Dissertations / Theses on the topic 'Sympathetic'
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Leshay, Ilana D. "A sympathetic lady /." South Hadley, Mass. : [s.n.], 2008. http://ada.mtholyoke.edu/setr/websrc/pdfs/www/2008/287.pdf.
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Manchanda, Rohit. "New insights into sympathetic transmission." Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.238131.
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Shatarat, Amjad. "ATP as a sympathetic neurotransmitter." Thesis, University of Nottingham, 2011. http://eprints.nottingham.ac.uk/12069/.
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ATP has been shown to be a sympathetic neurotransmitter in blood vessels. However, its relative importance has been shown to be influenced by the experimental conditions employed such as alteration of the vascular tone. Thus the main aim was to raise the tone of vascular preparations and to further examine sympathetic neurotransmission in these preparations. Porcine whole mesenteries were perfused with physiological buffer and changes in pressure recorded or different sized mesenteric arteries were isolated and set up for isometric recording. Responses to electrical field stimulation (EFS) were obtained under basal and raised tone conditions induced by U46619, a thromboxane A2 mimetic. The nature of the neurotransmitters involved in the mediation of the electrically-evoked responses was assessed using an α1-adrenoceptor antagonist, prazosin and/or the P2X receptor desensitizing agent, α,β-methyleneATP, an α2-adrenoceptor RX811059 antagonist, and a neuropeptide Y Y1 receptor antagonist BIBP3226. In separate experiments, responses to nerve stimulation were investigated in rat mesenteric small arteries pressurized to 90 mmHg. The effects of a selective α1-adrenoceptor antagonist, YM-12617, and selective P2X1 receptor antagonist, NF-449, on the electrically-evoked response were determined. Under basal tone conditions the electrically-evoked contractile responses in porcine whole mesenteric bed and isolated arteries were exclusively mediated by noradrenaline (NA) since they were inhibited by prazosin. However, under conditions of raised tone, the electrically-evoked responses were enhanced and a role for ATP was evident since these responses were sensitive to α,β-methyleneATP. Responses to exogenous NA and α,β-methyleneATP were also enhanced at raised tone indicating a postjunctional mechanism of enhancement. Nifedipine attenuated the enhanced responses to EFS and α,β-methyleneATP suggesting a possible role for L-type calcium channels in the mediation of the enhanced responses. In rat pressurised mesenteric arteries the electrically-evoked vasocontractile responses were sensitive to YM-12617 and NF-449, indicating that NA and ATP were involved in the mediation of these responses. Raising tone with U46619 in these arteries enhanced the electrically-evoked contractile response; under these conditions responses were sensitive to both YM-12617 and NF-449. The present study supports the observation that ATP becomes a more important sympathetic neurotransmitter under conditions of raised tone in contrast to when tone is absent. In porcine mesenteric vascular preparations NA predominates as the main sympathetic neurotransmitter under conditions of basal tone. However, when tone was raised the responses were enhanced and a role for ATP became evident.
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Chang, Hong-Shiu. "Dynamic synchronization of sympathetic oscillators." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312647.
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Kennard, James A. G. "Junctional modulation of sympathetic transmission." Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:09b63f51-0373-4a17-955d-48d3b4e46ccb.
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This project involved the study of mechanisms which modulate autonomic transmission within the sympathetic nervous system using the mouse vas deferens as a model tissue. Data was collected using contraction studies, electrophysiological techniques with sharp microelectrodes, and fluorescent calcium imaging of both smooth muscle cells and nerve terminal varicosities. An additional series of experiments was conducted using the PC12 cell line, derived from a phaeochromocytoma of the rat adrenal medulla, for flow cytometry experiments using fluorescence-activated cell sorting. During the course of this project a novel technique for studying the activity of the norepinephrine transporter within a whole organ preparation was developed using the neurotransmitter uptake assay. The uptake of this assay within the nerve terminals of the vas deferens was abolished by desipramine whilst its rate of washout was increased by amphetamine. However, some non-neuronal, peri-nuclear staining which could not be prevented by a range of pharmacological means was also observed. This new technique was then used in other work exploring putative NET regulation by cannabinoids. The modulatory effects of two pharmacological groups were assessed: testosterone and cannabinoids. Testosterone was found to have a rapid, non-genomic effect inhibiting neurotransmission within the vas deferens. This was a postjunctional effect which appeared to involve modulation of the opening of L-type calcium channels on the smooth muscle cells. For the studies of cannabinoids, two broad areas of research were conducted. First the effects of Δ9-tetrahydrocannabinol were investigated with regard to the pre-junctional release of neurotransmitters and the effect of THC on calcium dynamics within individual nerve terminal varicosities. Secondly, a surprising novel effect upon the norepinephrine transporter was identified and examined. This inhibitory effect was revealed initially by contraction experiments demonstrating a decrease in the rate of uptake of noradrenaline from the junction. This work demonstrates that there are still novel modes of regulation of sympathetic transmission to be uncovered. The ongoing challenge is to establish their role within physiology and pathophysiology.
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Scriven, Anthony James Ivor. "Plasma noradrenaline and cardiovascular sympathetic activity." Thesis, Imperial College London, 1990. http://hdl.handle.net/10044/1/46541.
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Jackson, V. Margaret. "Calcium dynamics in postganglionic sympathetic neurones." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365441.
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Wassall, Richard David. "High resolution studies of sympathetic neurotransmission." Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.497141.
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Graham, Lee Nicholas. "Sympathetic mechanisms following acute myocardial infarction." Thesis, University of Leeds, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.403027.
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Correia, Marcelo Lima De Gusmao. "Sympathetic vascular tone in human obesity." Diss., University of Iowa, 2007. http://ir.uiowa.edu/etd/134.
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King, Andrew J. "Sympathetic mechanisms of salt-sensitive hypertension." Diss., Connect to online resource - MSU authorized users, 2008.
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Thesis (Ph.D.)--Michigan State University. Dept. of Pharmacology and Toxicology, 2008.Title from PDF t.p. (viewed on Mar. 30, 2009) Includes bibliographical references (p.177-201). Also issued in print.
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Shanks, Julia A. "Cardiac sympathetic neural signalling in hypertension." Thesis, University of Oxford, 2013. https://ora.ox.ac.uk/objects/uuid:5d0c9f81-2a76-4acf-807f-a2003d362464.
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The work presented in this thesis examines the role of cardiac sympathetic signalling in the development and maintenance of hypertension in the spontaneously hypertensive rat (SHR); and the role the norepinephrine re-uptake transporter (NET) plays in the sympathetic phenotype during hypertension. Chapter One: reviews (i) cardiac impairment observed in hypertension, (ii) the mechanisms underlying sympathetic neurotransmission and signal termination, (iii) the structure, function, mechanism of action, and role of the norepinephrine (NE) re-uptake transporter in a number of diseases related to sympathetic dysfunction including hypertension. Chapter Two: comprises a detailed rational for the approach taken to; (i) record NET rate in single isolated cells from major sympathetic ganglia using a novel fluorescent assay (NTUA); (ii) measure norepinephrine release from isolated sympathetic cells using a method of carbon fibre based amperometry; (iii) measure autonomic function on living tissue in-vivo and in-vitro using organ bath and whole animal preparations; (iv) quantification of protein expression and protein levels within single cells and isolated ganglia. Chapter Three: examined the cardiac autonomic phenotype of the young pre-hypertensive SHR. Baseline haemodynamics were comparable between the SHR and age matched WKY controls, apart from in-vivo heart rate which the SHR displayed a small, but significant tachycardia. Release of sympathetic neurotransmitter NE, and the co-transmitter NPY were also elevated in the young SHR compared to WKY even though the SHR showed no elevation in arterial blood pressure at this age. Tyrosine hydroxylase levels were unaltered. 3H-NE release studies also revealed there may be a dysfunction in NET in the SHR at this age, as DMI treatment normalised the difference in 3H-NE overflow between the SHR and WKY. Chapter Four: described an investigation in to the activity of the NE re-uptake transporter between older, SHR with established hypertension and age matched normotensive WKY. A novel fluorescent assay of the monoamine transporter family was used to monitor NET activity within isolated sympathetic cells from three ganglia associated with hypertension. Direct evidence for the first time is reported that NET activity was lower in cardiac stellate neurons of the SHR compared to the WKY, but not in the other ganglia tested (superior cervical ganglion (SCG) â vascular innervation of head and neck, and celiac/superior mesenteric ganglia (CG/SMG)â renal and abdominal organs). The data support the notion that NET is regulated in a site-specific fashion, which may account for the sympathetic heterogeneity of NE spillover reported in humans. Chapter Five: examined differences in NET activity and expression levels between four-week-old pre-hypertensive SHR and age matched WKY. The NTUA assay revealed a significantly lower rate of NET activity within stellate neurons of the young SHR compared to WKY, with no difference in NET protein expression. No difference again was seen in the other ganglia. The SCG was the only ganglia in which NET significantly decreased with age, indicating the NET dysregulation within the vasculature may develop at a later stage of hypertension than observed in cardiac ganglia. Chapter Six: examined the ability to modulate NET activity in WKY and SHR stellate neurons in response to a number of pharmacological agents that stimulate cGMP (BNP, SNP, 8-Br-cGMP) and inhibition of PKC. These were agents previously implicated in NET modulation in other cell types. All activators of cGMP reduced NET rate to a similar degree in the WKY. No change in NET rate was observed in the SHR, indicating that NET modulation either intrinsically, and/or receptor membrane insertion, was faulty in the SHR. PKC inhibition increased NET rate in both groups. Chapter Seven: is a concluding discussion summarising the main findings from this thesis, placing them in to physiological context, and discusses avenues of further research.
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Edwards, Susan N. "Regulation of cell death in sympathetic neurons." Thesis, University of Oxford, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316898.
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Walker, Ryan G. "Plasticity of adult sympathetic neurons following injury." Miami University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=miami1250091703.
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Churcher, Millicent. "The Sympathetic Imagination: Recognition, Reciprocity, and Difference." Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/14735.
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In light of the limitations of top-down measures to adequately address the injustices that are suffered by devalued social identities, this thesis examines the sympathetic imagination as a resource for achieving recognition of racial and sexual difference. Adam Smith’s rich and sophisticated account of sympathy in The Theory of Moral Sentiments (1759) is central to this project. Smith claims that our capacity to imaginatively adopt others’ standpoints and to be emotionally affected by their experiences is what binds individuals together as moral agents. Smith acknowledges that the extent to which identify with others’ experiences is often influenced by a lack of understanding, bias and prejudice. Hence, if sympathy is to produce moral behaviour, it must be harnessed to an informed and reflective imaginative exercise. Harmonious social communities in Smith’s view are underpinned by reciprocal exercises of imaginative perspective-taking between individuals, wherein each person strives to grasp the other’s point of view, and to critically scrutinise their response to the other’s feelings. Given the general plausibility of Smith’s naturalistic moral theory, this thesis analyses the massive failures of sympathy that mark contemporary societies, with reference to the concept of the social imaginary. I suggest that the dominant social imaginary of a society has the capacity to systematically undercut fellow-feeling with the experiences of identities that are prevented from shaping prevailing values, norms and meanings, owing to their membership within a marginalised and devalued group. It achieves this by structuring implicit and widely held assumptions about different social identities that exclusively reflect the perspectives of privileged groups, and which render certain possibilities inconceivable or implausible. This research discusses the value and limitations of Smith’s appeal to a form of critical self-regulation as a means of repairing the failures of sympathy engendered by dominant imaginings of sexual and racial difference. This discussion draws attention to the important role played by informal, everyday embodied encounters with others, in addition to institutional structures and bottom up initiatives in facilitating sympathetic identification between privileged and devalued identities.
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Lei, Saobo. "Trophic regulation of ion channels in sympathetic neurons." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq23014.pdf.
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Kurvers, Henricus Anna Johannes Maria. "Reflex sympathetic dystrophy a clinical and experimental study /." [Maastricht : Maastricht : Universiteit Maastricht] ; University Library, Maastricht University [Host], 1997. http://arno.unimaas.nl/show.cgi?fid=5817.
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Tandon, Anurag. "Adenosine and acetylcholine synthesis in a sympathetic ganglion." Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=28539.
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The role of adenosine in modulating synaptic transmission in the cat superior cervical ganglion was investigated in this thesis. The first study showed that perfusion of ganglia with exogenous adenosine increased their acetylcholine (ACh) content. The effect was reduced by blockade of nucleoside transport, as if adenosine's action was mediated at an intracellular site. Isotopic labelling of the extra ACh with radiolabelled choline showed that the additional transmitter was due to increased ACh synthesis, and associated with increased choline transport. After its formation, preganglionic stimulation could release the extra ACh, but not if vesamicol, a vesicular ACh transport inhibitor, was present. Thus, the extra ACh appears to require mobilization from a reserve pool of transmitter.Activity-dependent modulation of synaptic transmission is known to occur in sympathetic ganglia. One such form of adaptive behavior is the increase in ACh content ('rebound ACh') after high frequency preganglionic stimulation. The possibility that adenosine might play a role in the rebound phenomenon was examined in the second study. The accumulation of rebound ACh was sensitive to nucleoside transport inhibitors; dipyridamole reduced rebound ACh if it wzs present only after the stimulation, but not if it was present only during stimulation. After its synthesis, rebound ACh was released by preganglionic stimulation, but not if vesamicol was present, as if the extra transmitter had to be mobilized from a reserve pool. Because the dipyridamole-sensitive step occurred after the conditioning period, it seemed possible that a retrograde messenger triggered the post-stimulation change in ACh synthesis.
Thus, the final series of experiments tested whether a postsynaptic signal could alter presynaptic ACh synthesis. Antidromic stimulation increased ganglionic ACh synthesis, and, consequently, ACh content. Subsequent evoked ACh release was potentiated, as if the additional transmitter was releasable. The antidromic stimulation-induced increase in AZh content was blocked by dipyridamole suggesting that adenosine might be involved.
Overall, the results presented in this thesis are consistent with the notion that adenosine acts as a retrograde messenger after high frequency orthodromic stimulation to induce an increase in presynaptic ACh synthesis.
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Smith, Amanda Bernadette. "Neurotransmitter release mechanisms in postganglionic sympathetic nerve terminals." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318470.
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Ramcharan, Eion J. "A study of receptors in mammalian sympathetic ganglia." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.256900.
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Zhu, Jinghua. "The transformation of chromaffin cells into sympathetic neurons." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386926.
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Elrick, Donald Brown. "Depolarisation-secretion coupling in postganglionic sympathetic nerve terminals." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260116.
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Miara, Amy. "Differences in sympathetic nervous response due to gender." Thesis, Boston University, 2013. https://hdl.handle.net/2144/12160.
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Thesis (M.A.)--Boston UniversityThe sympathetic nervous system, in addition to its many roles as part of the autonomic nervous system, utilizes contact with many organs in the body to recruit them for an immediate response to danger. The multiple survival responses that the sympathetic nervous system manifests are typically known as the fight, flight or freeze response. The freeze response, otherwise referred to as tonic immobility, is being explored here for its survival value in the specific context of gender. It is our belief that in situations of interpersonal aggression, females may be more suited to survive by utilizing a tonic response when they are confronted with violence. Research in the areas of both tonic immobility and gender differences will be explored and compared, as well as animal origins of tonic immobility. It is our hope that by looking at the various studies already conducted on these topics, a path for future research on gender and sympathetic response may be illuminated in the field of physiological psychology.
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Pijeira, Díaz H. J. (Héctor Javier). "Electrodermal activity and sympathetic arousal during collaborative learning." Doctoral thesis, Oulun yliopisto, 2019. http://urn.fi/urn:isbn:9789526222196.
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Abstract This dissertation investigates high school students’ individual and interpersonal physiology of electrodermal activity (EDA) during collaborative learning in naturalistic settings. EDA is an index of sympathetic arousal, which is concomitant with cognitive and affective processes. Two data collections were organized with students working collaboratively in triads. The first one took place during the performance of a science task, and the second during two runs of a six-week advanced physics course. The data collected included EDA (measured unobtrusively using Empatica® E3 and E4 wristbands), performance measures (pre- and post-tests, task solutions, and course exam), and questionnaires on cognitive, affective, and collaborative aspects of learning. The work was reported in three articles. The results indicate that, on average, students spent more than half (60%) of the class at a low arousal level, possibly signaling relaxation, disengagement, or boredom. Most of the time (≈60–95% of the lesson), triad members were at a different arousal level, which might indicate that students took turns (alternating task-doers) in executing the task or applied some division of labor rather than truly collaborating. In terms of achievement, sympathetic arousal during the exam was a predictor of the exam grades, and pairwise directional agreement of EDA was positively and highly correlated to the dual learning gain. Arousal contagion could have occurred in up to 41% of the high arousal intervals found. The possible arousal contagion cases took place mostly on a 1:1 basis (71.3%), indicating that interactions in a collaborative learning triad seem to occur mainly between two members rather than among the three. The findings provide an ecologically-valid picture of the students’ EDA responses in the classroom, both individually and collaboratively, benefiting from the connection of arousal to cognitive and affective processes to increase the saliency of otherwise elusive phenomena. Methodologically, the study contributes to the exploration and exploitation of psychophysiological approaches for collaborative learning research. On a practical level, it provides physiological indices that could be incorporated into learning analytics dashboards to support students’ awareness and reflection, and teachers’ pedagogical practicesTiivistelmä Tässä väitöstutkimuksessa tarkastellaan elektrodermaalista aktiivisuutta (EDA) ja tästä johdettua sympaattista vireystilaa ja fysiologisia indeksejä, samanaikaisesti yksilöiden ja yksilöiden välisten kognitiivisten ja affektiivisten prosessien kanssa. Tutkimusaineisto kerättiin yhteisöllisen oppimisen tilanteista, joissa oppilaat työskentelivät kolmen hengen ryhmissä. Ensimmäinen osa aineistosta kerättiin oppilaiden suorittaessa luonnontieteiden alan tehtävää ja toinen kahden fysiikan syventävän kurssin aikana. Aineistoon sisältyi EDA (Empatica® E3- ja E4-rannekkeista), oppimisen mittaukset (alku- ja lopputestit, tehtävien ratkaisut ja kurssikokeet) sekä kyselylomakkeet oppimisen kognitiivisista, affektiivisista ja yhteisöllisen työskentelyn näkökulmista. Tutkimus on raportoitu kolmessa artikkelissa. Tulokset osoittavat, että opiskelijoiden sympaattisen hermoston vireystila oli keskimäärin yli puolet (60 %) luokkatyöskentelystä alhainen, mikä viittaa mahdolliseen rentoutumiseen, osallistumisen puutteeseen tai tylsistymiseen. Ryhmänjäsenet olivat suurimman osan ajasta (≈60-95 %) eri vireystilan tasoilla, mikä voi tarkoittaa, että he suorittivat tehtävää vuorotellen (tehtävän suorittajaa vaihdellen) tai jonkinlaista työnjakoa käyttäen, yhteisöllisen työskentelyn sijaan. Sympaattinen vireystila kurssikokeessa ennusti kokeen arvosanoja. Lisäksi oppilasparien EDA:n samansuuntaisuus korreloi vahvasti oppimistulosten kanssa. Yksilöiden välillä tapahtuvaa sympaattisen vireystilan ”tarttumista” on voinut esiintyä jopa 41 prosentissa todetuista korkean vireystilan intervalleista. Mahdolliset ”tarttumiset” ilmenivät enimmäkseen (71,3%) 1:1 suhteessa, mikä viittaa siihen, että vuorovaikutus yhteisöllisessä oppimisessa näyttäisi tapahtuvan pääasiassa kahden yksilön välillä kaikkien kolmen sijaan. Tulokset tarjoavat ekologisesti validin kuvan opiskelijoiden EDA-reaktioista luokkahuoneessa sekä yksilöllisesti että yhteisöllisesti tarkasteltuna, selventäen samalla kuvaa sympaattisen vireystilan yhteydestä kognitiivisiin ja affektiivisiin prosesseihin. Menetelmällisesti tutkimus kartoittaa psykofysiologisen lähestymistavan mahdollisuuksia yhteisöllisen oppimisen tutkimuksessa. Se esittelee fysiologisia indeksejä, jotka voitaisiin visualisoida oppimisen analytiikan sovelluksissa opiskelijoiden tietoisuuden ja reflektion sekä opettajien pedagogisten käytäntöjen tukemiseksi
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Du, Toit Nagib. "Evisceration and sympathetic ophthalmia : is there a risk ?" Master's thesis, University of Cape Town, 2006. http://hdl.handle.net/11427/2893.
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Kasemeier-Kulesa, Jennifer Caroline. "Sympathetic ganglia formation in the chick peripheral nervous system." Diss., Montana State University, 2005. http://etd.lib.montana.edu/etd/2005/kasemeier-kulesa/Kasemeier-KulesaJ1205.pdf.
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Tabrizchi, Reza. "The vascular role of vasopressin and sympathetic nervous system." Thesis, University of British Columbia, 1986. http://hdl.handle.net/2429/26090.
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The aim of my study was to investigate the influence of arginine vasopressin (AVP) and the sympathetic nervous system in the control of peripheral resistance and to examine the constrictor actions of various pressor agents in capacitance vessels.
In the first set of experiments, the vascular effect of AVP in the presence and absence of influence from angiotensin II (Ag II) or a-adrenergic system was investigated in pentobarbital anaesthetized rats. Cardiac output (CO) and the distribution of blood flow (BF) were determined by the microspheres technique prior to and following the injection of an AVP pressor antagonist [d(CH₂)₅Tyr(Me)AVP] in three Groups of rats: saline-treated (I), saralasin-treated (II) and phentolamine-treated (III). The AVP antagonist decreased MAP and TPR in all Groups and it caused a greater depressor effect in Groups II and III than in I. In Group I, AVP antagonist increased BF to the stomach and skin. In Group II, AVP antagonist increased BF to the muscle and skin. In Group III, AVP antagonist markedly increased BF to the muscle.
The second set of experiments investigates the physiological role of the α-adrenoceptors in the vasculature. The effects of prazosin (α₂-blocker), rauwolscine (α₁-blocker) and phentolamine (nonselective α -blocker) on MAP, CO and its distribution were investigated in halothane anaesthetized rats. All three a-antagonists caused similar decreases of MAP and all increased of % distribution of CO to the lungs and muscle. During the infusion of prazo- sin, TPR was decreased but CO was not changed. In contrast, CO was decreased but TPR was not altered during the infusions of rauwolscine and phentolamine. Since CO was reduced after the blockade of α₂-but not α₁ receptors, it appears that α₂ receptors are responsible for the control of venous capacitance.
A final set of experiments were carried out to investigate the actions of various vasoconstrictor agents on the capacitance vessels of conscious rats. We investigated the dose-response relationships of methoxamine (α₁-agonist), B-HT 920 (α₂--agonist), noradrenaline (NA, non-selective α-agonist), AVP and Ag II on MAP, mean circulatory filling pressure (MCFP) and heart rate (HR) in conscious rats. The infusions of all the agonists, but not saline, caused dose-dependent increases in MAP and decreases in HR. The infusions of saline and methoxamine did not affect MCFP while the infusions of B-HT 920, NA and Ag II increased MCFP. Therefore, receptors for α₂ adrenergic agonists and Ag II are involved in the control of venous tone.Medicine, Faculty of
Anesthesiology, Pharmacology and Therapeutics, Department of
Graduate
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Wilson, Jennifer M. M. "Mechanisms of neuronal integration in adrenomedullary sympathetic preganglionic neurons." Thesis, University of Ottawa (Canada), 2002. http://hdl.handle.net/10393/6334.
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Sympathetic preganglionic neurons innervating the adrenal medulla (AD-SPN) regulate the release of adrenal catecholamines into the bloodstream. This research was undertaken to investigate the intrinsic properties and synaptic pathways characteristic of AD-SPN in neonatal rat spinal cord slice preparation. The presence of Lucifer Yellow from the patch pipette and Rhodamine-Dextran-Lysine from the adrenal medulla in the same neuron post recording identified AD-SPN. Active intrinsic properties revealed and characterised include: a potassium-mediated transient outward rectification present in 96% of AD-SPN and separable into a short 4-aminopyridine- and a long barium-sensitive component; a potassium-mediated sustained outward rectification revealed in TTx, activated positive to -50mV and blocked with quinine. These conductances contribute to the repolarising phase of the action potential. 89% of AD-SPN possessed potassium-mediated anomalous inward rectification. All AD-SPN displayed a high voltage-activated calcium spike that prolongs the action potential. The addition of internal caesium (140mM) revealed a low threshold spike mediated by T-type calcium channels that serve to facilitate burst firing. 75% of AD-SPN exhibited evidence of electrotonic coupling, indicated by characteristic oscillations in membrane potential and confirmed with dual recordings from electrotonically coupled AD-SPN. Electrotonic coupling promoted synchronous activity. An enhanced afterhyperpolarising potential facilitated transient termination of action potential firing forming bursts of activity. A role for calcium in the regulation of neuronal activity via action on electrotonic coupling was suggested by caffeine (10mM) decreasing, BAPTA-AM (15muM) and calcium free aCSF increasing the junctional conductance. Electrical stimulation of the descending fibres in both the ipsi- and contralateral funiculi evoked fast EPSPs in all AD-SPN that were mediated by both NMDA and non-NMDA receptors. A subpopulation of AD-SPN received fast IPSPs mediated by GABA acting via GABAA receptors. A train of stimuli (4 x 10Hz) in ipsi- and contralateral funiculi also evoked a slow IPSP mediated by noradrenaline acting via alpha 2-adrenergic receptors to increase a potassium conductance. The results provide insight into central mechanisms that contribute to the regulation of adrenomedullary catecholamine secretion.
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Eerdmans, Pedro Henry Alfred. "Sympathetic nerves and alterations in vascular structure and reactivity." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 1997. http://arno.unimaas.nl/show.cgi?fid=6816.
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Atwal, Jasvinder K. "Signalling mechanisms underlying Trk function in neonatal sympathetic neurons." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=37645.
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NGF acting through the TrkA tyrosine kinase receptor promotes survival and axon growth of developing sympathetic neurons in vivo and in vitro. This thesis examines the signalling pathways and proteins used by Trk receptors to mediate neuronal survival, local axon growth, and growth cone regulation in neonatal rat sympathetic neurons of the superior cervical ganglion (SCG).First, I examined the involvement of key signalling motifs on the Trk receptor in mediating neurotrophin-dependent survival and local axon growth. Using recombinant adenoviruses, I expressed the BDNF receptor TrkB, which is not endogenously expressed in SCG neurons, either in wild-type form or mutated at defined effector binding sites. Ectopically expressed wild-type TrkB activated signalling pathways similarly to endogenous TrkA, and supported both neuronal survival and local axon growth in compartmented Campenot chambers. However, TrkB mutated at the Shc-binding site was impaired in its ability to activate PI3-kinase/Akt and MEK/ERK, and was a poor mediator of both neuronal survival and local axon growth. Furthermore, by using pharmacological inhibitors, I found that TrkB-mediated survival and local axon growth required both PI3-kinase and MEK/ERK signalling.
Next, I investigated the contribution of Trk signalling to growth cone maintenance in sympathetic neurons. Acute inhibition of NGF/TrkA signalling rapidly collapsed growth cones, as did inhibition of either PI3-kinase or MEK/ERK. I then asked whether the chemorepellent Sema3F collapsed sympathetic growth cones by inhibiting TrkA-mediated growth signals. Sema3F did not disrupt NGF-induced activation of TrkA, Shc, or PLC-gamma but significantly reduced PI3-kinase and MEK/ERK activation. Furthermore, sustained hyper-activation of PI3-kinase and MEK/ERK partially blocked Sema3F-induced collapse, suggesting that Sema3F acts, at least in part, by inhibiting Trk-dependent pathways.
Together, these data describe the role of Trk signalling in survival, local axon growth, and growth cone maintenance in cultured sympathetic neurons. The Shc-binding site was found to be critical for TrkB-mediated survival and local axon growth. The PI3-kinase and MEK/ERK pathways were found to be important for survival, local axon growth and growth cone maintenance. Furthermore, the chemorepellent Sema3F collapses sympathetic growth cones, at least in part, by interfering with key neurotrophin-induced signalling pathways.
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Zagon, Aniko. "Origin of descending projections to identified sympathetic preganglionic neurons." Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.303087.
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Williams, Damian John. "High-resolution studies of drug action on sympathetic nerves." Thesis, University of Oxford, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.409943.
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Anderson, C. N. G. "Induction of apoptosis by cytosine arabinoside in sympathetic neurons." Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.595508.
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To test whether araC interfered with NGF signalling, I examined the effect of araC treatment on signalling pathways both before and during apoptosis. Using a solid-phase kinase assay and antibodies to active forms of signalling proteins, I found that treatment of neurons with araC induced apoptosis without affecting NGF-maintained signalling. AraC caused no reduction in the activity of either mitogen activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) or protein kinase B/Akt, a kinase implicated in NGF-mediated survival. AraC also did not activate c-Jun N-terminal kinase (JNK) or cause c-Jun N-terminal phosphorylation, processes that are implicated in apoptosis induced by NGF withdrawal. In investigating a role for p53 in araC-induced apoptosis, I established that p53 protein levels were elevated before and during apoptosis by treatment with araC. There was, however, no increase in the levels of p53 protein after NGF withdrawal. Furthermore, neurons from p53 null mice were resistant to treatment with araC, although in response to NGF withdrawal, these neurons and neurons from wild type animals died at a similar rate. It was found previously that MAPK/ERK activity was not necessary for NGF-induced survival. I found, by contrast, that MAPK/ERK activity protected against araC-induced toxicity as inhibition of the MAPK pathway by PD98059 resulted in a significant increase in the rate of apoptosis induced by araC in the presence of NGF. Consistent with this finding, ciliary neurotrophic factor, which induces survival but not sustained activation of MAPK/ERK, failed to protect against araC toxicity. The data presented here suggests that araC does not inhibit NGF-mediated signalling, but instead causes apoptosis by a p53-dependent mechanism which can be inhibited by MAPK/ERK activity.
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Williams, K. "Adrenoceptors in smooth and cardiac muscle after sympathetic denervation." Thesis, University of Nottingham, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377446.
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Smith, Paul Andrew. "A possible cause of sympathetic hyperactivity in essential hypertension." Thesis, University of Leeds, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399912.
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Holmes, Sharon Rosa. "Individual sympathetic nervous system activity and motion sickness susceptibility." Thesis, University of Southampton, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.245301.
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Suidan, Hana S. "Regulation of cyclic AMP metabolism in cultured sympathetic neurons." Thesis, University of Cambridge, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333392.
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Brock, James Alexander Clinton. "Analysis of factors controlling transmitter release from sympathetic nerves." Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670358.
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Du, Xiao-Jun. "Modulation of sympathetic neurotransmitter release in acute myocardial ischaemia." Thesis, University of Edinburgh, 1991. http://hdl.handle.net/1842/19706.
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There is substantial evidence to suggest that the sympathetic nervous system is intimately involved in the development of ventricular arrhythmias during acute myocardial ischaemia. Nevertheless factors controlling myocardial noradrenaline (NA) release during ischaemia are only partly understood. Therefore, the effect or duration and severity of ischaemia on neuronal NA release (left stellate ganglion stimulation, 5Hz) was studied using a perfused, innervated rat heart model. The effect of ischaemia on presynaptic inhibition by α-adrenergic, muscarinic and purinergic receptors was also examined. There is higher density of α-adrenoceptors in female tissues but it is not clear whether there is a gender difference in presynaptic inhibitory mechanisms. NA overflow progressively declined during 10 min stop-flow ischaemia, but was maintained for up to 60 min during less severe ischaemia (95% flow reduction). α-Adrenergic or purinergic antagonists increased NA overflow during low-flow but not stop-flow ischaemia. In normoxic hearts, neuronal NA overflow was inhibited by vagal nerve stimulation (VS, 15 Hz) but not after 10 min low-flow or 1-5 min stop-flow ischaemia. The loss of VS-induced inhibition of NA overflow during ischaemia may be due to enhanced α-adrenergic presynaptic inhibition of acetylcholine release, since an α-adrenoceptor antagonist could restore this effect. The inhibitory effect of the muscarinic agonist methacholine on NA overflow was also attenuated by low-flow or stop-flow ischaemia, indicating a dysfunction of muscarinic presynaptic receptors. The effect of gender on α-adrenergic presynaptic inhibition of neuronal NA release was also studied. In normoxic hearts, NA overflow by control nerve stimulation was similar. The α-adrenergic inhibitor rauwolscine potentiated NA overflow more in female (F) than in male (M) hearts, both during normoxia and ischaemia. Ovariectomy attenuated α-adrenergic presynaptic inhibition of NA overflow. During normoxia, presynaptic inhibition of neuronal NA overflow by VS was greater in F than in M hearts but methacholine reduced NA overflow equally in F and M hearts. In conclusion, sympathetic nerve stimulation leads to ischaemic-reperfusion arrhythmias. The antiarrhythmic effect of VS and of dietary polyunsaturated fatty acids cannot be explained by presynaptic modulation of NA release. Cardiac neuronal function, especially sympathetic neurotransmitter release and presynaptic modulation, is affected by the severity of ischaemia, parasympathetic nervous activity and gender.
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Heister, Hilmar. "The sympathetic imagination in the novels of J.M. Coetzee." Doctoral thesis, Humboldt-Universität zu Berlin, Kultur-, Sozial- und Bildungswissenschaftliche Fakultät, 2015. http://dx.doi.org/10.18452/17186.
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In dieser Studie wird umfassend untersucht, wie sich die sympathetic imagination im Werk von J.M. Coetzee entwickelt. Zugrunde liegt die Annahme, dass die Art und Weise wie J.M. Coetzee seine sympathetic imagination zum Einsatz bringt die Empathiefähigkeit des Lesers zu steigern vermag. Ausgangspunkt für die Untersuchung und deren zentrale Analysekategorien für die Besprechung der Romane Coetzees ist ein Blick auf Spiegelneuronen als neuronale Grundlage für Empathie, ein relative neues und stetig sich erweiterndes Feld. Geteilte Aufmerksamkeit (shared attention) und Perspektivübernahme (perspective-taking) bilden den Mittelpunkt bei neurowissenschaftlichen Diskussionen über den Zusammenhang zwischen Spiegelneuronen und Empathie. Eine Analyse von Coetzees Romanen zeigt, dass in seiner Literatur vergleichbare Mechanismen zur Wirkung kommen.The following study attempts a comprehensive evaluation of how the sympathetic imagination evolves in the works of J.M. Coetzee. The underlying assumption is that the way Coetzee employs his sympathetic imagination in his fiction enhances the reader’s empathetic capabilities. A starting point for the central categories of analysis and the close readings of his novels will be a brief exploration of the neuronal basis of empathy as discussed in the context of the discovery of and continuously extending research on mirror neurons as the neurological basis for empathy. Shared attention and perspective-taking constitute the focus of neuroscientific discussions of the connection between empathy and mirror neurons. A close look at Coetzee’s fiction will reveal comparable mechanisms in literary representation.
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Howard, A. Jean (Ava Jean). "Functional Significance of Sympathetic Fiber Ingrowth in the Habenula." Thesis, North Texas State University, 1986. https://digital.library.unt.edu/ark:/67531/metadc798080/.
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The physiological significance of noradrenergic sympathohabenular ingrowth following medial septal lesions was investigated. Following septal lesions, sympathetic fibers originating in the superior cervical ganglia are known to sprout into the medial habenular nuclei, and into the hippocampal formation. Previous work involving sympathohippocampal ingrowth showed that firing rates in septal animals with no ingrowth showed that firing rates in septal animals with no ingrowth were higher than rates of septal animals with ingrowth and controls. Those results suggested that sympathetic ingrowth in the hippocampus had some functional capability in a modulatory manner. The primary aim of the present study was to determine if the peripheral sympathetic ingrowth into the medial habenular nuclei following a septal lesion is functionally significant. The results showed that firing rates of neurons of the medial habenulae in animals receiving septal lesions were significantly higher than rates of control animals and septal lesioned + ganglionectomized animals.
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Clark, Craig R. "Sympathetic heating and cooling of trapped atomic and molecular ions." Diss., Georgia Institute of Technology, 2012. http://hdl.handle.net/1853/43757.
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Laser-cooled atomic ions have led to an unprecedented amount of control over the quantum states of matter. The Coulombic interaction allows for information to be transferred between neighboring ions, and this interaction can be used to entangle qubits for logic operations in quantum information processors. The same procedure for logic operations can be used for high resolution atomic spectroscopy, and is the basis for the most accurate atomic optical clocks to date. This thesis describes how laser-cooled atomic ions can impact physical chemistry through the development of molecular ion spectroscopy techniques and the simulation of magnetic systems by ion trap quantum computers.
A new technique developed for spectroscopy, Sympathetic Heating Spectroscopy (SHS), takes advantage of the Coulombic interaction between two trapped ions: the control ion and a spectroscopy ion. SHS uses the back action of the interrogating laser to map spectroscopy ion information onto the Doppler shift of the control ion for measurement. SHS only requires Doppler cooling of the ions and fluorescence measurement and represents a simplification of quantum logic spectroscopy. This technique is demonstrated on two individual isotopes of calcium: Ca-40(+) for cooling and Ca-44(+) as the spectroscopy ion.
Having demonstrated SHS with atomic ions, the next step was to extend the technique by loading and characterizing molecular ions. The identification of an unknown molecular ion is necessary and can be achieved by monitoring the change in motion of the two ion crystal, which is dependent on the molecular ion mass. The motion of two trapped ions is described by their normal modes, which can be accurately measured by performing resolved sideband spectroscopy of the S(1/2)-D(5/2) transition of calcium. The resolved sidebands can be used to identify unknown ions (atomic and molecular) by calculating the mass based on the observed value in axial normal mode frequencies. Again, the trapped molecular ion is sympathetically cooled via the Coulombic interaction between the Ca-40(+) and the unknown molecular ion. The sensitivity of SHS could be improved by implementing sympathetic sideband cooling and determining the heating by measuring single quanta of motion.
The ultimate limit of control would be the development of an ion trap quantum computer. Many theoretical quantum computing researchers have made bold claims of the exponential improvement a quantum computer would have over a classical computer for the simulation of physical systems such as molecules. These claims are true in principle for ideal systems, but given non-ideal components it is necessary to consider the scaling due to error correction. An estimate of the resource requirements, the total number of physical qubits and computational time, required to compute the ground state energy of a 1-D quantum Transverse Ising Model (TIM) of N spin-1/2 particles, as a function of the system size and the numerical precision, is presented. This estimate is based on analyzing the impact of fault-tolerant quantum error correction in the context of the quantum logic array architecture. The results show that a significant amount of error correction is required to implement the TIM problem due to the exponential scaling of the computational time with the desired precision of the energy. Comparison of this result to the resource requirements for a fault-tolerant implementation of Shor's quantum factoring algorithm reveals that the required logical qubit reliability is similar for both the TIM problem and the factoring problem.
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Walker, Stephen. "Studies on the sympathetic nervous system in experimental renovascular hypertension." Thesis, University of Leicester, 1987. http://hdl.handle.net/2381/34265.
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1. In these studies the role of the sympathetic nervous system (SNS) has been investigated in two models of renovascular hypertension in the rat and after surgical reversal. 2. Plasma noradrenaline (NA), heart rate and blood pressure (BP) were measured simultaneously in conscious rats with one-kidney, one-clip (1K1C) (4-6 weeks) and two-kidney, one-clip (2K1C) (4-6 and >16 weeks) hypertension, and parallel loose clip controls, before and 48 hours after unclipping. BP in all hypertensive groups fell to normal after unclipping. 3. Plasma NA was elevated in 1K1C hypertension and fell on unclipping. Conversely, in early 2K1C hypertension plasma NA was unaltered before and rose after unclipping. Plasma NA did not change with unclipping in chronic 2K1C hypertension and was not different from controls. Heart rate showed a similar pattern. Unclipping loose clip control rats produced no change in BP, plasma NA or heart rate. 4. Heart rate was correlated with plasma NA in 1K1C hypertension, and changes in these variables on unclipping were correlated in all three models. BP was only correlated with plasma hypertensive rats. 5. In contrast, renal and cardiac NA levels showed a remarkably similar pattern in 1K1C and 2K1C hypertension of 4-6 weeks duration. Ipsilateral renal NA was reduced in loose clip rats compared to sham-operated controls. This is most likely due to renal denervation during clipping. Hypertension produced a further reduction in ipsilateral renal NA and a reduction in cardiac and contralateral renal (2K1C) NA. 6. It is concluded that the SNS may have a minor role in 1K1C, but not in 2K1C, renovascular hypertension. However, changes in SNS activity upon reversal of hypertension do not explain the BP fall in either model. Changes in renal and cardiac levels of NA in renovascular hypertension are primarily secondary to sustained elevation of BP.
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Senger, Donna Lorraine. "Retrograde signaling by nerve growth factor in cultured sympathetic neurons." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ29105.pdf.
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Ramer, Matthew Stephen. "Sympathetic and sensory neuronal plasticity, peripheral substrates of neuropathic pain." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ31950.pdf.
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Milliano, Paul Augustinus René de. "Influence of medical intervention on sympathetic activity in heart failure." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2002. http://dare.uva.nl/document/85802.
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Bachoo, Manjit. "Central mechanisms responsible for generating respiratory-modulated sympathetic nerve discharge." Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=75943.
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The experimental work presented in this thesis explores, in anaesthetized and mid-collicular decerebrate, unanesthetized, cats, the properties of two components of the discharge of sympathetic nerves which are time-locked to the central respiratory cycle and are presumably generated within the central nervous system. One is the inspiration-synchronous burst, the other is a previously unknown late-expiratory burst. The properties of the inspiration-synchronous burst and its temporal relation to the phrenic nerve burst were studied under conditions in which the frequency of the latter was changed over a wide range by superior laryngeal nerve stimulation, by changes in ventilation frequency while the phrenic nerve burst was locked to the pump, and by hypocapnic hyperthermia. The data obtained are consistent with the hypothesis of a common rhythmic driver for phrenic motoneurons and sympathetic preganglionic neurons. Stimulation of low-threshold afferents in the superior laryngeal nerve selectively suppressed the phrenic burst together with the inspiration-synchronous sympathetic discharge and produced vasodilatation. The contribution of the inspiration-synchronous sympathetic discharge to neurogenic vasoconstriction was estimated, in the hindlimb of the cat, from the magnitude of the vasodilatation. A late-expiratory burst of sympathetic discharge was produced by systemic hypercapnia and by raising end-expiratory pressure to between 2 and 7 cmH$ sb2$O. Circumstantial evidence suggests this late-expiratory burst is due to input from late-expiratory neurons to sympathetic preganglionic neurons. As a background to the experimental data a survey is presented of present knowledge of the mechanisms providing mechanical and neural coupling between respiration and circulation. The functional significance of respiratory modulation of sympathetic activity is discussed.
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Fletcher, G. C. "The role of caspases in the death of sympathetic neurons." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.599084.
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Primary neurons from the rat superior cervical ganglion (SCG) are dependent on nerve growth factor (NGF) for their survival both in vivo and in vitro and die by apoptosis after NGF withdrawal. This study examines the involvement of caspases in SCG neuronal death and the circumstances under which caspase inhibitors both prevent apoptosis and allow the functional recovery of SCG neurons. Firstly, the effects of three caspase inhibitors on NGF-deprivation-induced apoptosis were tested. The most effective inhibitor at non-toxic concentrations was BOC-aspartyl(O-methyl) fluoromethylketone (BAF), which was further characterised in assays examining caspase activity during SCG neuronal apoptosis. The long-term survival of cells in which BAF treatment had prevented apoptosis was followed and it was found that newly-isolated cells could not survive after the readdition of NGF, in contrast to established neuronal cultures. The reasons to account for the lack of long-term survival of the newly-isolated NGF-deprived, BAF-treated neurons were examined. The most striking observation was the increased autophagic activity at the time of NGF addition and the selective loss of mitochondria three days later. Thus, newly-isolated cultures appear to become committed to death as a result of mitochondrial damage upstream of caspase activation. In contrast established neuronal cultures, which were rescued after caspase inhibition had prevented apoptosis, appear to become committed to death coincident with caspase activation. The data presented here suggest that the mechanism that commits neurons to die must be established before it can be predicted whether survival factors can rescue neurons when death has been prevented by caspase inhibition.
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Dalziel, Hugh H. "The role of purines in sympathetic neurotransmission in smooth muscles." Thesis, University of Glasgow, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.278487.
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Huggett, Robert John. "Sympathetic neural mechanisms in normotensive and hypertensive type 2 diabetics." Thesis, University of Leeds, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.423199.
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