 2 (TET2) protein for understanding specific functions in different body systems.
In Part I, I characterized the molecular mechanisms of Tet2 in the hematological system. As the second member of Ten-Eleven Translocation protein family, TET2 is frequently mutated in leukemic patients. Previous studies have shown that the TET2 mutations frequently occur in 20% myelodysplastic syndrome/myeloproliferative neoplasm (MDS/MPN), 10% T-cell lymphoma leukemia and 2% B-cell lymphoma leukemia. Genetic mouse models also display distinct phenotypes of various types of hematological malignancies. I performed 5-hydroxymethylcytosine (5hmC) chromatin immunoprecipitation sequencing (ChIP-Seq) and RNA sequencing (RNA-Seq) of hematopoietic stem/progenitor cells to determine whether the deletion of Tet2 can affect the abundance of 5hmC at myeloid, T-cell and B-cell specific gene transcription start sites, which ultimately result in various hematological malignancies. Subsequent Exome sequencing (Exome-Seq) showed that disease-specific genes are mutated in different types of tumors, which suggests that TET2 may protect the genome from being mutated. The direct interaction between TET2 and Mutator S Homolog 6 (MSH6) protein suggests TET2 is involved in DNA mismatch repair. Finally, in vivo mismatch repair studies show that the loss of Tet2 causes a mutator phenotype. Taken together, my data indicate that TET2 binds to MSH6 to protect genome integrity.
In Part II, I intended to better understand the role of Tet2 in the nervous system. 5-hydroxymethylcytosine regulates epigenetic modification during neurodevelopment and aging. Thus, Tet2 may play a critical role in regulating adult neurogenesis. To examine the physiological significance of Tet2 in the nervous system, I first showed that the deletion of Tet2 reduces the 5hmC levels in neural stem cells. Mice lacking Tet2 show abnormal hippocampal neurogenesis along with 5hmC alternations at different gene promoters and corresponding gene expression downregulation. Through the luciferase reporter assay, two neural factors Neurogenic differentiation 1 (NeuroD1) and Glial fibrillary acidic protein (Gfap) were down-regulated in Tet2 knockout cells. My results suggest that Tet2 regulates neural stem/progenitor cell proliferation and differentiation in adult brain.
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Morgenstern, Daniel Alexander. "Chondroitin sulphate proteoglycans in the peripheral and central nervous systems." Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.620931.
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Jansson, Björn. "Models for the transfer of drugs from the nasal cavity to the central nervous system /." Uppsala : Acta Universitatis Upsaliensis: Univ.-bibl. [distributör], 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3905.
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Marsh, Barnaby C. L. "The Role of Osteopontin in the Peripheral and Central Nervous Systems." Thesis, University of Bristol, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.486122.
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The glycoprotein osteopontin (OPN) is a secreted and heavily phosphorylated peptide that plays a role in a variety of cellular processes from cell adhesion to apoptosis. These actions are principally thought to be mediated via interactions with CD44.and integrins. OPN is expressed in a wide variety of tissues including the peripheral and central nervous systems (PNS and CNS respectively), although its exact function in these tissues remains unclear. We identified OPN as a putative axotomy response gene from a previously generated dorsal root ganglia (DRG) subtractive cDNA library. Immunohistochemical ,staining demonstrated that OPN protein colocalises with neurofilament but not other nociceptive markers. Mechanosensory thresholds in osteopontin knockout (OPN KO) animals are significantly increased compared to wild-type (WT) controls, although there are no differences in allodynia between genotypes after a spared nerve injury (SNI) model of neuropathic pain. Moreover, exogenous recombinant OPN has no effect on neurite outgrowth from adult WT sensory neurons, and no differences in neurite outgrowth were observed in OPN KO animals compared to WT controls. Within the CNS, previous studies have demonstrated that OPN expression increases in a number of cell types after injury, although its precise function is equivocal. Here, I demonstrate that organotypic hippocampal OPN KO cultures display increased apoptosis following glutamate induced cell death compared to WT controls. Moreover, exogenous recombinant OPN is neuroprotective to OPN KO and WT cultures. This neuroprotective effect is integrin mediated and involves activation ofthe Akt and ERK pathways. In summary, these studies further extend our understanding of the neuroprotective and possible cell survival roles played by OPN in the nervous system. Further studies are now warranted to extend those presented here and define the mechanisms that underlie the observed effects thus far delineated.
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Linneweber, Gerit Arne. "Interactions between the nervous, digestive and respiratory systems in Drosophila melanogaster." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648735.
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Shanbhag, Mihir S. Wheatley Margaret A. "Development of a multi-functional construct for central nervous system repair /." Philadelphia, Pa. : Drexel University, 2008. http://hdl.handle.net/1860/2906.
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Gonçalves, Vanessa Santos Silva. "Overcoming Central Nervous System-barriers by the development of hybrid structured systems for nose-to-brain drug delivery using clean technologies." Doctoral thesis, Universidade Nova de Lisboa, Instituto de Tecnologia Química e Biológica António Xavier, 2016. http://hdl.handle.net/10362/56395.
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The effective delivery of therapeutics into the brain is challenging since drugs or drug delivery systems (DDS) candidates are not able to cross the blood-brain barrier (BBB), making the development of new drugs alone not enough to ensure progresses in Central Nervous System (CNS) drug therapy. Due to several problems related with other routes of brain drug administration, the interest has increased towards exploring the possibility of intranasal administration. The nose-to-brain transport and the therapeutic viability of this route have been investigated for rapid and effective transport of drugs to CNS, but the development of nasal drug products for brain targeting is still faced with many challenges.(...)info:eu-repo/semantics/publishedVersion
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Mounger, David Kyle, Kynlee Hillard, Brooke Tipton, Grayson D. White, and Matthew R. Zahner. "GLP-1 agonist liraglutide increases metabolic- and cardiovascular-related sympathetic activity of the central nervous system." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/asrf/2019/schedule/58.
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Metabolic syndrome is associated with pathologies that include type 2 diabetes, hypertension, and dyslipidemia, all of which increase the risks of heart disease. Glucagon-like peptide (GLP-1) is a hormone produced by intestinal enteroendocrine L‑cells. GLP-1 increases insulin sensitivity, augments glucose-dependent insulin secretion, and suppresses glucagon release. GLP-1 also works centrally to decrease appetite and increase metabolism. Evidence suggests that the beneficial effect is mediated by metabolically related sympathetic neurons within the hypothalamus. Although the hypothalamus contains neurons that control metabolism, there are also neurons that control cardiovascular activity. Considering that one main goal of obesity and diabetes treatments is to reduce cardiovascular-related comorbidities, any drug‑induced increase in blood pressure is unacceptable. Therefore, a better understanding of GLP-1 agonists on sympathetic activity and the role of the hypothalamus in central GLP‑1 activity is essential. In this study, we tested the hypothesis that the long‑acting FDA approved GLP-1 receptor agonist liraglutide activates both metabolic and cardiovascular‑related hypothalamic neurons and augments reflex cardiovascular sympathetic activity in rats. To test this hypothesis, we administered liraglutide (125 mg/kg, SC, n=10) or vehicle (saline, n=10) to rats for 15 days and measured food intake and body weight. Next, we recorded blood pressure and renal sympathetic nerve activity (RSNA) in the anesthetized rat before and after liraglutide treatment. Finally, to determine the activation of hypothalamic neurons we performed neuroanatomical tracing studies and turned metabolically-related (raphe‑projecting) neurons green, and cardiovascular-related (rostroventrolateral medulla, RVLM) neurons red. After treating rats with liraglutide, (75 mg/kg IV) we performed immunohistochemical (IHC) labeling to identify neurons expressing cFos, a marker of neuronal activation. Daily liraglutide significantly (p < 0.05) reduced both food intake and body weight from the pretreatment baseline. In vehicle-treated rats, the mean baseline food intake was 27.9 ± 0.5g. During vehicle treatment, the mean food intake was 28.6 ± 0.8 g and body weight was 110 ± 1.5% of its baseline. In liraglutide-treated rats, the mean baseline food intake was 29.9 ± 0.7g. During liraglutide treatment, the mean food intake was 22.7 ± 1.4g and body weight was 105 ± 1.1% of its baseline. At the end of liraglutide treatment, food intake and body weight returned to that of the vehicle-treated rats. In the anesthetized rat, liraglutide significantly (p < 0.05) increased basal RSNA and augmented baroreflex and chemoreflex activity. Lastly, our cFos data show that liraglutide activates metabolic, but not cardiovascular hypothalamic neurons. Collectively, these data suggest that although liraglutide elevates sympathetic activity, it is not by activation of pre-sympathetic hypothalamic neurons.
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Harley, Linda Rosemary. "The application of a knowledge based system to micro-electrode guided neurosurgery." Thesis, Available online, Georgia Institute of Technology, 2004, 2004. http://etd.gatech.edu/theses/available/etd-02042004-131540/unrestricted/harley%5Flinda%5Fr%5F200405%5Fms.pdf.
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Thesis (M. S.)--Civil and Environmental Engineering, Georgia Institute of Technology, 2004.Dr. Michael Hunter, Committee Member ; Dr. Alexander M. Puzrin, Committee Member ; Dr. Nelson Baker, Committee Chair. Includes bibliographical references.
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McClure-Sharp, Jilliane Mary, and mikewood@deakin edu au. "Regulation of corticotropin-releasing factor concentration and overflow in the rat central nervous system." Deakin University. School of Biological and Chemical Sciences, 1998. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20060802.143911.
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Corticotropin-releasing factor (CRF) is the primary hormone of the hypothalamo-pituitary adrenal axis (HPA-axis). In addition to its endocrine function, it has been proposed that CRF acts as a neurotransmitter. The widespread distribution of CRF immunoreactivity and CRF receptors in the rat central nervous system (CNS) supports this theory. Immunohistochemical studies have demonstrated high levels of CRF immunoreactivity the rat hypothalamus, a brain region involved in the regulation and integration of a variety of endocrine and autonomic homeostatic mechanisms. CRF has been shown to be involved in a number of these activities such as blood pressure control, food and water intake, behaviour and emotional integration. Many of these activities demonstrate progressive dysfunction as ageing proceeds. The aim of this thesis was to investigate the regulation of CRF in the rat CNS, particularly over the period of maturation and ageing. Tissue extraction and peptide radioimmunoassay (RIA) techniques were developed in order to measure regional CRF concentrations as a function of age in the rat CNS. Seven brain regions were examined including the hypothalamus, pituitary, medulla oblongata, pons, cerebral cortex, cerebellum and midbrain. Three age ranges were investigated: 3 4 weeks, 4 5 months and 14 18 months, representing young, mature and old age groups. Data for the tissues of individual rats from each age group were analysed using one-way analysis of variance (ANOVA) with post-hoc Scheffé tests (SPSS Release 6 for Windows, 1989 1993). CRF were detected in measurable quantities in all brain regions examined. Different age-related patterns of change were observed in each brain region. CRF concentrations (ng/g tissue) were highest in the pituitaries of young rats and were significantly reduced over the period of maturation (P< 0.05). However, the high CRF concentration of the young rat pituitary was likely to be a factor of the smaller tissue mass. Although the absolute CRF content (ng/tissue) of this tissue appeared to decline with maturation and ageing, the reduction was not significant (P>0.05). Therefore the pituitary of the young rat was relatively enriched with CRF per gram tissue. The highest CRF concentration in mature and aged rats was measured in the hypothalamus, in accordance with previous immunohistochemical studies. Hypothalamic CRF concentrations (ng/g tissue) demonstrated no significant alterations with maturation and ageing. The absolute CRF content (ng/tissue) of the hypothalamus was significantly less in the young rat compared to mature and aged animals, however this was accompanied by a smaller tissue mass (P<0.05). The CRF concentrations (ng/g tissue) of the rat cerebral cortex and medulla oblongata demonstrated significant reduction with advancing age (P<0.05), however in both cases this appeared to be due to significant increases in mean tissue mass. The absolute CRF content of these tissues (ng/tissue) were not significantly different over the period of maturation and ageing (P>0.05). CRF concentration (ng/g tissue) and absolute content (ng/tissue) of the pons demonstrated a trend to increase with advanced age in the rat, however this was not significant in both cases (P>0.05). Of interest were the significant increases observed in the CRF concentrations of the cerebellum and midbrain (ng/g tissue with advanced ageing (P<0.05). Significant increases were also observed in the mean tissue mass and absolute CRF content (ng/tissue) of these regions in aged rats (P<0.05). These findings perhaps indicate increased CRF synthesis and or decreased CRF turnover in these tissues with advancing age. The second stage of these studies examined age-related alterations in basal and potassium-stimulated hypothalamic CRF and overflow over the period of maturation and ageing in the rat, and required the preliminary development of an in vitro tissue superfusion system. The concomitant release of the co-modulatory compound, neuropeptide Y (NPY) was also measured. NPY has been shown to positively regulate CRF release and gene expression in the hypothalamus. In addition, NPY has been demonstrated to be involved in a number of hypothalamic activities, including blood pressure control and food intake regulation. Hypothalamic superfusion data were analysed using one factor repeated measures ANOVA (SPSS Release 6 for Windows, 1989-1993) followed by least significant difference tests ( Snedecor and Cochran, 1967) to enable both time and age comparisons. Basal hypothalamic CRF overflow was unaltered with maturation and ageing in the rat. Potassium stimulation (56 mM) elicted a significant 2 3 fold increase in hypothalamic CRF overflow across age groups (P<0.05). Stimulated hypothalamic CRF overflow was significantly greater in the young rat compared to the mature and aged animals (P<0.05). The enhanced response to depolarizing stimulus was observed at an age when the absolute CRF content of the hypothalamus was significantly less that of other age groups. It is possible that the enhanced responsiveness of the young rat may be of survival advantage in life threatening situations. Basal hypothalamic NPY overflow was much less than that of CRF, and potassium stimulation resulted in a very different age-related profile. The hypothalamic NPY response to depolarization was significantly reduced in the young rat and declined significantly with advanced ageing (P<0.05). The contrasting profiles of stimulated CRF and NPY overflow may indicate the activity of alternative regulatory factors present in the hypothalamus, whose activity may also be affected in an age-related manner. The final stage of these studies examined the nature of NPY modulation of hypothalamic CRF overflow in the mature rat. The facilitatory effect of NPY on hypothalamic CRF overflow was confirmed. The application of NPY (0.1 µM) significantly increased CRF overflow approximately 4 fold of basal (P<0.05). In addition, the role of the NPY-Y1 receptor was investigated by the prior application of Y1 receptor antagonists, GW1229 (0.05 µM). At this concentration GW1229 significantly reduced hypothalamic CRF overflow induced by perfusion with NPY (0.1 µm), P<0.05. It was concluded the Y1 receptor does have a role in the regulation of hypothalamic CRF overflow by NPY.
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Madge, Paul. "Exploring C4-Modified Sialosides in Siglec Affinity and Selectivity." Thesis, Griffith University, 2018. http://hdl.handle.net/10072/379286.
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The family of Sialic-acid-binding ImmunoGlobulin-like LECtins, known as Siglecs, play a vital
role in the hematopoietic, immune and nervous systems of many mammals, including humans.
These membrane-bound proteins mediate cell to cell adhesion and signalling, and act as
regulatory systems for a variety of biological functions. All functional Siglecs bind to sialic acid
(Neu5Ac) moieties displayed on the terminus of cell surface glycan structures. Although the
Siglec family displays remarkably distinct selectivity for different glyosidic linkages (such as
Neu5Ac-α2,6 or Neu5Ac-α2,3) and modifications (such as Neu5Ac or Neu5Gc), the
carbohydrate binding pocket of the V-set domain is highly conserved. There are two major
groups of Siglecs; the conserved Siglecs, including Siglec-1 (Sialoadhesin, Sn), Siglec-2 (CD22),
Siglec-4 (myelin-associated glycoprotein, MAG) & Siglec-15, and the CD33-related Siglecs. The
research detailed within this PhD thesis is predominately focused on the conserved Siglecs, in
particular Siglec-2, Siglec-1 and Siglec-4.
Since the discovery of the Siglec family, their role in a wide variety of disease states has been
well established. Siglec-2 for example, is found on B cells which are known to play a significant
role in autoimmune diseases such as rheumatoid arthritis, type 1 diabetes, and systemic lupus
erythematosus. Additionally, some non-Hodgkins lymphomas and certain leukemias involve B
cells which express Siglec-2. Siglec-1 (primarily expressed on macrophages) is known to bind to
Neu5Ac terminating glycans on the surface of pathogens including Neisseria meningitidis,
Campylobacter jejuni, Trypanosoma cruzi and HIV-1. This binding can lead to the phagocytosis
of the pathogen or, as is the case with HIV, further the spread of the virus to other cells. Siglec-
4 functions as an essential part of the maintenance of myelinated axons as well as an inhibitor
of neurite outgrowth and axon regeneration. It has been demonstrated in vitro that blocking
Siglec-4 binding stimulates axon outgrowth, which could pave the way for therapies that allow
axon regeneration in patients with nerve injuries.
It has been hypothesised that synthetic Siglec ligands with high affinity and selectivity could be
used as potential therapeutics for these diseases. In the 19 years since the X-ray crystal
structure of Siglec-1 was first resolved, many research groups have ventured to synthesise
Siglec inhibitors, with the majority of these based upon the natural ligand, Neu5Ac. The
research in this thesis seeks to explore the C4 position of Neu5Ac and how modifications at
this position can influence the binding affinity of Siglecs to this novel class of Siglec ligands.
Chapter 1 provides a general introduction to sialic acids, lectins and, more specifically, the
Siglecs. The structure and function of Siglec-2, Siglec-1 and Siglec-4 are then described in
detail. Previous research conducted within the Siglec inhibitor space is also briefly reviewed.
Finally, an overview of the chemical synthesis that was carried out throughout the research
project is described.
Although the chemistry of Neu5Ac has been exhaustively documented for some four decades,
Neu5Ac derivatives that incorporate modifications at C2, C3 and C4 are relatively
underrepresented in the literature. Chapter 2 describes the development of methodologies
required to functionalise Neu5Ac at the C2 position via the 2,3-β-epoxide intermediate. The
described versatile synthesis allows for the introduction of various anomeric aglycon
substituents and maintains the C3 hydroxyl group which could be further functionalised (for
different research paths) or subsequently reduced to yield C3-anhydro derivatives.
Chapter 3 describes the use of STD NMR to explore the interactions between novel C4-
modified synthetic Siglec-2 ligands and the Siglec-2 protein. Initially we discovered that the
addition of aromatic amides to the C4 position of Neu5Acα2Me improved Siglec-2 binding by
up to 15-fold whilst also reducing Siglec-4 binding compared to the parent compound. By
combining C4 modifications with the 9-biphenylcarboxamido (9-BPC) moiety described in the
literature, we were able to enhance Siglec-2 binding by over 10,000-fold (compared to
Neu5Acα2Me). Using STD NMR we were able to resolve the ligand binding epitope, which
showed that the C4 and C9 substituents acted synergistically to enhance affinity. Furthermore,
we used a novel whole cell STD NMR technique to visualise how synthetic ligands overcome
cis-binding to recognise Siglec-2 in a cellular environment. This in turn led to the synthesis of
potent Siglec-2 ligands that were functionalised at the anomeric position (C2), in addition to C4
and C9.
Finally, we wanted to further explore the role that C2 and C4 modifications play in enhancing
affinity and, more importantly, selectivity. The research outlined in Chapter 4 involves the
synthesis and biological evaluation of a suite of C4-modified benzyl glycosides and C2-modified
meta-nitrophenylcarboxamido (4-mNPC) Neu5Ac derivatives. Addition of the 9-BPC
functionality to a select number of these compounds vastly improved Siglec-2 binding affinity
to nanomolar inhibitory concentrations. Selectivity towards Siglec-2 could potentially be
controlled by modifying the C2 and C4 substituents, however binding to Siglec-4 and Siglec-1
could not be abolished completely. Preliminary research in multivalent ligands and drug
delivery systems is described in Chapter 5, along with the thesis conclusions.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
Institute for Glycomics
Science, Environment, Engineering and Technology
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Passaro, Peter A. "Multi-electrode array recording and data analysis methods for molluscan central nervous systems." Thesis, University of Sussex, 2012. http://sro.sussex.ac.uk/id/eprint/43341/.
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In this work the use of the central nervous system (CNS) of the aquatic snail Lymnaea stagnalis on planar multi-electrode arrays (MEAs) was developed and analysis methods for the data generated were created. A variety of different combinations of configurations of tissue from the Lymnaea CNS were explored to determine the signal characteristics that could be recorded by sixty channel MEAs. In particular, the suitability of the semi-intact system consisting of the lips, oesophagus, CNS, and associated nerve connectives was developed for use on the planar MEA. The recording target area of the dorsal surface of the buccal ganglia was selected as being the most promising for study and recordings of its component cells during fictive feeding behaviour stimulated by sucrose were made. The data produced by this type of experimentation is very high volume and so its analysis required the development of a custom set of software tools. The goal of this tool set is to find the signal from individual neurons in the data streams of the electrodes of a planar MEA, to estimate their position, and then to predict their causal connectivity. To produce such an analysis techniques for noise filtration, neural spike detection, and group detection of bursts of spikes were created to pre-process electrode data streams. The Kohonen self-organising map (SOM) algorithm was adapted for the purpose of separating detected spikes into data streams representing the spike output of individual cells found in the target system. A significant addition to SOM algorithm was developed by the concurrent use of triangulation methods based on current source density analysis to predict the position of individual cells based on their spike output on more than one electrode. The likely functional connectivity of individual neurons identified by the SOM technique were analysed through the use of a statistical causality method known as Granger causality/causal connectivity. This technique was used to produce a map of the likely connectivity between neural sources.
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Forest, David L. "The Nervous Systems of Spionid Polychaetes: Structure, Composition, and Effects of Serotonin on Behavior." Fogler Library, University of Maine, 2005. http://www.library.umaine.edu/theses/pdf/ForestDL2005.pdf.
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EPELBAUM, EVA. "Tratamento de eficiência neurosensorial por laser de baixa intensidade e sua associação à acumputura a laser." reponame:Repositório Institucional do IPEN, 2007. http://repositorio.ipen.br:8080/xmlui/handle/123456789/11638.
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Made available in DSpace on 2014-10-09T12:54:12Z (GMT). No. of bitstreams: 0Made available in DSpace on 2014-10-09T14:07:44Z (GMT). No. of bitstreams: 1 12697.pdf: 655472 bytes, checksum: 17722971c9d58d20dbb9095955c414c4 (MD5)
Dissertacao (Mestrado Profissionalizante em Lasers em Odontologia)
IPEN/D-MPLO
Instituto de Pesquisas Energeticas e Nucleares - IPEN/CNEN-SP; Faculdade de Odontologia, Universidade de Sao Paulo , Sao Paulo
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Visser, Claire. "Evaluation of model systems for the study of protein association / incorporation of Beta-Methylamino-L-Alanine (BMAA)." Thesis, Nelson Mandela Metropolitan University, 2011. http://hdl.handle.net/10948/1451.
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β-methylamino-L-alanine (BMAA) is thought to be a contributing factor of Amyotrophic Lateral Sclerosis-Parkinsonism Dementia Complex (ALS/PDC). It has been shown that the levels of toxin ingestion by humans are too low to cause disease. However, it has recently been theorized that this toxin is bioaccumulated within cells. Via a process of slow release from this reservoir, the BMAA is able to bring about neurotoxicity. Mechanisms of uptake and bioaccumulation of BMAA have been proposed in several publications; however the mechanism of protein incorporation of BMAA has not yet been identified. Identifying suitable model systems would be a prerequisite in order for future studies on BMAA protein incorporation. Three specific models were therefore chosen for investigation; mammalian cell lines including C2C12 and HT29, a prokaryotic (E. coli) expression system and yeast cells. The cytotoxity of BMAA was established for the mammalian cell lines and further investigation of BMAA incorporation into cellular proteins was performed on all three above mentioned models. Samples were run on HPLC-MS in order to determine uptake of BMAA into cells or lack thereof. Results indicate negligible cytotoxicity as measured by MTT and CellTitre Blue assays, limited uptake and protein incorporation of BMAA within the prokaryotic model and insignificant uptake of BMAA by yeast cells. Although the uptake of BMAA in the prokaryotic model was not extensive, there was indeed uptake. BMAA was not only taken up into the cells but was also observed in inclusion body protein samples after hydrolysis. After further investigation and use, this model could very well provide researchers with information pertaining to the mechanism of association of BMAA with proteins. Although the other models provided negative results, this research was valuable in the sense that one can narrow down the number of possible model systems available. Also, in seeking models for studying protein association/incorporation, the use of the final target cell is not relevant or necessary as the purpose of the research was to identify a model system in which the mechanism of protein association/incorporation can, in future, be studied.
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Laguna, Tuset Ariadna. "Study of Dyrk1a kinase in central nervous systems development: implication in mouse retina development." Doctoral thesis, Universitat Pompeu Fabra, 2008. http://hdl.handle.net/10803/7115.
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El gen DYRK1A es troba situat en una regió del cromosoma 21 humà que s'ha associat a alteracions en el neurodesenvolupament. Aquest treball mostra com canvis en la dosis gènica de Dyrk1A en el ratolí causen una alteració en la cel.lularitat de les capes internes de la retina i provoquen alteracions funcionals severes. A més a més, la sobreexpressió de Dyrk1A és la única responsable de les alteracions en la retina dels animals Ts65Dn, un model murí de Síndrome de Down. El control de la mort cel.lular programada és fonamental pel correcte desenvolupament del sistema nerviós central. Aquest treball demostra que la proteïna quinasa DYRK1A és un regulador negatiu de la via intrínseca d'apoptosis durant el desenvolupament de la retina. DYRK1A no afecta la proliferació o especificació de les cèl.lules progenitores, sinó que regula el nombre de cèl.lules que moren per apoptosis. La caspasa-9 és un nou substracte de DYRK1A, i la fosforilació de la caspasa al residu treonina 125 per DYRK1A protegeix les cèl.lules de la retina de la mort apoptòtica. Aquestes dades suggereixen un model en el qual una desregulació de la resposta apoptòtica en neurones en diferenciació podria participar en la neuropatologia de malalties que pesenten una alteració en la dosis gènica de DYRK1A.DYRK1A is located in a region of human chromosome 21 (HSA21) that has been associated to the neurodevelopmental impairments shown by individuals with HSA21 aneuploidies. This work shows changes in Dyrk1A gene dosage in the mouse strongly alter the cellularity in inner retina layers and results in severe functional alterations. Moreover, overexpression of Dyrk1A is solely responsible for the retina alterations shown by Ts65Dn mice, a mouse model for Down syndrome. The precise regulation of programmed cell death is critical for the normal development of the nervous system. This work demonstrates that DYRK1A protein kinase is a negative regulator of the intrinsic apoptotic pathway in the developing retina. DYRK1A does not affect the proliferation or specification of retina progenitor cells, but rather regulates the number of cells that die by apoptosis. Caspase-9 is a novel DYRK1A substrate, and the phosphorylation on caspase-9 at threonine residue 125 by DYRK1A protects retina cells from apoptotic cell death. This data suggests a model in which dysregulation of the apoptotic response in differentiating neurons participates in the neuropathology of diseases that display DYRK1A gene dosage imbalance effects.
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Pätschke, Arne [Verfasser]. "Anatomical and chemical approaches to the development of model insect nervous systems / Arne Pätschke." Hannover : Technische Informationsbibliothek und Universitätsbibliothek Hannover (TIB), 2012. http://d-nb.info/1026932807/34.
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Martel, Jean-Claude. "Autoradiographic and pharmacological studies of neuropeptide Y receptors in central and peripheral nervous systems." Thesis, McGill University, 1990. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=74569.
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The distribution of neuropeptide Y (NPY) receptor sites was investigated in certain mammalian species using receptor autoradiography and membrane binding assay techniques. NPY receptor sites are discretely distributed throughout the central nervous systems of hamster, rat, guinea pig and monkey but are particularly concentrated in cortex and hippocampus. NPY receptor autoradiography techniques also revealed important labelling of numerous thalamic nuclei while most hypothalamic nuclei showed surprisingly low densities of NPY receptor sites, considering the high levels of NPY-like immunoreactivity in this brain area. The widespread distribution of NPY receptor sites suggests that this peptidergic system must have important roles in mammalian central nervous system. In particular, the possible involvement of NPY in cognitive function deserves further investigation since we observed that ($ sp3$H) NPY receptor site densities are decreased in temporal cortex and hippocampus of individuals decreased with Alzheimer's disease.The possible existence of NPY/peptide YY (PYY) receptor subtypes was investigated in the rat brain. Overall, the similar autoradiographic distribution of ($ sp{125}$I) BH-NPY and ($ sp{125}$I) PYY in most areas suggests that these two receptor probes most likely interact with the same population of NPY/PYY receptor sites. ($ sp{125}$I) PYY may recognize both a high and low affinity state/subtype of NPY/PYY receptors while ($ sp{125}$I) BH-NPY recognize a single affinity state of receptor having the binding characteristics of the low affinity ($ sp{125}$I) PYY receptor state/subtype. The exact nature of this high affinity receptor state/subtype remains to be established.
Finally, the structural requirements of NPY receptors in central (CNS) and peripheral (PNS) nervous systems were also examined with a binding assay on rat brain membrane preparation and with the rat vas deferens bioassay preparation. The amino acid residues responsible for the activation of NPY receptors in the rat vas deferens preparation lie in the C-terminal half of the NPY molecule as revealed by the loss of potency, but not of biological activity with C-terminal fragments up to NPY$ sb{18-36}$. The N-terminal portion of the NPY molecule appears to be mostly important to insure adequate affinity for central and peripheral NPY receptors. Moreover, a series of NPY analogs revealed that the two tyrosine residues in position 20 and 21 are not directly involved in NPY receptor activation in this bioassay preparation, although they appear relatively important for the maintenance of adequate affinity for the receptors. Interestingly, modifications of the tyrosine residue in position 20 led to the development of two analogs demonstrating a certain degree of selectivity for the PNS receptors while other modifications of tyrosine residues in position 21 may provide some selectivity for CNS receptor sites. (Abstract shortened by UMI.)
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Tulgar, Metin. "New approaches to electrical stimulation of the nervous systems for the relief of pain." Thesis, University of Liverpool, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267910.
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Smith, Jacqueline Anne McInnes. "Characterisation of kappa opioid receptors in the guinea-pig and rat central nervous systems." Thesis, University of Cambridge, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333423.
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Britt, Nicholas Mason, Madeleine Kate Miller, Donald B. Ph D. Hoover, and John B. M. D. Schweitzer. "IMMUNODEFICIENT R2G2 MOUSE STRAIN YIELDS SPLEENS WITH UNUSUAL CYTOARCHITECTURE AND SYMPATHETIC INNERVATION." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/asrf/2018/schedule/205.
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The nervous system and immune system contact one another through two-way communication in order to establish and preserve homeostasis. The sympathetic neurotransmitter norepinephrine has an impact on how the immune system responds by affecting regional blood flow and activation of adrenergic receptors on leukocytes. Former studies showed that immune cells are capable of releasing nerve growth factor allowing for the establishment and continuation of sympathetic nerves in targeted tissues. From this gathered information, it was hypothesized that sympathetic nerves would prove to be less frequent in spleens from the immunodeficient R2G2 mouse strain (Envigo) when compared to 129P3/J (129) and C57BL/6 (C57) strains. R2G2 mice are an immunodeficient strain that lacks functional T, B, and natural killer cells. Ten to eleven week aged-matched male mice were measured by body weight, spleen weight, and temperature. Spleens were cut and fixed for histological investigation. Sympathetic nerves were labeled by immunostaining tyrosine hydroxylase (TH). Hematoxylin & eosin (H&E) was used to stain spleen sections in order to evaluate cytoarchitecture. Von Willebrand factor (VWF) was used to immunostain for megakaryocytes. R2G2 mice showed slightly higher temperatures and body weights but yielded a significantly smaller spleen weight (R2G2, 38.20 ± 1.48; 129, 65.08 ± 11.71; C57, 81.33 ± 8.38; P< 0.0001, ANOVA). TH stain revealed sympathetic innervation in all strains but location and morphology differed in R2G2 mice compared to controls. Control spleens had nerves which entered white pulp regions of the spleen and were closely related to leukocytes. Fiber profiles in the controls were filamentous with small acute bends. R2G2 differed by having (TH+) nerve fibers more associated with arteries and less localized in the surrounding parenchyma. The fibers were abnormally swollen and held a more granular shape instead of a filamentous shape. The H&E stain showed clear red and white pulp zones in the control spleens with 129 showing more distinct germinal centers than C57. R2G2 H&E sections showed cytoarchitecture with indistinct pulp areas. VWF staining revealed R2G2 mice had an abundant amount of megakaryocytes versus control mice megakaryocyte counts (R2G2, 11.28 ± 3.87 per 20X field; 129, 1.73 ± 0.70; C57, 1.42 ± 0.13; P< 0.0001, ANOVA) and extramedullary hematopoiesis was highly prominent. This evidence supports that leukocytes secrete neurotrophic factors or are vital to establishing normal growth of TH+ nerves toward the white pulp. Leukocytes may not be required for sympathetic innervation of blood vessels in the spleen, however, lack of leukocytes shows TH+ nerve fibers with abnormal morphology in severely immune threatened mice.
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Hermann, Heike. "The cannabinoid receptor type 1 in the murine nervous system physiological roles and cross-talk with other receptor systems /." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=971837341.
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Pereira, Francisco Carlos. "Estudo experimental e quantitativo da reinervação muscular após regeneração de nervos no interior de próteses tubulares." Universidade de São Paulo, 1993. http://www.teses.usp.br/teses/disponiveis/42/42131/tde-16052012-152634/.
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Objetivamos o estudo quantitativo e temporal do padrão de inervação do músculo extensor longo dos dedos (edl), após transecção do nervo ciático em camundongos e reparo imediato pela técnica de tubulização. Assim, o músculo edl apresentou-se desnervado na segunda semana após a tubulização. Todas as fibras musculares do edl estavam reinervados na sexta semana após o implante da protese tubular. Entre a sexta e a quadragesima semanas pós-implante a proporção de fibras musculares do edl com mono e poli-inervação aumentou de 3:1 para 4:1. Na quadragésima semana após o implante do tubo foi atingida a porcentagem máxima (80%) de inervação troncular das placas motoras do edl mono-inervadas. Mesmo com tempos prolongados de sobrevivencia após implante, não houve estabilização do padrão de origem das fibras nervosas que convergiam para as placas poli-inervadas do edl. A mono-inervação troncular foi readquirida por 65% das fibras musculares do edl dos animais tubulizados, padrão encontrado em 100% das fibras musculares do edl dos animais não operados. Os padrões morfometricos de reinervação do músculo edl foram idênticos, a partir do terceiro mes, entre o grupo de animais com secção e tubulização do nervo ciatico e o grupo com simples esmagamento do nervo, evidenciando padrão similar de reinervação muscular a longo prazo.We aimed to study the quantitative and temporal pattern of muscle innervation extensor digitorum longus (EDL), following transection of the sciatic nerve in mice and immediate repair technique for tubing. Thus, the EDL muscle denervation presented in the second week after the tubing. All of the EDL muscle fibers were reinnervated in the sixth week after the implantation of prosthetic tube. Between the sixth and FORTY weeks post-implantation, the proportion of muscle fibers of the EDL with mono-and poly-innervation increased from 3:1 to 4:1. The forty weeks after the implantation of the tube was reached maximum percentage (80%) of trunk innervation of motor endplates of the EDL mono-innervated. Even with prolonged survival times after implantation, there was no stabilization of the pattern of origin of nerve fibers that converged on the plates of poly-innervated EDL. The mono-innervation trunk was regained by 65% of EDL muscle fibers of animals tubularized, pattern found in 100% of EDL muscle fibers of animals not operated. The morphometric patterns of reinnervation of the EDL muscle were identical, from the third month, the group of animals with tubing and resources section of the sciatic nerve and the group with simple nerve crush, showing similar pattern of muscle reinnervation in the long term.
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Mathews, Nithin. "Beyond self-assembly: Mergeable nervous systems, spatially targeted communication, and supervised morphogenesis for autonomous robots." Doctoral thesis, Universite Libre de Bruxelles, 2018. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/267717.
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The study of self-assembling robots represents a promising strand within the emerging field of modular robots research. Self-assembling robots have the potential to autonomously adapt their bodies to new tasks and changing environments long after their initial deployment by forming new or reorganizing existing physical connections to peer robots. In previous research, many approaches have been presented to enable self-assembling robots to form composite morphologies. Recent technological advances have also increased the number of robots able to form such morphologies by at least two orders of magnitude. However, to date, composite robot morphologies have not been able to solve real-world tasks nor have they been able to adapt to changing conditions entirely without human assistance or prior knowledge.In this thesis, we identify three reasons why self-assembling robots may not have been able to fully unleash their potential and propose appropriate solutions. First, composite morphologies are not able to show sensorimotor coordination similar to those seen in their monolithic counterparts. We propose "mergeable nervous systems" -- a novel methodology that unifies independent robotic units into a single holistic entity at the control level. Our experiments show that mergeable nervous systems can enable self-assembling robots to demonstrate feats that go beyond those seen in any engineered or biological system. Second, no proposal has been tabled to enable a robot in a decentralized multirobot system select its communication partners based on their location. We propose a new form of highly scalable mechanism to enable "spatially targeted communication" in such systems. Third, the question of when and how to trigger a self-assembly process has been ignored by researchers to a large extent. We propose "supervised morphogenesis" -- a control methodology that is based on spatially targeted communication and enables cooperation between aerial and ground-based self-assembling robots. We show that allocating self-assembly related decision-making to a robot with an aerial perspective of the environment can allow robots on the ground to operate in entirely unknown environments and to solve tasks that arise during mission time. For each of the three propositions put forward in this thesis, we present results of extensive experiments carried out on real robotic hardware. Our results confirm that we were able to substantially advance the state of the art in self-assembling robots by unleashing their potential for morphological adaptation through enhanced sensorimotor coordination and by improving their overall autonomy through cooperation with aerial robots.Doctorat en Sciences de l'ingénieur et technologie
info:eu-repo/semantics/nonPublished
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Sandberg, Arne. "Dynamic Changes in the Peripheral and the Central Nervous Systems in Patients with Prior Polio." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4617.
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Seal, L. H. "Studies on glycogen in the nervous systems of Haemopis sanguisuga (L) and Planorbis corneus (L)." Thesis, University of Salford, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.372154.
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Peck, Jennifer L. "The Effects of Acute Restraint Stress on Renal Vasculature Reactivity and the Sympathetic Nervous Systems." University of Akron / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=akron1289840898.
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Kniel, Peter Christian. "The sympathetic, parasympathetic and enteric nervous systems of rats are differently affected by streptozotocin-diabetes /." [S.l : s.n.], 1985. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.
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Tigerholm, Jenny. "Mechanisms of excitability in the central and peripheral nervous systems : Implications for epilepsy and chronic pain." Doctoral thesis, KTH, Beräkningsbiologi, CB, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-93496.
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The work in this thesis concerns mechanisms of excitability of neurons. Specifically, it deals with how neurons respond to input, and how their response is controlled by ion channels and other active components of the neuron. I have studied excitability in two systems of the nervous system, the hippocampus which is responsible for memory and spatial navigation, and the peripheral C–fibre which is responsible for sensing and conducting sensory information to the spinal cord. Within the work, I have studied the role of excitability mechanisms in normal function and in pathological conditions. For hippocampus the normal function includes changes in excitability linked to learning and memory. However, it also is intimately linked to pathological increases in excitability observed in epilepsy. In C–fibres, excitability controls sensitivity to responses to stimuli. When this response becomes enhanced, this can lead to pain. I have used computational modelling as a tool for studying hyperexcitability in neurons in the central nervous system in order to address mechanisms of epileptogenesis. Epilepsy is a brain disorder in which a subject has repeated seizures (convulsions) over time. Seizures are characterized by increased and highly synchronized neural activity. Therefore, mechanisms that regulate synchronized neural activity are crucial for the understanding of epileptogenesis. Such mechanisms must differentiate between synchronized and semi synchronized synaptic input. The candidate I propose for such a mechanism is the fast outward current generated by the A-type potassium channel (KA). Additionally, I have studied the propagation of action potentials in peripheral axons, denoted C–fibres. These C–fibres mediate information about harmful peripheral stimuli from limbs and organs to the central nervous system and are thereby linked to pathological pain. If a C–fibre is activated repeatedly, the excitability is altered and the mechanisms for this alteration are unknown. By computational modelling, I have proposed mechanisms which can explain this alteration in excitability. In summary, in my work I have studied roles of particular ion channels in excitability related to functions in the nervous system. Using computational modelling, I have been able to relate specific properties of ion channels to functions of the nervous system such as sensing and learning, and in particular studied the implications of mechanisms of excitability changes in diseases.QC 20102423
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Rahman, Bootan Mohammed. "Dynamics of neural systems with time delays." Thesis, University of Sussex, 2017. http://sro.sussex.ac.uk/id/eprint/67773/.
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Complex networks are ubiquitous in nature. Numerous neurological diseases, such as Alzheimer's, Parkinson's, epilepsy are caused by the abnormal collective behaviour of neurons in the brain. In particular, there is a strong evidence that Parkinson's disease is caused by the synchronisation of neurons, and understanding how and why such synchronisation occurs will bring scientists closer to the design and implementation of appropriate control to support desynchronisation required for the normal functioning of the brain. In order to study the emergence of (de)synchronisation, it is necessary first to understand how the dynamical behaviour of the system under consideration depends on the changes in systems parameters. This can be done using a powerful mathematical method, called bifurcation analysis, which allows one to identify and classify different dynamical regimes, such as, for example, stable/unstable steady states, Hopf and fold bifurcations, and find periodic solutions by varying parameters of the nonlinear system. In real-world systems, interactions between elements do not happen instantaneously due to a finite time of signal propagation, reaction times of individual elements, etc. Moreover, time delays are normally non-constant and may vary with time. This means that it is vital to introduce time delays in any realistic model of neural networks. In this thesis, I consider four different models. First, in order to analyse the fundamental properties of neural networks with time-delayed connections, I consider a system of four coupled nonlinear delay differential equations. This model represents a neural network, where one subsystem receives a delayed input from another subsystem. The exciting feature of this model is the combination of both discrete and distributed time delays, where distributed time delays represent the neural feedback between the two sub-systems, and the discrete delays describe neural interactions within each of the two subsystems. Stability properties are investigated for different commonly used distribution kernels, and the results are compared to the corresponding stability results for networks with no distributed delays. It is shown how approximations to the boundary of stability region of an equilibrium point can be obtained analytically for the cases of delta, uniform, and gamma delay distributions. Numerical techniques are used to investigate stability properties of the fully nonlinear system and confirm our analytical findings. In the second part of this thesis, I consider a globally coupled network composed of active (oscillatory) and inactive (non-oscillatory) oscillators with distributed time delayed coupling. Analytical conditions for the amplitude death, where the oscillations are quenched, are obtained in terms of the coupling strength, the ratio of inactive oscillators, the width of the uniformly distributed delay and the mean time delay for gamma distribution. The results show that for uniform distribution, by increasing both the width of the delay distribution and the ratio of inactive oscillators, the amplitude death region increases in the mean time delay and the coupling strength parameter space. In the case of the gamma distribution kernel, we find the amplitude death region in the space of the ratio of inactive oscillators, the mean time delay for gamma distribution, and the coupling strength for both weak and strong gamma distribution kernels. Furthermore, I analyse a model of the subthalamic nucleus (STN)-globus palidus (GP) network with three different transmission delays. A time-shift transformation reduces the model to a system with two time delays, for which the existence of a unique steady state is established. Conditions for stability of the steady state are derived in terms of system parameters and the time delays. Numerical stability analysis is performed using traceDDE and DDE-BIFTOOL in Matlab to investigate different dynamical regimes in the STN-GP model, and to obtain critical stability boundaries separating stable (healthy) and oscillatory (Parkinsonian-like) neural ring. Direct numerical simulations of the fully nonlinear system are performed to confirm analytical findings, and to illustrate different dynamical behaviours of the system. Finally, I consider a ring of n neurons coupled through the discrete and distributed time delays. I show that the amplitude death occurs in the symmetric (asymmetric) region depending on the even (odd) number of neurons in the ring neural system. Analytical conditions for linear stability of the trivial steady state are represented in a parameter space of the synaptic weight of the self-feedback and the coupling strength between the connected neurons, as well as in the space of the delayed self-feedback and the coupling strength between the neurons. It is shown that both Hopf and steady-state bifurcations may occur when the steady state loses its stability. Stability properties are also investigated for different commonly used distribution kernels, such as delta function and weak gamma distributions. Moreover, the obtained analytical results are confirmed by the numerical simulations of the fully nonlinear system.
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Foa, Lisa Catherine, and mikewood@deakin edu au. "The ontogeny of putative GABAergic neurons and their receptors in the nervous system of the crayfish Cherax destructor." Deakin University, 1996. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20060728.141951.
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Inhibitory neurons exert control the expression of many aspects of behaviour by regulating the effectiveness of excitatory neural function. By comparison with excitatory neural systems, relatively little is known about the development of inhibitory neurons and the influence which these neurons exert on the development of other neural systems. Two issues which relate to the development of inhibitory neurons are of particular interest. First, a paradox arises when inhibitory neurons are considered in terms of modern models of synaptic development which involve activity-dependent mechanisms of synaptic plasticity. Second, there is some evidence that inhibitory neurotransmitters may act in a special trophic manner during the early development of nervous systems. Investigations of these issues would be greatly facilitated in a neural system in which it was possible to experimentally control aspects of the development of individual pre- and postsynaptic cells. The aim of the results presented in this thesis was to characterise the normal development of one such system: the GABAergic inhibitory system of the Australian freshwater crayfish, Cherax destructor.
The ontogeny of the inhibitory neurotransmitter GABA across the embryonic period of 30% to 100% development was investigated using immunohistochemical techniques. GABA-like immunoreactive cells and fibres were first detected in the embryonic brain region. The expression of GABA-like immunoreactivity progressed along a rostro-caudal gradient, with GABA-like immunoreactive cells being detected in the most anterior thoracic ganglia at 45% development and in all ganglia by 65% development. GABA-like immunoreactive fibres were evident in peripheral nerves as early as 55% development and ramified extensively throughout the neuropil of the nervous system by 65% development. By contrast, immunoreactivity to the primary excitatory neurotransmitter, glutamate, was not detected until 60-65% development. Glutamate-like immunoreactivity at 60-65% development was evident only in the form of punctate staining in the midline of the ventral nerve cord. Cell body staining was observed only at 90% development and was restricted to only a few cells on the periphery of the ventral nerve cord.
Radio-labelled ligand binding methods and autoradiography were used to study the expression of putative GABA receptors in the Cherax embryos from 30% to 100% development. Specific binding was evident in the earliest embryos studies at 30% development. There was an initial increase in binding from 30% to 40% development, followed by a dramatic drop to almost zero binding at 50-55% development. This was followed by a gradual increase in binding levels with age, reaching a plateau at 85% development. Preliminary pharmacological evaluation of binding indicated that at least three GABA receptor types were expressed during embryonic development.
Methods for culturing, dissociated neural tissues explanted form Cherax embryos at 85% development were established. The success of cultures was demonstrated by neurite extension, and neuronal networks in which neurons appeared to form connections with other neurons and with explanted muscle cells after two days in culture. Immunohistochemical studies demonstrated that some explanted neurons expressed GABA-like immunoreactivity within two days of explanting.
These studies have provided a comprehensive description of the development of GABAergic neurons and their receptors in Cherax destructor embryos. The very early expression of GABA-like immunoreactivity, coupled with the early onset of specific GABA binding, strongly indicates that the GABAergic neurons are functional and able to exert an effect on other cells during much of the period of nervous system development in crayfish embryos. These results support the hypothesis that inhibitory neurons may play an important role as regulators of the overall process of assembly and maturation of the nervous system and provide a substantial basis for future experimental studies in which the specific action of inhibitory neurons on the development of discrete components of the crayfish nervous system may be investigated.
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Bridge, Suzanne Kathleen. "Interactions between the sympathetic nervous systems and endothelial factors in the short-term regulation of the circulation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/MQ63273.pdf.
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Hillard, Kynlee, Matthew Zahner, David Kyle Mounger, Brooke Tipton, and Grayson Jo White. "The effect of leptin on metabolic- and cardiovascular-related pre-sympathetic hypothalamic neurons in mice." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/asrf/2019/schedule/11.
Full textAbstract:
Obesity has risen 75% in the United States since 1980 and an estimated 80 million American adults are considered obese. Obesity activates the sympathetic nervous system and is associated with neurogenic hypertension. Leptin is an obesity-related neuropeptide released from fat cells which reduces appetite and increases metabolism. Leptin activates metabolic and cardiovascular responsive pre‑sympathetic neurons within the hypothalamus. Although leptin increases metabolism and curbs appetite, it also increases blood pressure. Considering that one main goal of obesity treatments is to diminish the cardiovascular-related co-morbidities this is an unacceptable side effect for potential treatments. Thus, a better understanding of the role hypothalamic sites involved in obesity-related hypertension is necessary for successful treatments. Our hypothesis is that leptin activates hypothalamic neurons that control metabolic (raphe pallidus) and cardiovascular activity (RVLM, rostroventrolateral medulla) within the brainstem. To test our hypothesis we created a line of transgenic mice using the cre-lox recombination system to express the reporter gene tdTomato under the control of the leptin (ObRb) receptor gene. First, we performed a behavioral study to verify the physiological effect and optimal dose of daily leptin treatment. To do this we implanted mini-osmotic pumps for continuous subcutaneous leptin (400 ng/hr) administration and measured food intake and body weight over 4 weeks. To determine if leptin activates pre‑sympathetic hypothalamic neurons we performed neuroanatomical tracer studies in these mice. At the end of the 4-week period, we injected fluorescent retrograde tracers into the raphe pallidus (green, metabolic center) and RVLM (magenta, cardiovascular). We then performed fluorescence immunohistochemical labelling to identify leptin-induced neuronal activation cFos a marker of neuronal activation of these neurons. Data from this behavioral, neurophysiological and neuroanatomical study will provide a better understanding of the role of the hypothalamus in controlling blood pressure and metabolism in obesity. Information from this study will provide groundwork for a better understanding of central autonomic mechanisms of cardiovascular risk as well as risk introduced by drugs intended to treat obesity.
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Pettit, Michael J. (Michael James). "Mechanisms of rapid receptive field reorganization." Thesis, University of North Texas, 1995. https://digital.library.unt.edu/ark:/67531/metadc332851/.
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Rapid receptive field (RF) reorganization of somatosensory neurons in the cat dorsal column nuclei (DCN) was studied using electrophysiological and histological methods. Soon after denervation of the peripheral RF by lidocaine injection, every DCN neuron tested exhibited a reorganized RF.
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Geiselbrecht, Hannes [Verfasser], and Roland [Akademischer Betreuer] Melzer. "Morphology and evolution of Malacostraca : structure of central nervous systems, mandibles and sensilla / Hannes Geiselbrecht. Betreuer: Roland Melzer." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2014. http://d-nb.info/1056876670/34.
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Rosin, Åsa. "Effects of joint cocaine and ethanol on the brain opioid systems /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-441-4/.
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Safdar, Shahana. "Peptide-targeted nitric oxide delivery for the treatment of glioblatoma multiforme." Diss., Georgia Institute of Technology, 2012. http://hdl.handle.net/1853/45797.
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Glioblastoma multiforme (GBM) is the most common malignant central nervous system tumor. The ability of glioma cells to rapidly disperse and invade healthy brain tissue, coupled with their high resistance to chemotherapy and radiation have resulted in extremely poor prognoses among patients. In recent years, nitric oxide (NO) has been discovered to play a ubiquitous of role in human physiology and studies have shown that, at sufficient concentrations, NO is able to induce apoptosis as well as chemosensitization in tumor cells. This thesis discusses the synthesis and characterization of targeted NO donors for the treatment of GBM.
Two glioma targeting biomolecules, Chlorotoxin (CTX) and VTWTPQAWFQWVGGGSKKKKK (VTW) were reacted with NO gas to synthesize NO donors. These NO donors, CTX-NO and VTW-NO, released NO for over 3 days and were able to induce cytotoxicity in a dose dependent manner in glioma cells. The biggest advantage, a result of the targeted delivery of NO, was that the NO donors did not have toxic effects on astrocytes and endothelial cells. To characterize the chemosensitizing effects of CTX-NO, cells were incubated with CTX-NO prior to exposure to temozolomide (TMZ) or carmustine (BCNU). These drugs are the most popular chemotherapeutics used in the treatment of GBM, but have only shown modest improvements in patient survival. Viability studies showed that CTX-NO selectively elicited chemosensitivity in glioma cells, whereas the chemosensitivty of astrocytes and endothelial cells remained unaffected. Further investigation showed that CTX-NO pretreatment decreased O6-methylguanine DNA methyltransferase (MGMT) and p53 levels, suggesting that a decrease in DNA repair ability may be the mechanism by which chemosensitivity is induced.
Lastly, the effects of CTX-NO on glioma cell invasion and migration were studied using Boyden chamber and modified scratch assays. Non-toxic doses of CTX-NO decreased glioma cell invasion in a dose dependent manner. Studies quantifying matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) surface expression demonstrated that while MMP-2 expression was decreased by both CTX and CTX-NO, MMP-9 expression was decreased only by CTX-NO. Furthermore quantifying MMP-2 and MMP-9 activity levels showed that NO and CTX work synergistically to decrease the activity of the enzymes. These studies demonstrate that the decrease in glioma invasion resulting from CTX-NO treatment was partially a consequence of decreased levels of surface and activated MMP-2 and MMP-9. The work presented in this thesis describes a novel approach to treating GBM that can be modified to develop treatments for various other tumors. Furthermore this is the first study to develop glioma-targeting NO donors.
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Sorensen, Michael Elliott. "Functional Consequences of Model Complexity in Hybrid Neural-Microelectronic Systems." Diss., Georgia Institute of Technology, 2005. http://hdl.handle.net/1853/6908.
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Hybrid neural-microelectronic systems, systems composed of biological neural networks
and neuronal models, have great potential for the treatment of neural injury and
disease. The utility of such systems will be ultimately determined by the ability of the engineered
component to correctly replicate the function of biological neural networks. These
models can take the form of mechanistic models, which reproduce neural function by describing
the physiologic mechanisms that produce neural activity, and empirical models,
which reproduce neural function through more simplified mathematical expressions.
We present our research into the role of model complexity in creating robust and flexible
behaviors in hybrid systems. Beginning with a complex mechanistic model of a leech
heartbeat interneuron, we create a series of three systematically reduced models that incorporate
both mechanistic and empirical components. We then evaluate the robustness
of these models to parameter variation, and assess the flexibility of the models activities.
The modeling studies are validated by incorporating both mechanistic and semi-empirical
models in hybrid systems with a living leech heartbeat interneuron. Our results indicate
that model complexity serves to increase both the robustness of the system and the ability
of the system to produce flexible outputs.
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Wixner, Jonas. "Gastrointestinal disturbances in hereditary transthyretin amyloidosis." Doctoral thesis, Umeå universitet, Institutionen för folkhälsa och klinisk medicin, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-88745.
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Background Transthyretin amyloid (ATTR) amyloidosis is a systemic disorder caused by amyloid deposits formed by misfolded transthyretin (TTR) monomers. Two main forms exist – wild-type and hereditary ATTR amyloidosis, the latter associated with TTR gene mutations. Wild-type ATTR amyloidosis has a late onset and primarily cardiac manifestations, whereas hereditary ATTR amyloidosis is a rare autosomal dominant condition with a considerable phenotypic diversity. Both disorders are present all over the world, but endemic areas of the hereditary form are found in Sweden, Portugal, Brazil and Japan. Gastrointestinal (GI) complications are common in hereditary ATTR amyloidosis and play an important role in the patients’ morbidity and mortality. Malfunction of the autonomic and enteric nervous systems has been proposed to contribute to the GI disturbances, but the underlying mechanisms have not been fully elucidated. The aims of this thesis were to assess the prevalence of GI disturbances for different subtypes of ATTR amyloidosis, to further explore the mechanisms behind these disturbances, and to evaluate the outcome of the patients’ GI function after liver transplantation, which currently is the standard treatment for hereditary ATTR amyloidosis. Methods The Transthyretin Amyloidosis Outcomes Survey (THAOS) is the first global, multicenter, longitudinal, observational survey that collects data on patients with ATTR amyloidosis. THAOS enrollment data were used to assess the prevalence of GI symptoms and to evaluate their impact on nutritional status (mBMI) and health-related quality of life (EQ-5D Index Score). Data from routine investigations of heart-rate variability and cardio-vascular response to tilt tests were utilized to evaluate the impact of autonomic neuropathy on the scintigraphically measured gastric emptying half-times in Swedish patients with hereditary ATTR amyloidosis. Gastric wall autopsy specimens from Japanese patients with hereditary ATTR amyloidosis and Japanese non-amyloidosis controls were analyzed with immunohistochemistry and computerized image analysis to assess the densities of interstitial cells of Cajal (ICC) and nervous tissue. Data from gastric emptying scintigraphies and validated questionnaires were used to evaluate the outcome of Swedish patients’ GI function after liver transplantation for hereditary ATTR amyloidosis. Results Sixty-three percent of the patients with TTR mutations and 15 % of those with wild-type ATTR amyloidosis reported GI symptoms at enrollment into THAOS. Subsequent analyses focused on patients with TTR mutations and, among them, unintentional weight loss was the most frequent symptom (32 %) followed by early satiety (26 %). Early-onset patients (<50 years of age) reported GI symptoms more frequently than late-onset cases (70 % vs. 50 %, p <0.01), and GI symptoms were more common in patients with the V30M mutation than in those with non-V30M mutations (69 % vs. 56 %, p <0.01). Both upper and lower GI symptoms were significant negative predictors of nutritional status and health-related quality of life (p <0.01 for both). Weak but significant correlations were found between gastric emptying half-times and the function of both the sympathetic (rs = -0.4, p <0.01) and parasympathetic (rs = -0.3, p <0.01) nervous systems. The densities of c-Kit-immunoreactive ICC were significantly lower in the circular (median density 0.0 vs. 2.6, p <0.01) and longitudinal (median density 0.0 vs. 1.8, p <0.01) muscle layers of the gastric wall in patients compared to controls. Yet, no significant differences in protein gene product 9.5-immunoreactive nervous cells were found between patients and controls either in the circular (median density 3.0 vs. 6.8, p = 0.17) or longitudinal (median density 1.4 vs. 2.5, p = 0.10) muscle layers. Lastly, the patients’ GI symptoms scores had increased slightly from before liver transplantation to the follow-ups performed in median two and nine years after transplantation (median score 7 vs. 10 vs. 13, p <0.01). However, their gastric emptying half-times (median half-time 137 vs. 132 vs. 125 min, p = 0.52) and nutritional statuses (median mBMI 975 vs. 991 vs. 973, p = 0.75) were maintained at follow-ups in median two and five years after transplantation. Conclusion GI disturbances are common in hereditary ATTR amyloidosis and have a negative impact on the patients’ nutritional status and health-related quality of life. Fortunately, a liver transplantation appears to halt the progressive GI involvement of the disease, although the patients’ GI symptoms tend to increase after transplantation. An autonomic neuropathy and a depletion of gastrointestinal ICC seem to contribute to the GI disturbances, but additional factors must be involved.