Dissertations / Theses: 'Heat stimulation'

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Livingston, Megan M., and n/a. "Stimulation of immune cells by heat-killed lactobacilli and exopolysaccharide." University of Otago. Department of Microbiology & Immunology, 2008. http://adt.otago.ac.nz./public/adt-NZDU20090108.142107.

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Lactobacilli are intestinal bacteria with known immunomodulatory competence. Numerous strains of this genus have been implicated in both the prevention and treatment of intestinal inflammation as well as in maintenance of immunological homeostasis. The frequent inclusion of lactobacilli in probiotic products attests to this ability. These lactic acid bacteria colonise the murine forestomach and burgeon in other environments similarly rich in carbohydrate-containing substrates. Accordingly, lactobacilli may utilise fermentable carbohydrates to synthesise exopolysaccharides (EPS). These polymers are secreted into the cellular milieu and, while the ecological function of EPS is yet to be defined, evidence points towards a protective role. This function may include bacterial protection from immunological attack, via EPS recognition by immune cells, resulting in modulation of immunological activity. Dendritic cells (DC) are potent antigen presenting cells, providing an essential link between the innate and adaptive arms of the intestinal immune system. DC efficiently sample intestinal antigens and present peptides to cognate naive CD4⁺ T cells in secondary lymphatic tissue. Under the influence of secreted cytokines, DC direct the differentiation of naive CD4⁺ T cells and therefore, instruct the resultant immune response. Anti-inflammatory Th2 and regulatory T cells can down-regulate the destructive Th1 pro-inflammatory effects associated with inflammatory bowel disease (IBD). As such, bioactives with the aptitude to direct DC activity and T cell differentiation have the potential to prevent or reduce intestinal inflammation. Therefore, this study aimed to determine whether heat-killed EPS-producing strains of lactobacilli, and their secreted EPS, exert an immunomodulatory effect on the murine gut which may down-regulate the immune reactions associated with IBD. Lactobacilli were screened for their ability to produce EPS when grown in the presence of glucose, sucrose or lactose. Heat-killed EPS-producing strains were then used to stimulate bone marrow-derived DC (BMDC) and the resultant cytokine profile was analysed. Nine Lactobacillus strains were found to produce EPS when grown in the presence of sucrose. Of these, L. reuteri 100-23 and L. johnsonii 100-33 exhibited potential anti-inflammatory effects. Therefore, these strains, as well as L. johnsonii 100-5 and L. johnsonii #21, with relatively weak BMDC stimulatory effect, were selected for further investigation. EPS of the potentially anti-inflammatory strain L. reuteri 100-23 was analysed. This sample contained approximately 85% carbohydrate and was composed of a (2[to]6)-β-fructofuranan (levan) and a mannan. The fructan, with an estimated molecular weight of 7 kDa, comprised at least 50% of the EPS, while the mannan made up at least 22%. The mannan component was likely linked to a protein and may have originated from the culture medium. The immunostimulatory capacity of heat-killed Lactobacillus bacterial cells and their EPS was determined in vitro. Firstly, the effect of lactobacilli and EPS on BMDC cytokine secretion, particularly levels of anti-inflammatory IL-10 and pro-inflammatory IL-12, as well as the expression of cell surface activation markers, was determined. L. reuteri 100-23 stimulated relatively high IL-10 secretion but low IL-12, while L. johnsonii 100-33-stimulated BMDC produced elevated levels of both IL-10 and IL-12. All bacterial cells up-regulated co-stimulatory molecules CD40 and CD80 on BMDC. The effect of these stimulated BMDC on T cell proliferation and cytokine production was then assessed, employing the ovalbuminDO11.10 T cell model. L. reuteri 100-23-stimulated BMDC down-regulated T cell production of the proliferation-stimulating cytokine, IL-2, up-regulated regulatory TGF-β secretion, but did not affect pro-inflammatory IFN-γ levels. The EPS of all strains did not stimulate significant BMDC cytokine production and failed to alter BMDC activation marker expression. However, BMDC stimulated with L. reuteri 100-23 and L. johnsonii 100-33 EPS significantly enhanced T cell IL-2 secretion, but did not alter TGF-β or IFN-γ levels. The effect of in vivo L. reuteri 100-23 and EPS intestinal stimulation on the reactivity of immune cells was subsequently investigated. Mesenteric lymph node (MLN) cells and splenic T cells from reconstituted Lactobacillus-free mice fed stimulant or PBS on two occasions were co-cultured with stimulated or unstimulated donor CD11c⁺ splenic DC ex vivo. Cellular proliferation as well as TGF-β and IFN-γ secretion was analysed, and IL-10 neutralisation assays were carried out to ascertain the involvement of this cytokine. Primary exposure of MLN cells to L. reuteri 100-23 resulted in suppressed cell proliferation in the presence of enhanced TGF-β levels, which may have also involved IL-10. Primed splenic T cells exhibited increased proliferation in the presence of elevated TGF-β levels following re-exposure to L. reuteri 100-23, and IL-10 may be involved in limiting this proliferation. L. reuteri 100-23 EPS did not alter MLN cell proliferation, possibly due to the suppressive activity of IL-10, but did enhance that of naive and primed splenic T cells. The effect of ingested L. reuteri 100-23 and EPS on intestinal sIgA concentration was assessed by quantifying IgA levels in the faecal supernatant of RLF mice previously ingesting L. reuteri 100-23 and EPS. L. reuteri 100-23 EPS-fed female mice exhibited significantly elevated levels of sIgA, while heat-killed bacteria did not affect antibody levels. The present study demonstrated that oral administration of heat-killed L. reuteri 100-23 and EPS exerts immunomodulatory effects on the murine intestine. These bioactives may promote a suppressive environment by conditioning DC to secrete a cytokine profile conducive to regulatory T cell induction and memory generation. Additionally, mucosal protection may be favoured by the stimulation of elevated sIgA levels. Therefore, a therapeutic composite is possibly obtained to preserve the intestinal barrier by defending against pathogen-induced injury and buffering inflammatory events. In these ways, L. reuteri 100-23 and EPS may confer long-lasting protection against, and down-regulate the immune reactions associated with, IBD.

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Bender, Robert William. "The Effects of Passive Heat Stress on Muscle Fatigue and Intracortical Excitability of the Wrist Flexors." Ohio University Honors Tutorial College / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=ouhonors1307493073.

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Deschamps, Alain. "Vascular capacitance and the control of venous return : effect of heat stress, baroreceptor stimulation, and neuropeptide Y." Thesis, McGill University, 1990. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=74611.

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The role of capacitance vessels and blood flow distribution (BFD) in the control of venous return and cardiac output were examined. First, saline infusion during exercise in humans maintained plasma volume, reduced heart rate and core temperature, but did not change endurance time. Second, the vascular mechanics of the skin were studied in dogs. The skin has a large venous compliance (C$ sb{ rm v})$ and a long time constant of venous drainage $( tau sb{ rm v}),$ and may act as a blood reservoir during heat stress. A rise in core or skin temperature increases C$ sb{ rm v}$ and decreases venous resistance (R$ sb{ rm v}),$ but does not change $ tau sb{ rm v}.$ The last three studies were performed in dogs on circulatory bypass. The third study examined the mechanisms of increase in venous return during heat stress. Splanchnic (SPL) unstressed volume (V$ sb{ rm u})$ decreases with no change in R$ sb{ rm v},$ C$ sb{ rm v},$ $ tau sb{ rm v}$ or BFD during heat stress. This decrease in V$ sb{ rm u}$ is abolished by ganglionic blockade but not by $ alpha$ or $ beta$-receptor blockade. The fourth study looked at the effects of the baroreflex on capacitance vessels and BFD. A decreases in carotid sinus pressure from 200 to 50 mm Hg increases SPL blood flow and C$ sb{ rm v},$ and decreases SPL R$ sb{ rm v},$ $ tau sb{ rm v}$ and V$ sb{ rm u}.$ The decrease in V$ sb{ rm u}$ is abolished by ganglionic blockade, but is only partially reversed by $ alpha$-receptor blockade. The last study examined the effects of neuropeptide Y (NPY) on capacitance vessels and BFD. NPY decreases SPL V$ sb{ rm u}$ with no change in R$ sb{ rm v},$ C$ sb{ rm v},$ $ tau sb{ rm v}$ or BFD. Thus, NPY may play a role in the control of venous return.

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Sobair, Abbas Taha Hamza. "The influence of body temperature on MAC of halothane in the rabbit determined using controlled mechanical and heat stimulation." Thesis, University of Edinburgh, 1995. http://hdl.handle.net/1842/30002.

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The determination of the minimum alveolar concentration (MAC) of any inhalation anaesthetic requires repeated application of the stimulus. The investigation of the influence of body temperature on MAC in the same animal, requires even more applications of the stimulus. The use of what is commonly known as a "supramaximal stimulus", beyond which there is no increase in MAC with any further increase in stimulus intensity, is generally held to provide for the reproducibility of MAC. However, there are many conflicting reports with regard to the MAC values obtained using "supramaximal stimuli" and with the interpretation of results. In this study the unreliability of the "supramaximal stimulus", in the form of tail clamping using a haemostat for the determination of MAC of halothane in the rabbit, was established. The use of this technique was demonstrated, both grossly and histologically, to cause severe trauma and lacerations that may have altered the sensitivity of the sensory mechanisms as indicated by the great variability in the values of MAC obtained on subsequent determinations in the same animal. Also, the technique appeared to disregard modern physiological concepts on receptor thresholds, inflammation and hyperalgesia. Therefore, it was decided to explore more reliable techniques of stimulation. Controlled mechanical and heat stimulators were devised and used for the determination of MAC of halothane in the rabbit as the body temperature was manipulated to test the effect of environmental heating or cooling on MAC. The mechanical stimulator is a form of pincer driven by compressed air, and is operated from a control panel with a manual trigger. It is capable of delivering a precise stimulus at a preselected pressure to the target site (ear pinna). The stimulus was calculated in terms of Newtons per unit surface area after calibration of the device using gram weights.

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Littmann, Andrew Edwards. "Use-dependent plasticity of the human central nervous system: the influence of motor learning and whole body heat stress." Diss., University of Iowa, 2012. https://ir.uiowa.edu/etd/2931.

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The human central nervous system (CNS) is capable of significant architectural and physiological reorganization in response to environmental stimuli. Novel sensorimotor experiences stimulate neuronal networks to modify their intrinsic excitability and spatial connectivity within and between CNS structures. Early learning-induced adaptations in the primary motor cortex are thought to serve as a priming stimulus for long term CNS reorganization underlying long-lasting changes in motor skill. Recent animal and human studies suggest that whole body exercise and core temperature elevation as systemic stressors also recruit activity-dependent processes that prime the motor cortex, cerebellum, and hippocampus to process sensorimotor stimuli from the environment, enhancing overall CNS learning and performance. A primary goal of rehabilitation specialists is to evaluate and design activity-based intervention strategies that induce or enhance beneficial neuroplastic processes across the lifespan. As such, an investgation of the influence of physical, non-pharmacological interventions on cortical excitability, motor learning, and cognitive function provide the central theme of this dissertation. The first study investigated the effects of a visually-guided motor learning task on motor cortex excitability at rest and during voluntary activation measured via transcranical magnetic stimulation (TMS). Motor learning significantly increased resting cortical excitability that was not accompanied by changes in excitability as a function of voluntary muscle activation. The cortical silent period, a measure of inhibition, increased after learning and was associated with the magnitude of learning at low activation. These findings suggest that separate excitatory and inhibitory mechanisms may influence motor output as a function of learning success. The following studies investigated the influence of systemic whole-body thermal stress on motor cortex excitability, motor learning and cognitive performance. We established the reliability of a novel TMS cortical mapping procedure to study neurophysiological responses after whole-body heat stress. Heat stress significantly potentiated motor cortex excitability, though acute motor learning and cognitive test performance did not differ between subjects receiving heat stress and control subjects. Future research is needed to delineate the potential of whole body heat stress as a therapeutic modality to influence central nervous system plasticity and performance.

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Picot, Alexis. "2P optogenetics : simulation and modeling for optimized thermal dissipation and current integration Temperature rise under two-photon optogenetics brain stimulation." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCB227.

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Depuis maintenant quinze ans, l’optogénétique a bouleversé la recherche en neurosciences en permettant de contrôler les circuits neuronaux. Le développement récent de plusieurs approches d’illumination, combinées à de nouvelles protéines photosensibles, les opsines, ont permis d’ouvrir une voie vers le contrôle neuronale avec la précision de la cellule unique. L’ambition nouvelle d’utiliser ces approches afin d’activer des dizaines, centaines, milliers de cellules in vivo a soulevé de nombreuses questions, notamment concernant les possibles dégâts photoinduits et l’optimisation du choix du couple illumination/opsine. Lors de mon doctorat, j’ai conçu une simulation vérifiée expérimentalement qui permet de calculer, dans toutes les conditions actuelles d’illumination, quel sera l’échauffement au sein du tissus cérébral dû à l’absorption de la lumière par le cerveau. Parallèlement, j’ai paramétré à partir de données expérimentales des modèles de dynamique des populations, à partir d’enregistrements d’électrophysiologie, qui permettent de simuler les courants intracellulaires observés lors de ces photostimulations, pour trois protéines différentes. Ces modèles permettront les chercheurs d’optimiser leurs protocoles d’illumination afin de garantir l’échauffement le plus faible possible dans l’échantillon, tout en favorisant des dynamiques de photocourant adaptées aux besoins expérimentaux Over the past fifteen years, optogenetics has revolutionized neuroscience research by enabling control of neuronal circuits. The recent development of several illumination approaches, combined with new photosensitive proteins, opsins, have paved the way to neuronal control with the single-cell precision. The new ambition to use these approaches in order to activate tens, hundreds, thousands of cells in vivo has raised many questions, in particular concerning the possible photoinduced damages and the optimization of the choice of the illumination / opsin couple. During my PhD, I developed an experimentally verified simulation that calculates, under all actual illumination protocols, what will be the temperature rise in the brain tissue due to the absorption of light. In parallel, I modeled, from electrophysiology recordings, the intracellular currents observed during these photostimulations, for three different opsins, allowing me to simulate them. These models will allow the researchers to optimize their illumination protocols to keep heating as low as possible in the sample, while helping to generate optimized photocurrent dynamics according to experimental requirements

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LeMaitre, John P. "Exercise training by neuromuscular stimulation in chronic heart failure." Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/29219.

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Methods: Studies 1-3 randomise stable patients to conventional bicycle training (Bike) or neuromuscular stimulation (NMS) of quadriceps and gastrocnemius leg muscles. A 6-week training programme is undertaken with functional performance assessed by 6-minute walk (6MW), quadriceps strength and fatigue testing, cardiopulmonary exercise testing and quality of life scoring. Body composition is assessed further in study 2 using dual-energy X-ray absorptionometry. Inflammatory markers are assessed before and after training in study 3. Study 4 is a controlled trial of NMS and Bike training including stable (S-CHF) and recently decompensated (RD-CHF) patients, with performance testing before and after a period of training. Study 5 explores the characteristics of a large group of CHF patients admitted to hospital with heart failure and compares the characteristics of these patients with those included in the exercise training trial described in study 4 and also with those patients included in a recent meta-analysis of exercise training trials. Results: Improvements in 6MW, treadmill exercise time, quadriceps strength and fatigue were observed following both Bike and NMS training for stable patients in study 1. In study 2, a significant improvement in peak VO2 following bike training but not NMS was observed when corrected for lean muscle mass. No change in body composition following training was observed. Pro-inflammatory state was attenuated following conventional training with a significant fall in sTNFαr2 in the Bike group only. NMS training resulted in significant improvement in NT-pro BNP when compared with controls and Bike patients in study 4. Overall, exercise training appeared to be effective when RD-CHF patients were included. Study 5 demonstrated that only 6.7% of the screened population was suitable for inclusion in the exercise training trial in study 4. Eligible patients were younger, more likely to be male, had fewer comorbidities and were on more optimal CHF medication than the non-eligible patients despite similar symptoms. The characteristics of the eligible patients were similar to those included in the large meta-analysis. Conclusions: NMS exercise training appears safe and effective in stable CHF patients, although it differs from Bike training in its effects on markers of inflammation. Body composition did not change following training despite functional improvements, implying qualitative changes in peripheral muscle. RD-CHF patients may benefit from training but recruitment into a trial of exercise training is difficult. NMS is more easily delivered than Bike training and it may be a useful alternative or bridging therapy for those who cannot exercise conventionally.

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Tang, Hsin-Yi. "Changes on physiologic and cognitive functioning through light/sound stimulation in older adults : a mind/body connection /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/7216.

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Flint, Nigel Stuart. "Arrhythmogenic potential of alpha-adrenoceptor stimulation in the rat heart." Master's thesis, University of Cape Town, 1985. http://hdl.handle.net/11427/26526.

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A recent proposal is that the alpha₁-adrenoceptor may mediate the arrhythmogenic effect of catecholamines during acute myocardial ischaernia. The purpose of this thesis was to explore the role of alpha₁ and alpha₂-adrenoceptor stimulation on vulnerability to ventricular fibrillation in the norrnoxic rat ventricular myocardium and further to evaluate the possible underlying cellular mechanism. The model used was the isolated perfused rat heart (Langendorff technique) in which ventricular fibrillation was electrically induced. The amount of current required to produce ventricular fibrillation was measured as the ventricular fibrillation threshold. Alpha₁-adrenoceptor stirnμlation with methoxamine to 10⁻⁶M to 10⁻⁵M increased the vulnerability to ventricular fibrillation. The arrhythmogenic effect of methoxamine could not be attributed to beta-adrenoceptor stimulation as it occurred in the setting of the beta-adrenoceptor antagonist agent, atenolol; furthermore no accumulation of cyclic AMP, the proposed arrhythmogenic second messenger of beta-adrenoceptor stimulation, occurred. Similarly no alteration in heart rate, coronary flow rate or myocardial high energy phosphate content accompanied the arrhythrnogenic effect of methoxamine. The QT interval increased with alpha₁-adrenoceptor stimulation, this being an indirect index of prolongation of the action potential duration. The arrhythmogenic action of methoxamine was associated with a positive inotropic effect. Prazosin 10⁻⁸M (an alpha₁-adrenoceptor antagonist agent) produced a tenfold displacement to the right of the log concentration response curve of the positive inotropic effect of methoxamine. Prazosin 10⁻⁸M prevented the methoxamine induced fall in ventricular fibrillation threshold. Alpha₂-adrenoceptor stimulation with B-HT 920 and B-HT 933 (azepexole), in the presence of the beta-adrenoceptor antagonist agent atenolol, did not alter the vulnerability to ventricular fibrillation. Alpha₂-adrenoceptor stimulation produced no alteration in heart rate, coronary flow rate or metabolic status. We next explored the possible mechanism underlying the arrhythmogenic effect of methoxamine. Alpha₁-adrenoceptor stimulation enhances transsarcolemmal calcium ion influx and may induce sarcoplasmic reticulum calcium release. To assess the role of transsarcolemmal calcium movement in alpha₁-adrenoceptor mediated effects experiments were undertaken with nisoldipine and low extracellular calcium. To evaluate the role of sarcoplasmic reticulum calcium release, experiments were undertaken with ryanodine (an agent reputed to inhibit sarcoplasmic reticulum calcium release without effecting the slow inward current). Nisoldipine 10⁻⁸M, reducing extracellular calcium (2.5 mM to 1.25 mM) and ryanodine 10⁻⁹M to 10⁻⁸M, prevented the arrhythmogenic and positive inotropic effect of methoxamine. Heart rate, metabolic status and cyclic AMP levels we're unchanged with these procedures. The mechanism underlying the arrhythmogenic action of alpha₁-adrenoceptor stimulation might be an increase in cytosolic calcium concentration. This increase may be secondary to (i) an enhanced transsarcolemmal calcium influx or (ii) an increase in the phasic release of calcium from the sarcoplasmic reticulum.

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Schmidt, Christopher Easthope. "Réduction de la fatigue musculaire en trail : mécanismes et stratégies." Phd thesis, Université Nice Sophia Antipolis, 2013. http://tel.archives-ouvertes.fr/tel-00923173.

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L'objectif de ce travail de thèse a été d'analyser les stratégies de réduction de la fatigue musculaire en course de trail et potentiellement d'identifier certains paramètres d'influence de cette fatigue. La course de trail est un nouveau sport en essor qui induit une combinaison spécifique de fatigue et dommages musculaires des principaux muscles locomoteurs. Afin de pouvoir conduire des études interventionnelles, une étude descriptive préliminaire a été conduite pour caractériser la fatigue spécifique et les dommages musculaires induits par ce type d'épreuve de trail. Ensuite, la reproductibilité du trail comme modèle de fatigue a été vérifiée afin de pouvoir l'utiliser dans un contexte d'intervention. Enfin, deux études visant à réduire la fatigue induite par le trail ont été conduites. D'une part l'utilisation des vêtements de compression - très à la mode en trail a été analysée comme stratégie d'optimisation de la performance. D'autre part, a aussi été étudié l'effet d'un réchauffement préalable du muscle sur les dommages musculaires : Dans cette optique, une étude contrôlée en laboratoire a été menée, examinant les effets d'un réchauffement passif sur les conséquences fonctionnelles de course en descente chez une population non-entraînée. En résumé, les travaux conduits au sein de cette thèse fournissent une description de la fatigue en trail, et valident l'utilisation du trail comme modèle reproductible de terrain pour investiguer les stratégies de réduction de la fatigue. De plus, ils relativisent l'effet positif des vêtements de compression sur la performance et montrent le lien fonctionnel entre le réchauffement musculaire et la réduction des dommages musculaires induits par un travail excentrique.

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Davies, P. "Artificial cardiac pacing stimulation thresholds in the in vitro rabbit heart." Thesis, Coventry University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383671.

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Guhde, Isabel C., and Conner Moss. "The Role of Vagal Nerve Stimulation in Mitigating Heart Failure Progression." Digital Commons @ East Tennessee State University, 2021. https://dc.etsu.edu/asrf/2021/presentations/54.

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Cardiovascular disease (CVD) is the leading cause of death worldwide and is expected to increase in prevalence. As a result of the individual and systemic healthcare impacts of CVD, heart failure, and its subsets, focusing on the alleviation of cardiac dysfunction and restoration of autonomic imbalance is paramount. Most research regarding cardiovascular disease is focused on mitigating heart failure from a cardiovascular perspective. However, this review will investigate heart failure from a neuroscientific perspective, highlighting the influence of the renin-angiotensin-aldosterone system, autonomic imbalance, and neuroinflammation on the progression of heart failure. By doing so, this research will bring light to how neuroscience may be applied to the cardiovascular system, and how interventions, such as vagal nerve stimulation, may be an untapped resource in mitigating the progression of heart failure. This review examined current relevant research to understand the brain regions implicated in the progression of heart failure, and to better understand how the nervous system may be modulated to improve heart failure outcomes through vagal nerve stimulation. This review sets the conceptual framework for future research to examine the structural changes observed in research animals who receive vagal nerve stimulation.

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Tran, Phillip. "Investigations of cochlear implant stimulation using a finite element head model." Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/14153.

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The cochlear implant (CI) is a medical technology that is widely used to treat hearing loss. In this, current pulses are injected at the electrode pads on the implanted intracochlear electrode array to stimulate the neurons in the modiolus. All the current must travel to the return electrode, which is located remotely on the side of the head for monopolar (MP) stimulation. Our understanding of the current conduction pathways and voltage distribution resulting from CI stimulation can help improve future designs and implementation strategies. A computational model would serve as a useful tool to improve our understanding of the current conduction pathways and voltage distributions as a result of MP stimulation. However, most of these models are only interested in the local cochlea region and assume particular boundary conditions. For a more reliable result, a Human Electro-Anatomical Total Head Reconstruction (HEATHER) was developed. This finite element (FE) model was created from the female Visible Human Project dataset to include twelve tissues and geometries of the cochlear implant and electrode array. A simulation of MP stimulation using HEATHER showed that current exits the cochlea via the modiolus, the basal end of the cochlea and the cochlear walls, and travels to the implant via the cranial cavity or scalp. All return locations were similar except for the internal auditory meatus. Blocking the basal end of the cochlea increased current going to the modiolus and cochlear walls. Global voltage distributions were sensitive to tissue resistivities of large tissues (scalp, bone, grey matter). Local voltages are also dependent on boundary conditions. With HEATHER, studies that would otherwise have been difficult or not feasible to perform in vivo can be tested in silico, making it valuable for CI research. Its flexibility allows it to be also used in other fields. The workflow used to generate HEATHER can be applied to other anatomical models.

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Khalili, Mohammad Amouzadeh. "Techniques including functional electrical stimulation for treatment of spastic limb contracture." Thesis, Glasgow Caledonian University, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263378.

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Sheehan, Scott E. (Scott Eugene). "The effect of head turn velocity on Cross-coupled Stimulation during centrifugation." Thesis, Massachusetts Institute of Technology, 2007. http://hdl.handle.net/1721.1/38652.

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Thesis (S.M.)--Massachusetts Institute of Technology, Dept. of Aeronautics and Astronautics, 2007. "February 2007." Includes bibliographical references (p. 88-93). Artificial Gravity (AG) has been suggested as a potential countermeasure to the deleterious physiologic effects of long-duration space flight. Short-radius centrifugation (SRC) provides a practical means of producing AG, though perceptual side-effects may potentially limit its operational feasibility. Head-turns in the rotating environment of SRC produce Cross-coupled Stimulation (CCS), which the subject perceives as a tumbling sensation. Acutely, the CCS tumbling sensation is nauseagenic, though adaptation has been shown to diminish this detriment over time. The force environment of CCS suggests that the head-turn velocity plays a role in determining the stimulus magnitude, though the degree to which has not been characterized. In order for SRC to be an operationally viable alternative for AG, it must be shown that the motion sickness symptoms can be controlled without sacrificing adaptation. Modulation of head turn velocity has been suggested as a means to that end. A total of 23 subjects were subjected to right quadrant head-turns of 8 different velocities while spinning at 19 and 23 RPMs in the rotating environment of SRC. (cont.) The perceptual effects were characterized with subjective and objective metrics, investigating the acute differences between velocities as well as the chronic effects on adaptation. The following key results were obtained: 1. A threshold of HT Velocity exists above which an asymptotic perceptual response is observed, and below which the resulting perceptual response diminishes at a logarithmically increasing rate. 2. The effects of HT Velocity are independent of HT direction, with differing head-turn directions produce contextually specific stimuli. 3. HT velocity modulation could provide a practical means of incremental adaptation. by Scott E. Sheehan. S.M.

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Soppa, Gopal Krishna Ranganathan. "Mechanical unloading and β2-adrenoceptor stimulation for the treatment of heart failure". Thesis, Imperial College London, 2009. http://hdl.handle.net/10044/1/5287.

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Background & Introduction: Heart transplantation is the most effective treatment for end-stage heart failure (HF) but is hindered due to an inadequate availability of donor organs. Left ventricular assist devices (LVADs) have been shown to be a suitable alternative and primarily used as a ‘bridge to transplantation’ wherein the failing heart can be supported by mechanical circulatory assistance until a suitable donor organ becomes available. In 4-9% of patients, the LVAD also acts as ‘bridge to recovery’, since it induces substantial functional improvement that allows LVAD explantation, without the need of transplantation. The rate for explantation of the LVAD remains low and the functional improvement observed, a transient phenomenon. LVADs cause mechanical unloading, which produces functional, structural, signalling and molecular changes in HF. Development of myocardial unloading-induced atrophy, time- dependent myocyte contractile dysfunction and excitation-contraction (EC) coupling changes may have detrimental consequences. However, when mechanical unloading is combined with pharmacological therapy, including the β2-AR agonist clenbuterol, an improved ‘bridge to recovery’ rate of 75% can be achieved. The effects of clenbuterol on functional, structural, signalling and molecular changes in a normal and failing hearts, during mechanical unloading, are unknown. This thesis investigates some of the key effects of mechanical unloading and β2-AR agonist stimulation with clenbuterol for HF treatment, based on the following hypotheses which have been individually addressed in Chapters 3, 4 and 5 respectively. • Chronic administration of clenbuterol alters myocardial structure and function and affects calcium handling in normal rat hearts. • Mechanical left ventricular unloading and the consequent left ventricular atrophy results in altered whole-heart and cellular function in non- failing/normal rat hearts. • Clenbuterol treatment during mechanical unloading of a normal rat heart normalises whole-heart and cellular function. • Clenbuterol has an additional benefit when combined with mechanical unloading in the treatment of failing rat hearts. Methods: Clenbuterol was administered by osmotic minipumps. Mechanical un- loading was achieved by heterotopic abdominal heart transplantation. Heart failure was induced by left coronary artery ligation in rats. In-vivo whole heart function was assessed by echocardiography and ex-vivo function by pressure- volume relationship. Only LV myocytes were isolated and studied using optical, fluorescence and electrophysiological techniques. Calcium handling protein expression was assessed by Western blotting. Theory and methodology of the single-cell studies is outlined, together with validation experiments and the necessary assumptions. Results: Data obtained and their interpretations are presented in three chapters according to the proposed hypotheses. The results show that clenbuterol with, without mechanical unloading, or on its own can affect both whole-heart and cellular function in normal hearts. The treatment of failing hearts with clenbuterol, alone or in combination with mechanical unloading, improves LV function at whole-heart and cellular level by effects on cell morphology, EC coupling and myofilament sensitivity to calcium. The details of individual experiments and their interpretation are discussed in the respective chapter. General Discussion: This thesis supports the use of clenbuterol in the strategy to improve recovery in HF patients treated with LVADs and also begins to elucidate some of the possible cellular mechanisms responsible for the improvement in LV function. The questions remaining unanswered are discussed and possible future experiments that could be performed to address them are described.

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ARICI, MARTINA. "Selective SERCA2a stimulation: a new promising therapeutic approach for heart failure treatment." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2023. https://hdl.handle.net/10281/404607.

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Lo scompenso cardiaco è una delle principali cause di morte improvvisa nei paesi sviluppati ed è noto che il cuore scompensato sia caratterizzato da una ridotta contrattilità causata da un’alterazione della dinamica del calcio tra il sarcoplasma e il reticolo sarcoplasmatico. In questo ambito, istaroxime è un farmaco in fase 2 preclinica che combina l’inibizione della pompa Na+/K+ e la stimolazione di SERCA2a, mostrando effetti promettenti per il trattamento dello scompenso cardiaco acuto. Tuttavia, l’uso di istaroxime è limitato al trattamento i.v. a causa della sua breve emivita (⁓ 1 h) e dalla sua estensiva metabolizzazione a livello epatico portando alla formazione di una molecola chiamata PST3093. Il primo obiettivo del mio progetto di tesi mirava allo studio del PST3093, il principale metabolita di istaroxime, per capire se fosse dotato di attività farmacologica e per comprendere meglio gli effetti in vivo dell’istaroxime. Sulla base dei risultati ottenuti, il secondo obiettivo era quello di sviluppare degli analoghi del PST3093, stimolatori di SERCA2a e dotati di un gruppo metabolicamente stabile per la somministrazione orale. Effetti in vivo e in vitro dei derivati del PST3093 venivano valutati in un modello di ratto con cardiomiopatia diabetica indotta da streptozotocina (STZ), in quanto caratterizzato da disfunzione diastolica associata a down-regolazione di SERCA2a. Innanzitutto, venivano studiati gli effetti del PST3093 sull’attività di SERCA2a e della pompa Na+/K+, sulla dinamica del calcio intracellulare in miociti ventricolari isolati e sull’emodinamica nei ratti STZ. A differenza di istaroxime, il PST3093 risultava uno stimolatore “selettivo” di SERCA2a, privo di effetti sulla pompa Na+/K+¸ con un profilo meno aritmogenico del composto di origine. Il PST3093 risultava attivo a concentrazioni nanomolari in preparazioni cardiache di cavia e di ratto STZ e, similmente a istaroxime, stimolava SERCA2a solo in presenza del fosfolambano, diminuendone l’inibizione su SERCA2a. L’infusione del composto (effetto acuto) nei ratti STZ migliorava complessivamente le prestazioni cardiache e revertiva molte anomalie causate da STZ. Grazie alla collaborazione con un gruppo di chimici del nostro dipartimento, sono stati sintetizzati dei derivati del PST3093 privi di attività inibitoria sulla pompa Na+/K+ e formulati per essere utilizzati nel trattamento cronico (orale) dello scompenso cardiaco. Molti di loro mantenevano l’azione stimolatoria su SERCA2a a dosi nanomolari. Il composto 5 e il composto 8 venivano selezionati per ulteriori analisi in cardiomiociti isolati e in vivo (in acuto). Entrambi i composti, stimolando SERCA2a, promuovevano la compartimentalizzazione nel calcio intracellulare e, in seguito a infusione, ripristinavano la funzione diastolica nei ratti STZ. Infine, venivano valutati gli effetti cronici in vivo del composto 8 nei ratti STZ dopo somministrazione orale. Venivano testate due diverse dosi (40 o 80 mg/kg) e gli effetti venivano valutati dopo 1 o 4 somministrazioni (1 al giorno), per valutare eventuali effetti dose-dipendenti e, indirettamente, esplorare la sua farmacocinetica. Il composto 8 migliorava in maniera dose-dipendente la disfunzione diastolica causata da STZ e la sua farmacocinetica risultava comparabile a quella del PST3093. Analisi delle interazioni molecolari con 50 diversi ligandi escludevano effetti off-target del composto 8. Infine, veniva valutata la tossicità in topo. Il composto 8 risultava meno tossico di PST3093 e istaroxime In conclusione, PST3093 e i suoi derivati agivano come stimolatori “selettivi” di SERCA2a. Mentre il PST3093 prolungava gli effetti benefici dati dall’infusione dell’istaroxime, i suoi derivati possono essere considerati il prototipo di una nuova classe farmacodinamica per la terapia dello scompenso cardiaco. In particolare, il composto 8 risultava un possibile candidato per la terapia cronica. Heart failure (HF) is one of the leading causes of sudden death in developed countries and it is known that failing hearts are characterized by reduced contractile properties caused by impaired Ca2+ cycling between the sarcoplasm and sarcoplasmic reticulum (SR). In this field, istaroxime is a small-molecule drug under phase 2 clinical trial that, combining inhibition of Na+/K+ ATPase and SERCA2a stimulation, shows an interesting profile for acute HF treatment. However, istaroxime use is restricted to acute i.v. infusion because of its plasma half-life of about 1 hour in humans and its extensive hepatic metabolism to a molecule, named PST3093. The first aim of my thesis project dealt with the investigation whether PST3093, the main metabolite of istaroxime, may, on its own, be endowed with pharmacological activity and at least partially explain in vivo istaroxime effects. In light of the results, the second aim was to develop PST3093 analogues with metabolically stable groups, with the purpose to generate orally administrable SERCA2a stimulators. In vivo and in vitro effects of PST3093 follow-on compounds were evaluated by using streptozotocin (STZ)-treated rats developing diabetic cardiomyopathy with diastolic dysfunction associated to SERCA2a downregulation. Firstly, we characterized PST3093 effects on SERCA2a and Na+/K+ ATPase activities, intracellular Ca2+ dynamics in isolated ventricular myocytes and in vivo hemodynamic effects in STZ rats. At variance with its parent compound, PST3093 is a “selective” (i.e. devoid of Na+/K+ ATPase inhibition) SERCA2a stimulator, showing a safer profile than istaroxime. It is active at nanomolar concentrations in cardiac preparations from normal guinea pig and STZ rats and, similarly to istaroxime, it stimulates SERCA2a only in the presence of phospholamban (PLN), thus relieving its inhibitory activity on SERCA2a. In-vivo PST3093 i.v. infusion (acute effects) in STZ rats improved overall cardiac performance and reversed most STZ-induced abnormalities. Thanks to a collaboration with chemists of our Department, we synthesized a panel of PST3093 derivatives devoid of Na+/K+ ATPase inhibitory activity to develop a class of compounds suitable for chronic (oral) HF treatment. Most of them retained SERCA2a stimulatory action with nanomolar potency. Two selected PST3093 analogues, compound 5 and compound 8, were further characterized in isolated cardiomyocytes and their acute in vivo effects were firstly evaluated after i.v. infusion in STZ rats. Both compounds, stimulating SERCA2a, improved intracellular Ca2+ handling (promoting SR Ca2+ compartmentalization) and restored diastolic function following acute i.v. infusion in STZ rats. Finally, we evaluated chronic in vivo effects of compound 8 in STZ rats after oral administration at two dosages (40 or 80 mg/kg) at 1 or 4 daily doses to evaluate potential dose-dependent effects and to indirectly explore its pharmacokinetic in rats. Compound 8 dose-dependently ameliorated STZ-induced diastolic dysfunction and its pharmacokinetic was comparable to that of PST3093, i.e. longer than istaroxime one. Off-target effects of compound 8 were excluded based on the analysis of its molecular interaction with a panel of 50 ligands. Acute toxicity in mice was finally evaluated, showing a safer profile of compound 8 than PST3093 and istaroxime. In conclusion, PST3093 and its derivatives act as “selective” SERCA2a stimulators. While PST3093 is suitable to prolong the cardiac beneficial effect of istaroxime infusion, PST3093 derivatives can be considered the prototype of a novel pharmacodynamic class for the ino-lusitropic approach of HF. In particular, compound 8 seems to be a favourable drug candidate for chronic HF therapy.

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18

Sivaswamy, Senthil Roppel Thaddeus A. "Microfabricated electrode arrays suitable for stimulation and recording in cardiac electrophysiological studies." Auburn, Ala, 2008. http://repo.lib.auburn.edu/EtdRoot/2008/SPRING/Electrical_and_Computer_Engineering/Thesis/Sivaswamy_Senthil_58.pdf.

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19

Wilson, Laura Catherine. "The Effects of Exercise-Induced Heart Rate Arousal on Stimulation Seeking and Aggression in College Students." Diss., Virginia Tech, 2012. http://hdl.handle.net/10919/73005.

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The current study aimed to test sensation seeking as a mediator in the relationship between arousal and aggression. In addition, an experimental design was used to test whether arousal can be manipulated to alter levels of sensation seeking and aggression, both measured behaviorally. A sample of 128 undergraduate students completed state and trait measures of sensation seeking and aggression, and baseline measures of physiology. It was hypothesized that trait sensation seeking would mediate the relationship between baseline physiology and trait aggression. Also, state sensation seeking would mediate the relationship between an arousal manipulation and state aggression. The results failed to support the proposed mediation models. Furthermore, the arousal manipulation was insufficient to result in sustained heart rate differences, and therefore the malleability of state sensation seeking and aggression could not truly be tested. Exploratory analyses supported an interaction between arousal and sensation seeking, such that in individuals low on experience seeking, disinhibition and boredom susceptibility, low heart rate was associated with greater aggression. These findings suggest that arousal and sensation seeking may conjointly predict aggression through moderation rather than mediation, though future studies with improved experimental designs are needed. Ph. D.

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20

Sutherland, Hazel. "The effects of pattern and frequency of stimulation on transformation and damage in mammalian skeletal muscle." Thesis, University of Liverpool, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367198.

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21

Moncada, Diaz Silvia Juliana. "Repopulation and Stimulation of Porcine Cardiac Extracellular Matrix to Create Engineered Heart Patches." BYU ScholarsArchive, 2018. https://scholarsarchive.byu.edu/etd/8806.

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Heart failure is the main cause of death for both men and women in the United States. The only proven treatment for patients with heart failure is heart transplantation. The goal of this research is to create patches of tissue that could mimic the function of the native heart to repair the damaged portions of the heart. In this study, whole porcine hearts were decellularized to create a 3D construct that was recellularized with cardiomyocytes (CM) differentiated from human induced pluripotent stem (IPS) cells. At day 4 of differentiation, IPS-derived CMs were implanted onto cardiac extracellular matrix (cECM) and ten days after recellularization, the cells started to beat spontaneously. After implantation, the progenitor CMs continued to proliferate and populate the cECM. A live/dead assay showed the potential of the cECM as a scaffold suitable for recellularization. Confocal microscopy images were taken to evaluate the organization of the cells within the matrix and the impact of the cECM on the growth and maturation of the CMs. Representative cardiac Troponin T (cTNT) and vimentin immunostaining images of CMs derived from iPSCs, on cECM and on standard cell culture plates showed that the cECM allowed the cells to organize and form fibrils with the fibroblasts, compared with CMs cultured in regular culture plates. The timeline of implantation of the cells was a key factor for the development of the heart tissue constructs. Progenitor CMs seeded onto cECM showed better organization and the ability to penetrate 96 µm deep within the collagen fibers and align to them. However, mature CMs seeded onto the matrix showed a disorganized network with very reduced interaction of CMs with fibroblasts, forming two different layers of cells; CMs on top of fibroblasts. In addition, the depth of penetration of the mature CMs within the matrix was only 20 µm. To evaluate the impact of the addition of support cells to the CM monolayer cultures, CMs were co-cultured with human umbilical vein endothelial cells (HUVEC) and it was demonstrated that at ratios of 2:1 HUVEC:CM the beating rate of the CMs was improved from 20 to 112 bpm, additionally, the CM monolayer cultures showed a more synchronized beating pace after the addition of HUVECs. Pharmacological stimulation was performed on CM monolayer cultures using norepinephrine as a stimulator and the results showed that the beating pace of the CMs was improved to 116 bpm after 5 minutes of drug exposure. For future studies, inosculation of the tissue constructs could be performed with the incorporation of membrane proteins to understand the mechanotransduction of the cells. As a preliminary study, the action of dual claudins was evaluated with HUVEC cultures and the results showed the potential of these membrane proteins in the healing of the damaged cell membrane.

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22

Cullen, John Patrick. "Receptor subtypes and associated mechanisms in the stimulation of ventricular cell hypertrophy by angiotensin II and endothelin-1." Thesis, Queen's University Belfast, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287435.

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23

Altakroury, Hamza Fawzi. "In-vivo Human Head Conductivity Estimation by SEEG and EEG Recorded in Simultaneous with Intracerebral Electrical Stimulation." Electronic Thesis or Diss., Université de Lorraine, 2017. http://www.theses.fr/2017LORR0304.

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La localisation de source d'EEG devient un outil important pour traiter les patients atteints d'épilepsie en localisant les zones épileptogènes avant d'effectuer une chirurgie de résection. Compte tenu d'un modèle de tête direct, la localisation de la source EEG est réalisée en résolvant le problème inverse. Le modèle de tête direct est un modèle biophysique de tête plus ou moins complexe qui décrit la distribution électrique. En considérant la propagation électrique expliquant la distribution de potentiels, outre la numérisation, le modèle nécessite le réglage deux paramètres lesquels sont la géométrie du modèle de tête et la valeur des conductivités de chaque compartiment du modèle de tête. En raison des progrès computationnel et des techniques d'imagerie (comme l'IRM et la CT), il est possible de générer des modèles de tête humaine qui représentent avec une grande précision la géométrie de la tête réelle. Cependant, il existe une incertitude sur les valeurs de conductivité de chaque compartiment et la méthode avec laquelle ils devraient être estimés. Dans la littérature, les valeurs communes pour les conductivités proviennent principalement des expériences in-vitro. Dans ce travail, nous effectuons une estimation de la conductivité in-vivo à partir de données EEG/SEEG/Stimulation électrique de trois patients épileptiques. Ces données sont constituées des images IRM et des CT SCAN pour la construction d'un modèle de tête FEM à cinq compartiments pour chaque patient, ainsi que les enregistrements SEEG et EEG qui ont été acquis en même temps que la stimulation électrique intracérébrale (IES). L'originalité de ce travail réside dans l'évaluation de la performance de l'estimation des conductivités in-vivo par des mesures EEG et / ou SEEG en fonction de différents paramètres spatiaux et de la localisation des IES. Le travail se compose de trois parties principales: la première partie vise à déterminer la méthode d’optimisation sous contraintes la plus robuste parmi les algorithmes courants pour optimiser les paramètres du modèle direct de tête. L'objectif de la deuxième partie est d'analyser la sensibilité des valeurs de conductivité à différentes conditions sur la position de stimulation, le conditionnement du problème avec les positions de mesure et leur nombre et le nombre de compartiments. Alors que dans la partie finale, les conductivités d'un modèle de tête FEM isotrope et homogène à cinq compartiments ont été estimées avec des paramètres précédemment déterminés pour les trois patients. Enfin, l'effet de la fréquence de stimulation sur les conductivités estimées est analysé EEG source localization is becoming an important tool for treating epileptic patients by localizing the epileptogenic zones before performing a resection surgery. Given a forward head model, EEG source localization is performed by solving the inverse problem. The forward head model is a biophysical model which describes the electrical distribution in the human head. When considering the propagation as the only way for the current distribution to move in the head, the focus is directed primarily on two parameters for having an accurate forward head model. These parameters are: the geometry of the head model and the conductivity value of each compartment of the head model. Due to the recent advances in computers and imaging techniques (like MRI and CT), it is possible to generate human head models that represent with a high accuracy the geometry of the real head. However, there is still an argument about the conductivity values and the method by which it should be estimated. In literature, the common values for conductivities come mostly from in-vitro experiments. In this work we are performing in-vivo conductivity estimation by considering the data of three epileptic patients. This data consists of MR images and CT scans for building a five-compartment FEM head model for each patient along with SEEG and EEG recordings that were acquired in simultaneous with intracerebral electrical stimulation (IES). The originality of this work lies in evaluating the performance of in-vivo conductivity estimation by EEG and/or SEEG measurements in function of different spatial parameters and locations of the IES. The following work consists of three major parts: the first part aims to determine the most robust optimization algorithm among common algorithms for optimizing the forward head model. The objective of the second part is to analyze the sensitivity of the conductivity values given different conditions on stimulation position, measurement positions and number of compartments. While in the final part, the conductivities of an isotropic and homogeneous five-compartment FEM head model were estimated with previously selected parameters for three drug-resistant epileptic patients. Finally the effect of changing the stimulation frequency on the estimated conductivities was determined

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Dayer, Mark. "Limitations to Exercise in Congestive Heart Failure: Insights from Peripheral and Transcranial Magnetic stimulation." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.486285.

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The aims of the experiments in this thesis were to describe and further understand changes that occur in patients with heart failure after exercise. The first chapter outlines the pathophysiology of heart failure and why the motor system, from the central nervous system to the muscles, may be important in the generation of symptoms and possibly the generation of the syndrome. It also lays qut the hypotheses that guided the work in this thesis. Chapter two explains the methodologies used. Chapters three and four describe the impact of exhaustive cycle exercise on respiratory muscle and quadriceps muscle function of patients with congestive heart failure (CHF). In chapter three, 12 patients and 13 control subjects were studied. Diaphragm contractility as determined by the twitch transdiaphragmatic pressure did not fall significantly. There was no evidence of low frequency diaphragm fatigue. In chapter four, 10 patients and 10 control subjects were studied. There was significant evidence of low frequency quadriceps fatigue after exercise, which was slightly, but not significantly, more marked in the normal subjects. Having studied the principal muscles of breathing and cycling, I went on to consider the impact of heart failure on the central nervous system. Transcranial magnetic stimulation (TMS) is a technique that is well established for studying cortical excitability and a small number of studies have documented changes in motor cortical excitability after exercise. TwoÃƒ?Ã‚??Ãƒ?Ã‚?Ãƒ?Ã‚Â· studies on healthy volunteers are described in chapter five which not only confirmed that we could successfully induce these changes at lower workloads (more comparable to the workloads that subjects with CHF might be expected to attain), but also suggested that the changes induced were more related to total body work done, rather than the work of an individual muscle group. Building on theseÃƒ?Ã‚??Ãƒ?Ã‚?Ãƒ?Ã‚Â· studies I went on to study the impact of exhaustive cycle exercise on patients with 9HF. 10 patients and 10 healthy age-matched control subjects were studied. The data suggested that, by some measures, central fatigue was not induced and that changes in cortical excitability, although present, were less marked in those with CHF compared to control Subjects. Pot~ntial reasons for this are explored. The final chapter brings together the' findings and suggests. future avenues for research. A number of appendices are attached; inclUding the' custom-written software to analyse exercise tolerance tests and the work of breathing, the two papers published so far from this work and an abstract presented at the European Society of Cardiology in 2005.

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25

Szebeni, Katalin, Attila Szebeni, T. DiPeri, N. Davis, Gregory A. Ordway, and J. L. Ardell. "Thoracic Spinal Cord Stimulation Protects the Hippocampus in a Canine Model of Heart Failure." Digital Commons @ East Tennessee State University, 2013. https://dc.etsu.edu/etsu-works/8635.

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26

Bian, Jin-song. "The role of protein kinase C upon K-opioid receptor stimulation in the heart /." Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21790863.

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27

Granget, Jules. "Soulagement de la dyspnée par stimulation olfactive." Electronic Thesis or Diss., Sorbonne université, 2024. http://www.theses.fr/2024SORUS114.

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Notre cerveau orchestre la respiration par un équilibre d'informations sensorielles afférentes et les commandes respiratoires efférentes, volontaires ou autonomes. Une anomalie dans cet équilibre déclenche des sensations d'inconforts respiratoire regroupés sous le terme de « dyspnée ». La dyspnée représente non seulement une douleur physique, mais aussi une détresse psychologique avec une crainte quotidienne de mourir, entraînant de fortes réductions de la qualité de vie. Des opportunités thérapeutiques existent pour corriger les anomalies respiratoires impliquées dans la dyspnée, cependant, elles ne sont pas toujours disponibles et parfois insuffisantes. Dans ces cas, la dyspnée est appelée « persistante » et nécessite de nouvelles approches thérapeutiques pour être soulagée. Dans ce contexte, une stimulation olfactive (SO) pourrait représenter un bon candidat pour traiter la dyspnée persistante. Premièrement, par un impact émotionnel positif car il existe un lien étroit entre le système olfactif et les régions cérébrales impliquées dans la régulation des émotions par rapport à d'autres modalités sensorielles. Ensuite, par son effet sur les paramètres respiratoires. Les odeurs agréables induisent une respiration lente et profonde qui synchronise les rythmes cérébraux, induisant un état de conscience altéré et de relaxation. Et enfin par la stimulation de la branche parasympathique du système nerveux autonome (SNA), favorisant la conscience de soi, le bien-être et la relaxation. Pour explorer cette question, nous avons commencé par identifier, avec des enregistrements électroencéphalographiques intracrâniens (iEEG), les réseaux cérébraux impliqués dans les manœuvres volontaires d'exploration olfactive telles que les sniffs et les apnées, notamment pour explorer son lien avec les régions cérébrales de traitement émotionnel. Ensuite, nous avons utilisé des odeurs agréables et désagréables spécifiques à chaque sujet comme SO pendant l'induction expérimentale de la dyspnée avec une charge mécanique et métabolique tout en enregistrant l'EEG, l'ECG et des tests psychométriques pour tester si les odeurs peuvent soulager la sensation de dyspnée et par quels processus physiologique ce soulagement passe. Concernant les réseaux cérébraux sous-jacents à l'exploration olfactive volontaire, nos résultats nous ont permis d'identifier une modulation de l'activité neuronale dans l'amygdale, l'hippocampe, l'insula postérieure et le cortex temporal. En particulier, nous montrons une augmentation significative de la puissance du theta (4-8Hz) et de l'alpha (8-12Hz) au cours de l'apnée, ainsi qu'une augmentation de la puissance avant le sniff et l'apnée dans ces régions. Ces résultats suggèrent que les manœuvres volontaires respiratoires recrutent des zones limbiques, telles que l'hippocampe et l'amygdale, couramment impliquées dans le processus émotionnel, ainsi que des zones corticales, telles que les cortex temporaux. En ce qui concerne l'impact des odeurs sur les sujets sains pendant la dyspnée expérimentale, nous avons pu mesurer que les odeurs agréables ou désagréables n'ont pas affecté les paramètres respiratoires et n'ont modulé l'effet de la charge mécanique ou métabolique sur le SNA. Lors de l'induction d'une dyspnée expérimentale, les odeurs agréables ou désagréables ont induit des réponses EEG plus élevées par rapport à l'absence d'odeur, avec une odeur désagréable recrutant un réseau plus important pendant l'inspiration par rapport à une odeur agréable. Nous avons également observé que les odeurs agréables induisaient une diminution significative de la dyspnée dans une sous-population de sujets que nous avons qualifiés de « répondeurs », par opposition à une sous-population de « non-répondeurs ». Ces résultats suggèrent qu'une odeur plaisante pourrait soulager la dyspnée en fonction de l'affinité qu'un sujet pourrait avoir pour cette dernière Our brain orchestrates breathing through a balance of afferent information and efferent volitional or autonomous respiratory signals. An anomaly in this balance triggers aversive sensations regrouped under the term of “dyspnea”. Dyspnea represents not only a physical pain, but also a psychological distress with a day-to-day life fear of dying with high decreases for quality of life. Therapeutical opportunities to correct respiratory abnormalities implicated in dyspnea exist, however they are not always available and sometimes not sufficient. In these cases, the dyspnea is called “persistent” and need new therapeutical approaches to be alleviated. In this context, an olfactory stimulation (OS) could represent a good candidate to address persistent dyspnea. Firstly, OS could alleviate dyspnea through a positive emotional impact, there is a close link between the olfactory system and brain regions implicated in emotions regulation comparing to other sensory modalities. Then, through its effect respiratory parameters. Pleasant odors induce a slow and deep breathing that synchronizes brain rhythms, inducing an altered state of consciousness and relaxation. And finally, the fact that an OS stimulates the parasympathetic branch of the autonomic nervous system (ANS), promoting self-awareness and well-being with relaxation. Thus, we propose that an OS can alleviate persistent dyspnea through the interplay of these different aspects.To do so we started by identifying with intracranial electroencephalographic recordings (iEEG) brain networks implicated in volitional olfactory sampling maneuvers such as sniffs and apnea, notably to explore the link between emotion processing brain region and olfactory exploration. Then we used subject specific pleasant and unpleasant odors as OS during experimental dyspnea induction with mechanical and metabolic load while recording EEG, ECG and psychometric tests to test if odors can alleviate dyspnea sensation. Regarding brain networks underlying volitional olfactory sampling, our results enabled us to identify modulation in the amygdala, hippocampus, posterior insula and temporal cortex. Specifically, we measured a significant power increase of theta (4-8Hz) and alpha (8-12Hz) over time during apnea, as well as power increase before sniff and apnea in these regions. These results suggest that both excitatory and inhibitory respiratory maneuvers recruit limbic areas, such as the hippocampus and the amygdala, which are commonly involved in emotional process, and also cortical areas, such as temporal cortices. Regarding odor impact on healthy subjects during experimental dyspnea, pleasant or unpleasant odors did not affect respiratory parameters, and did not potentiate or remove ANS effect for mechanical or metabolic load. During experimental dyspnea, pleasant or unpleasant odors induced higher EEG responses comparing with no odor, with unpleasant odor recruiting a larger network during inspiration comparing to pleasant odor. We also identified that pleasant odor decrease significantly dyspnea in a subpopulation of subjects that we called “responder” in opposition to “non-responder”. Comparing the various physiological recordings measured this study, we can indicate that this dyspnea positive effect is primarily related to changes in brain rhythms given the fact that no alterations in the ANS or respiration were measured

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28

Schmidt, Christian Alexander Peter. "Stimulating angiogenesis into biomaterials through the delivery of growth factors." Doctoral thesis, University of Cape Town, 2007. http://hdl.handle.net/11427/26618.

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lschemic disease in form of ischemic heart disease (IHD), ischemic stroke and peripheral arterial disease (PAD) due to atherosclerosis represents a massive clinical and economic burden to healthcare and is currently the number one cause of death in the world. Treatment modalities for peripheral arterial disease include bypass surgery involving autologous vein or synthetic materials such as ePTFE. Long term patency of small diameter vascular grafts used for infra-inguinal reconstructions, however, is below 50 % 5 years after implantation. Therefore, novel vascular graft concepts and materials are needed. The concept of transmural in vivo endothelialisation of vascular grafts holds great promise for increasing long term patency. To achieve complete luminal endothelial cell coverage and optimal integration of the porous synthetic graft material into the host tissue, transmural ingrowth of tissue and vasa vasorum might have to be facilitated. Since VEGF1ss and PDGF-BB are growth factors known to stimulate and consolidate angiogenesis, this PhD thesis hypothesized, that neovascularisation of porous polyurethane (PU) can be increased by delivery of vascular endothelial growth factor (VEGF1ss) and platelet derived growth factor (PDGF-BB). To prove this hypothesis, subcutaneous implantation of PU discs was established as a valid, reproducible, relatively simple and quantifiable neovascularisation model. Three different ways of growth factor delivery were investigated. The gene encoding for human VEGF15s was cloned into the genome of adeno associated viruses (AAV), which served as a vector for gene transduction of autologous wound healing cells in vivo using the "Gene Activated Matrix" approach. Genetically modified matrix embedded AAV-VEGF155 was loaded into porous PU and transduced autologous ingrowing wound cells. In contrast to the excellent transduction efficiency in myocytes, AA V showed a poor tropism for wound healing cells. The second approach to increase neovascularisation into porous PU was the surface modification of PU by covalent attachment of nitrous acid degraded heparin. Neovascularisation into the biomaterial was increased by 77 % after 10 days of subcutaneous implantation. Since certain angiogenic growth factors show a high affinity for heparin, additional loading of heparin surface modified PU with VEGF165 increased neovascularisation even further up to 115 % at 10 days compared to control. Dual growth factor delivery of VEGF 165 and PDGF-BB not only initiated increased vascularisation of porous PU, but also created a stable vascular network 2 months after implantation. In contrast, PU loaded with VEGF165 alone showed regression of total vascular area of 61 % compared to vascular area at 10 days. Thirdly, to study the effects of controlled, prolonged growth factor delivery, a "Neovascularisation Construct" was developed which was implanted subcutaneously in rats. The construct consisted of an osmotic mini pump and a tube of porous PU lined with ePTFE, into which a defined amount of VEGF16s was pumped for 10 days. After implantation, granulation tissue was growing into the pores of the PU and neovascular area was increased up to 265 % compared to PBS control. Furthermore, using different growth factor concentration, a dose dependency was shown. In addition, this thesis investigated the functional perfusion of the micro vascular network growing into PU by four different vascular quantification techniques. lntravital perfusion with biotinylated lycopersicon esculentum followed by microscopical analysis, vascular corrosion casting quantified by scanning electron microscopy as well as the novel micro-CT analysis of silicone rubber perfused vessels were compared to conventional immunhistochemical analysis of endothelial cells by CD31. Interestingly, PBS perfused "Neovascularisation Constructs" showed a relatively poor perfusion; therefore CD31 immunohistochemistry "overestimated" functional neovascularisation 3 fold. All perfusion techniques indicated a strong effect of VEGF 165 delivery on vessel perfusion (10 to 20 fold increases of vascular area and volume compared to PBS control). Micro-CT scanning was shown to be an excellent tool to study micro vascular networks in a three-dimensional fashion across the whole length of the sample in a limited amount of time and to provide reliable and reproducible data on vessel density, vascular volume, and connectivity. Since resolution is still limited today to about 10 μm using a commercially available bench top scanner, this new technology still needs to be complemented by immunohistochemistry and perfusion studies such as lectin perfusion and corrosion casting. In summary, the induction of neovascularisation was achieved by heparin surface modification alone, which was even increased through additional delivery of growth factors into the biomaterial PU. The development of a stable micro vascular network at 2 months was achieved and the functionality was shown using four different, independent techniques including the novel micro-CT scanning of neovascularisation into biomaterials. Towards the development of an in vivo, spontaneously and transmurally endothelialising vascular graft with superior long-term patency further investigations are necessary. As an initial step, increased spontaneous neovascularisation of the possible graft material polyurethane was achieved. Future steps are clearly indicated to study the translation of increased neovascularisation of the biomaterial polyurethane towards increased endothelialisation in a vascular graft model.

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Hugo, Jenine. "Feel + learn + heal - a children's development centre and clinic." Diss., University of Pretoria, 2012. http://hdl.handle.net/2263/30101.

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Although human beings continuously learn through their experiences and impressions, the most important years in determining all actions and decisions which will be made in life, are during childhood. In designing spaces for children, their perception of the built environment and interaction with their surroundings needs to be understood in terms of the influence that elements of architecture and the landscape have on their sensorial and motoric actions as well as social activities. FEEL + LEARN + HEAL, the subject of this dissertation, is a centre for childhood development and an ambulatory clinic, which will demonstrate how built environments enhance perceptual experience by means of sensory stimulation and healing environments. The study area is located on the urban edge, north east of Pretoria's Central Business District and forms a gateway into the city at a large intersection, where Boom, Soutpansberg, Dr. Savage and du Toit Street intersect. Dissertation MArch(Prof)--University of Pretoria, 2012. Architecture MArch(Prof) Unrestricted

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Davis, Danisha Marie, Suman Dalal, Connor James, Cerrone R. Foster, and Krishna Singh. "The Role of Osteopontin in Extracellular Matrix Remodeling Following Chronic Sympathetic Stimulation in The Aging Heart." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/asrf/2019/schedule/122.

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Cardiovascular disease (CVD) is the leading cause of death in the United States. A common feature in most cardiac pathologies is the dysregulation of beta-adrenergic receptors (β-AR) and changes in the extracellular matrix (ECM). The ECM maintains strength and normal organization of cardiac tissue, while fibrosis (connective tissue scarring) is necessary for repair of damaged cardiac tissue. However, the dysregulation of the ECM leads to a number of cardiac disease pathologies. Osteopontin (OPN) is a protein with diverse biological functions in regulating the ECM such as bone resorption and calcification, wound healing, cell adhesion, cell survival, and apoptosis. OPN is expressed at low levels in the heart but increases with injury by promoting collagen synthesis, cardiac fibroblast growth, and adhesions to ECM proteins. Furthermore, as the heart ages, increases in ECM reorganization leads to cardiac damage and failure. Several studies have examined the role of OPN in the heart, but to date, no studies exist on the role of OPN in response to β-AR signaling and cardiac remodeling or the role that aging plays in this response. The goal of this study was to examine the effects of OPN on cardiac ECM remodeling following chronic beta-adrenergic stimulation. We proposed that OPN expression increases cardiac remodeling and dysfunction following ISO treatment in the aging heart evidenced by increased fibrosis. For this study, young (4 months) and middle age (14 months) mice with (WT) and without (KO) the OPN gene were treated with isoproterenol (ISO) for 28 days. Echocardiography was used to assess cardiac function. Mice were euthanized, and the hearts were analyzed for fibrosis using Masson’s Trichrome Staining. Results showed ISO increased fibrosis in the WT-ISO, but not KO-ISO compared to the respective controls (SHAM, no ISO treatment) for the middle age mice (p≤0.05). Furthermore, the aged WT-ISO group exhibited a 3-fold increase in fibrosis compared to the young WT-ISO group. Results from echocardiography will be analyzed and we expect to see compromised cardiac function in the WT-ISO groups compared to KO-ISO groups. OPN is currently being examined as a potential biomarker in heart failure. The results from this study will provide new insight on changes in the cardiac vasculature in the aging heart following injury and the role OPN plays in this process.

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Radcliffe, Emma. "A role for protein S-nitrosylation in the cardioprotective effects of vagal nerve stimulation in heart failure." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/a-role-for-protein-snitrosylation-in-the-cardioprotective-effects-of-vagal-nerve-stimulation-in-heart-failure(a4b61102-fd35-4a52-9e6a-935ddd897cbb).html.

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Heart failure is a prevalent health concern within the western world. It has huge economic, financial and personal implications. Despite the development of several clinically available treatments, heart failure associated mortality remains high. Heart failure patients display with dysfunction of the autonomic nervous system, including a high degree of vagal withdrawal. Consequently, the up-regulation of cardiac vagal tone, using vagal nerve stimulation (VNS) has recently gained attention as a potential new therapeutic approach to the treatment of heart failure. Clinical trials of VNS have produced mixed outcomes and very little is known about the mechanisms mediating the cardioprotective effects of VNS. This study has therefore implemented VNS in an ovine tachypaced model of heart failure, with the primary aim of quantifying its therapeutic effect in this model. Secondly, two potential underlying mechanisms of VNS have been investigated: 1) the effects of VNS on cellular calcium handling and 2) the effects of VNS on myocardial S-nitrosylation (S•NO).VNS treatment in this model of heart failure had a modest therapeutic effect. However, no differences in echocardiographic parameters, including those used as outcome measures in ongoing clinical trials, were observed between treated and untreated animals. Similarly, no differences in calcium handling parameters were observed between ventricular myocytes isolated from treated and untreated animals. Finally, VNS caused an increase in S•NO of several identified myocardial proteins when compared to untreated heart failure controls. However, this was a relatively small change compared to that observed between control and heart failure tissues. This data, as with studies before, highlights the need for a greater understanding of autonomic regulation and VNS in the heart failure setting, so that treatment strategies can be more effectively optimised. Given the limited therapeutic effect observed in this study, these potential mechanisms cannot be excluded as contributing to the cardioprotective effects of VNS observed in other studies.

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Altakroury, Hamza Fawzi. "In-vivo Human Head Conductivity Estimation by SEEG and EEG Recorded in Simultaneous with Intracerebral Electrical Stimulation." Thesis, Université de Lorraine, 2017. http://www.theses.fr/2017LORR0304/document.

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La localisation de source d'EEG devient un outil important pour traiter les patients atteints d'épilepsie en localisant les zones épileptogènes avant d'effectuer une chirurgie de résection. Compte tenu d'un modèle de tête direct, la localisation de la source EEG est réalisée en résolvant le problème inverse. Le modèle de tête direct est un modèle biophysique de tête plus ou moins complexe qui décrit la distribution électrique. En considérant la propagation électrique expliquant la distribution de potentiels, outre la numérisation, le modèle nécessite le réglage deux paramètres lesquels sont la géométrie du modèle de tête et la valeur des conductivités de chaque compartiment du modèle de tête. En raison des progrès computationnel et des techniques d'imagerie (comme l'IRM et la CT), il est possible de générer des modèles de tête humaine qui représentent avec une grande précision la géométrie de la tête réelle. Cependant, il existe une incertitude sur les valeurs de conductivité de chaque compartiment et la méthode avec laquelle ils devraient être estimés. Dans la littérature, les valeurs communes pour les conductivités proviennent principalement des expériences in-vitro. Dans ce travail, nous effectuons une estimation de la conductivité in-vivo à partir de données EEG/SEEG/Stimulation électrique de trois patients épileptiques. Ces données sont constituées des images IRM et des CT SCAN pour la construction d'un modèle de tête FEM à cinq compartiments pour chaque patient, ainsi que les enregistrements SEEG et EEG qui ont été acquis en même temps que la stimulation électrique intracérébrale (IES). L'originalité de ce travail réside dans l'évaluation de la performance de l'estimation des conductivités in-vivo par des mesures EEG et / ou SEEG en fonction de différents paramètres spatiaux et de la localisation des IES. Le travail se compose de trois parties principales: la première partie vise à déterminer la méthode d’optimisation sous contraintes la plus robuste parmi les algorithmes courants pour optimiser les paramètres du modèle direct de tête. L'objectif de la deuxième partie est d'analyser la sensibilité des valeurs de conductivité à différentes conditions sur la position de stimulation, le conditionnement du problème avec les positions de mesure et leur nombre et le nombre de compartiments. Alors que dans la partie finale, les conductivités d'un modèle de tête FEM isotrope et homogène à cinq compartiments ont été estimées avec des paramètres précédemment déterminés pour les trois patients. Enfin, l'effet de la fréquence de stimulation sur les conductivités estimées est analysé EEG source localization is becoming an important tool for treating epileptic patients by localizing the epileptogenic zones before performing a resection surgery. Given a forward head model, EEG source localization is performed by solving the inverse problem. The forward head model is a biophysical model which describes the electrical distribution in the human head. When considering the propagation as the only way for the current distribution to move in the head, the focus is directed primarily on two parameters for having an accurate forward head model. These parameters are: the geometry of the head model and the conductivity value of each compartment of the head model. Due to the recent advances in computers and imaging techniques (like MRI and CT), it is possible to generate human head models that represent with a high accuracy the geometry of the real head. However, there is still an argument about the conductivity values and the method by which it should be estimated. In literature, the common values for conductivities come mostly from in-vitro experiments. In this work we are performing in-vivo conductivity estimation by considering the data of three epileptic patients. This data consists of MR images and CT scans for building a five-compartment FEM head model for each patient along with SEEG and EEG recordings that were acquired in simultaneous with intracerebral electrical stimulation (IES). The originality of this work lies in evaluating the performance of in-vivo conductivity estimation by EEG and/or SEEG measurements in function of different spatial parameters and locations of the IES. The following work consists of three major parts: the first part aims to determine the most robust optimization algorithm among common algorithms for optimizing the forward head model. The objective of the second part is to analyze the sensitivity of the conductivity values given different conditions on stimulation position, measurement positions and number of compartments. While in the final part, the conductivities of an isotropic and homogeneous five-compartment FEM head model were estimated with previously selected parameters for three drug-resistant epileptic patients. Finally the effect of changing the stimulation frequency on the estimated conductivities was determined

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Hashimoto, Tadashi. "Temporal profile of visual evoked responses to pattern reversal stimulation analyzed with whole-head magnetometer." Kyoto University, 1999. http://hdl.handle.net/2433/181243.

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Campbell, Annabel Sarah. "A study on the effect of β-adrenergic stimulation on the electrophysiology of the isolated heart". Thesis, University of Glasgow, 2017. http://theses.gla.ac.uk/8001/.

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Background: A coordinated heart beat relies on the propagation of a rapid depolarising event throughout the atria and ventricles and the subsequent coupling of this electrical signal to a transient contraction in every atrial and ventricular cardiomyocyte. The rate of propagation, known as conduction velocity (CV) is mainly determined by cellular expression of Na channels and gap junctional proteins (connexins), however there is emerging evidence that both proteins may be functionally regulated by intrinsic signaling processes. Previous studies indicate that stimulation of the β-adrenergic pathway increases CV, but little consistent data exists on the magnitude, associated adrenoreceptor pharmacology or time course of the effect. This study investigates the effect of β-AR stimulation – using either the β-agonist isoproterenol (ISO) or by directly raising cAMP via addition of Forskolin (Fsk) and/or 3-Isobutyl-1-methylxanthine (IBMX) - on ventricular CV in the intact rat heart. The aim was to measure the response of CV to β-AR stimulation and investigate the mechanisms behind this response. Action potential (AP) and intracellular Ca2+ measurements were also made to determine the effect of β-AR stimulation on cellular electrophysiology over the same time-course as the CV response to β-AR stimulation. Methods: Adult male Wistar rats (250-350g) were euthanized by cervical dislocation and excised hearts retrogradely perfused with modified Tyrode's solution. CV measurements were taken using a custom-built probe, consisting of bipolar stimulating and recording electrode pairs placed flat against the epicardium of the left ventricle (LV). The CV probe also incorporated a fibre-optic light guide, allowing ratiometric measurements of voltage and intracellular Ca2+ from the LV epicardium. Results and Conclusions: β-AR stimulation increased LV longitudinal CV by approximately 10%. This increase in CV was found to be cAMP mediated. This effect was not due to changes in Ca2+ handling alone and although an increase in AP amplitude (APA) suggested that INa was increased, the magnitude was thought insufficient to explain the change in CV. This suggested a potential role for gap junction conductance (GJC) in mediating CV changes. This view was supported by preliminary data indicating the magnitude of the response was larger when measuring transverse CV: transverse conduction involves proportionally more GJC than longitudinal conduction. β-AR stimulation was confirmed to increase CV, a response mediated via β1AR subtype, and which required an increase in cAMP: cAMP was increased by activation of adenylyl cyclase (AC) with forskolin (Fsk) or through inhibition of phosphodiesterases (PDEs) by IBMX. The increase in CV was shown to be mediated through the cAMP sensitive kinase, PKA; another cAMP target, Epac, appeared not have a role in this pathway. Understanding the regulation of CV by β-AR stimulation is crucial to understanding sympathetic regulation of the heart and may lead to further understanding of the interplay between downregulated β-AR signaling and arrhythmia generation in the diseased heart.

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Dodd-o, Jeffrey M. (Jeffrey Michael). "The effects of coronary α₁-adrenergic stimulation on coronary blood flow and left ventricular function". Thesis, University of North Texas, 1991. https://digital.library.unt.edu/ark:/67531/metadc332773/.

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This study examines the α-adrenergic constrictor tone varies with intensity of exercise, the effects of coronary α1-adrenergic blockade on left ventricular contractile function and regional myocardial perfusion, and compares the effects of increasing coronary blood flow by removing α1-constrictor tone.

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Hachem, Dany. "Méthodes et analyses physico-expérimentales des mécanismes liés à la résistance dynamique dans les composants HEMT GaN de puissance." Thesis, Toulouse 3, 2020. http://www.theses.fr/2020TOU30035.

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Pour contrôler le flux d'énergie électrique de la source à la charge, l'électronique de puissance constitue un des éléments phares dans l'acheminement de cette énergie. La gestion et la conversion de cette énergie électrique nécessitent des convertisseurs de puissance efficaces, basés sur des interrupteurs présentant des performances élevées en commutation et en conduction, à haute puissance et haute fréquence. Bien que les dispositifs à base de silicium dominent depuis longtemps l'électronique de puissance, les propriétés physiques de ce matériau limitent les performances des dispositifs en termes de température maximale d'opération, de tension de claquage, de résistance à l'état passant et de vitesse de commutation. La recherche des matériaux prometteurs présentant des performances supérieures à celles du silicium est donc nécessaire. Le nitrure de gallium (GaN) est l'un des matériaux qui permet, grâce à ses propriétés physiques, de répondre aux exigences de fabrication des convertisseurs de puissance. En outre, le transistor à haute mobilité électronique (HEMT) à hétérostructure AlGaN/GaN est un composant qui contribue à l'innovation des technologies de conversion de puissance. Cependant, de nombreux problèmes de fiabilité affectent les performances électriques de ces dispositifs et nécessitent un effort d'analyse et de compréhension. Les contributions du présent travail s'inscrivent précisément dans ce domaine. La caractérisation de la résistance à l'état passant de ce transistor, qui est un problème critique, est nécessaire pour comprendre la dynamique de certains phénomènes tels que le piégeage. Dans ce travail, on s'intéresse tout particulièrement à la caractérisation des effets du piégeage induit par des défauts qui peuvent exister dans les différentes couches de la structure. Nous proposons une nouvelle méthodologie générale de mesure permettant d'obtenir des résultats fiables et reproductibles et montrant l'importance de maîtriser les conditions initiales avant chaque mesure. Les phénomènes dynamiques sont caractérisés à l'aide des mesures du courant en fonction du temps, réalisées sur des structures TLM issues de différents lots technologiques, sous stimulations électrique et/ou optique. Deux méthodes de caractérisation de ces défauts sont ainsi proposées. Le but de la première est de stresser le dispositif par une tension négative appliquée sur le substrat pour stimuler les défauts présents entre ce dernier et le canal 2DEG, alors que la deuxième consiste à illuminer le dispositif sous test par une source lumineuse dont l'énergie de photon correspondante est choisie de façon à ce qu'elle n'affecte que les pièges présents dans les matériaux. L'effet de l'illumination sur les résistances de contact est ensuite étudié, montrant une contribution non négligeable de ces résistances dans la résistance totale et mettant ainsi en évidence, pour la première fois, que la dynamique de la résistance à l'état passant peut-être due non seulement à des phénomènes dans le canal 2DEG mais également à des phénomènes au niveau des contacts ohmiques[...] To control the flow of electrical energy from source to load, power electronics is one of the key elements for the management of this energy. Managing and converting electrical energy requires efficient power converters, based on switches exhibiting high switching and conduction performance, at high power and high frequency. Although silicon-based devices have dominated power electronics for long time, the physical properties of this material limit the performance of these devices in terms of maximum operating temperature, breakdown voltage, dynamic On-state resistance and switching speed. The search for promising materials exhibiting superior performance compared to silicon is therefore contemplated. Gallium nitride (GaN) is one of the materials that, thanks to its physical properties, meet the manufacturing requirements of power converters. Furthermore, the AlGaN/GaN heterostructure high electronic mobility transistor (HEMT) is one a power device that contributes to the innovation in power conversion technologies. However, many reliability issues affect the electrical performance of these devices and require efforts of analysis and understanding. The contributions of this work fit precisely in this topic. The characterization of the dynamic On-state resistance of GaN HEMT transistors, which is a critical problem, is necessary to understand the dynamics of certain phenomena such as trapping. In this work, we focus on characterizing the effects of trapping induced by defects that may exist in the different layers of the structure. We propose a new general measurement methodology allowing reliable and reproducible results and showing the importance of mastering the initial conditions before each measurement. These dynamic phenomena are characterized using current measurements as a function of time, realized on TLM structures coming from different technological batches, under electrical and/or optical stimulations. Two characterization methods of these defects are proposed. The purpose of the first method is to stress the device by a negative voltage applied to the substrate to stimulate the defects located between the 2DEG channel and the substrate, while the second one consists in illuminating the device under test with a light source whose corresponding photon energy is chosen to affect only the traps present in the materials. The effect of the illumination on the contact resistances is then studied, showing a non-negligible contribution of these resistances in the total resistance and thus highlighting, for the first time, that the degradation of the dynamic on-state resistance may be due not only to phenomena in the 2DEG channel but also to phenomena at the ohmic contacts.[...]

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Dalal, Suman, Cerrone R. Foster, Bhudev C. Das, Mahipal Singh та Krishna Singh. "β-Adrenergic Receptor Stimulation Induces Endoplasmic Reticulum Stress in Adult Cardiac Myocytes: Role in Apoptosis". Digital Commons @ East Tennessee State University, 2012. https://dc.etsu.edu/etsu-works/8572.

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Accumulation of misfolded proteins and alterations in calcium homeostasis induces endoplasmic reticulum (ER) stress, leading to apoptosis. In this study, we tested the hypothesis that β-AR stimulation induces ER stress, and induction of ER stress plays a pro-apoptotic role in cardiac myocytes. Using thapsigargin and brefeldin A, we demonstrate that ER stress induces apoptosis in adult rat ventricular myocytes (ARVMs). β-AR-stimulation (isoproterenol; 3h) significantly increased expression of ER stress proteins, such as GRP-78, Gadd-153, and Gadd-34, while activating caspase-12 in ARVMs. In most parts, these effects were mimicked by thapsigargin. β-AR stimulation for 15 min increased PERK and eIF-2α phosphorylation. PERK phosphorylation remained higher, while eIF-2α phosphorylation declined thereafter, reaching to ∼50% below basal levels at 3 h after β-AR stimulation. This decline in eIF-2a phosphorylation was prevented by β1-AR, not by β2-AR antagonist. Forskolin, adenylyl cyclase activator, simulated the effects of ISO on eIF-2α phosphorylation. Salubrinal (SAL), an ER stress inhibitor, maintained eIF-2α phosphorylation and inhibited β-ARstimulated apoptosis. Furthermore, inhibition of caspase-12 using z-ATAD inhibited β-AR-stimulated and thapsigargininduced apoptosis. In vivo, β-AR stimulation induced ER stress in the mouse heart as evidenced by increased expression of GRP-78 and Gadd-153, activation of caspase-12, and dephosphorylation of eIF-2α. SAL maintained phosphorylation of eIF-2α, inhibited activation of caspase-12, and decreased β-AR-stimulated apoptosis in the heart. Thus, β-AR stimulation induces ER stress in cardiac myocytes and in the heart, and induction of ER stress plays a pro-apoptotic role.

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Meyers, Erin Elizabeth. "Afferent vs. efferent cervical vagal nerve stimulation: effects on blood glucose, insulin, and glucagon concentrations in rats." Thesis, University of Iowa, 2016. https://ir.uiowa.edu/etd/3144.

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Cervical vagal nerve stimulation (VNS) has been studied in the context of several conditions including epilepsy and depression. However, its effects on glucose metabolism, and its potentially beneficial effects in type II diabetes, have not yet been evaluated in humans. Efferent parasympathetic activation reduces hepatic glucose release and increases pancreatic insulin secretion, while afferent parasympathetic activation may increase hepatic glucose release and inhibit insulin secretion potentially through sympathetic activation. Thus, the effect of combined afferent and efferent cervical VNS is difficult to predict. We hypothesized that selective efferent VNS would decrease blood glucose concentration [Glu] and that selective afferent VNS would increase [Glu]. To investigate these potentially contrasting effects of efferent vs. afferent parasympathetic signaling, we recorded [Glu] and serum insulin and glucagon levels before and during 120 min of VNS in anesthetized rats. The nerve was left intact for combined afferent and efferent VNS (n=9) or sectioned proximal or distal from the stimulation electrode for selective efferent (n=8) of afferent (n=7) VNS, respectively. We found that afferent VNS caused a strong and sustained increase in [Glu] (+108.9±20.9% or +77.6±15.4% after 120 min of combined afferent and efferent VNS or selective afferent VNS) that was not accompanied by an increase in serum insulin concentration. Combined afferent and efferent VNS significantly increased serum glucagon concentration (57.6±23.4% at 120 min of VNS), while selective afferent VNS did not increase glucagon levels. Conversely, selective efferent VNS increased [Glu] only temporarily (+28.8±11.7% at 30 min of VNS). This response coincided with a transient increase in serum glucagon concentration at 30 min of VNS (31.6±8.3%) and a strong and sustained increase in serum insulin concentration (+71.2±27.0% after 120 min of VNS). These findings demonstrate that afferent VNS may increase [Glu] by suppressing pancreatic insulin release, while efferent VNS transiently increases [Glu] by stimulating glucagon secretion before reducing levels to or below baseline values by stimulating the release of insulin. Thus, selective efferent VNS may be potentially effective in the treatment of type II diabetes.

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Gutierrez, Juan Claudio. "Improved Late-gestation Cardiac Morphology in Fetuses of Diabetic Mothers After Maternal Immune Stimulation: Potential Role of Dysregulated Apoptosis." Diss., Virginia Tech, 2009. http://hdl.handle.net/10919/26117.

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The incidence of malformed newborns is higher in human pregnancies complicated by diabetes mellitus, as compared to non-diabetic pregnancies. Neural tube and cardiac defects predominate among the fetal malformations induced by hyperglycemia. Non-specific maternal immune stimulation is protective in mice against birth malformations caused by chemical or physical teratogens, or by maternal diabetes mellitus. Insulin dependent diabetes was induced in ICR females to study the late gestation fetal heart by morphometric analysis. Diabetic females treated with Freundâ s compete adjuvant (FCA) or interferon-gamma (IFNÎ³) were also generated to elucidate potential positive effects of maternal immune stimulation during the diabetic pregnancy by morphometric analysis and pathologic scoring. Insulin-dependent CD1 females were generated to analyze late gestation fetal myocardial apoptosis by flow cytometric analysis and by real time-polymerase chain reaction (RT-PCR) analysis of a panel of 5 genes involved in apoptosis/proliferation (Bcl-2, P53, Caspase3, Caspase9 and PkC-e). The morphometric analysis of fetal hearts revealed visibly obvious dilation of ventricular chambers and outflow channel of the left ventricle, and reduction of total myocardial ventricular area in late gestation fetuses, as predominant changes seen in the offspring of diabetic dams. Pathologic scoring revealed that maternal immune stimulation, particularly with FCA, in part alleviated fetal heart changes of cavitary dilation and myocardial reduction. Increased rate of apoptosis/necrosis in the fetal myocardium in late gestation during the diabetic pregnancy was evidenced by flow cytometric analysis. Particularly there was a significant increase in percentage of early apoptotic cells in the fetal myocardium detected by cell markers annexin V and propidium iodide. There was also a significant increase in percentage of late apoptotic/necrotic fetal myocardial cells in the diabetic group compared to the control group. These results suggest that maternal treatment with FCA may in part protect the heart from high hyperglycemia by reducing the number of myocardial cells undergoing apoptosis and necrosis. The RT-PCR analysis revealed subtle changes in gene expression for all the genes except Bcl-2. A paradoxical and dramatic up-regulation of this anti-apoptotic gene was observed in late gestation fetal myocardium from the insulin-dependent hyperglycemic groups. Possibly, this could be a mechanism to protect the fetal myocardial cell from the chronic exposure to a severe hyperglycemic insult and consequent apoptosis. In conclusion, maternal insulin-dependent diabetes caused morphological changes in the late gestation fetal heart. Such changes were in part related to dysregulation of myocardial apoptosis. Maternal immune stimulation with FCA improved fetal heart morphology, by a mechanism that may in part relate to normalizing fetal myocardial apoptosis. Ph. D.

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TORRE, ELEONORA. "Role of SERCA stimulation and voltage-dependent Ca2+ channels in improving Ca2+ handling and sustaining heart automaticity." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2020. http://hdl.handle.net/10281/261917.

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Parte 1. La cardiomiopatia diabetica (DCM) è una malattia caratterizzata da una precoce disfunzione diastolica (DD). I meccanismi che possono ripristinare il rilassamento cardiaco, migliorando la dinamica intracellulare di Ca2+, rappresentano un promettente approccio terapeutico per le malattie cardiovascolari associate alla DD. Istaroxime è un inibitore di NaK-ATPase (NKA) e stimolatore del recupero di Ca2+ nel reticolo sarcoplasmatico (SR) attraverso la pompa del SR per il Ca2+ (SERCA2a). Il progetto mira a caratterizzare gli effetti di Istaroxime a una concentrazione che minimamente influenza NKA per isolare i suoi effetti dipendenti da SERCA2a in un modello di diabete di tipo 1. I ratti trattati con streptozotocina (STZ) sono stati valutati a 9 settimane dopo l'iniezione di STZ rispetto ai controlli (CTR). I ratti STZ hanno mostrato una riduzione del livello e dell'attività della proteina SERCA2a e un aumento del rapporto PLNmonomerico/SERCA2a. Le dinamiche del Ca2+ intracellulare e l'attività elettrica sono state valutate in miociti ventricolari isolati. Nei miociti STZ, la downregulation di SERCA ha causato 1) aumento di Ca2+ diastolico 2) riduzione del contenuto di Ca2+ nel SR e dell’ampiezza del transiente di Ca2+, 3) ricarica del SR più lenta con inibito lo scambiatore Na/Ca, 4) stabilità del SR e numero di sparks di Ca2+ invariati. I potenziali d'azione (AP) sono stati significativamente prolungati, con conseguente aumento della short-term variability (STV) dell'APD. Istaroxime (100 nM) ha stimolato in modo significativo l'attività di SERCA2a ripristinando gli effetti indotti da STZ 1) riducendo Ca2+ diastolico, 2) aumentando l’ampiezza del transiente e il contenuto del SR di Ca2+ e 3) accelerando il recupero di Ca2+ nel SR nel gruppo STZ. Inoltre, Istaroxime, stimolando SERCA2a, ha parzialmente ripristinato le caratteristiche delle sparks di Ca2+. La stimolazione di SERCA2a da parte di Istaroxime ripristina le anomalie delle dinamiche del Ca2+ intracellulare indotte da STZ. Pertanto, la stimolazione SERCA2a può essere considerata un promettente approccio terapeutico per il trattamento della DD. Parte 2. L'automaticità cardiaca è generata nel nodo seno-atriale (SAN) attraverso i canali ionici della membrana plasmatica e il rilascio di Ca2+ dipendente dal recettore intracellulare della rianodina (RyR). Le cellule del SAN sono caratterizzate dall'espressione dei canali Cav1.3 di tipo L e Cav3.1 di tipo T (Cav). Per studiare il significato dell'espressione di Cav nell'automaticità cardiaca abbiamo usato topi mutanti con delezione genetica individuale o concomitante di Cav1.3 e Cav3.1. La delezione del CaV ha ridotto in modo additivo la frequenza cardiaca nei topi. Le registrazioni ECG dei cuori intatti di Cav1.3-/-/Cav3.1-/- hanno mostrato una dissociazione del ritmo atrioventricolare e una ritmicità prevalentemente giunzionale, anziché del SAN. La mappatura ottica dell'automatismo ha mostrato l'interruzione dell'automaticità primaria in SAN Cav1.3- -/Cav3.1-/- e uno spostamento dei principali siti di pacemaker al di fuori dell'area SAN. Abbiamo anche studiato il ruolo dei canali f- (HCN) attivati dall'iperpolarizzazione e dei canali Na+ (Nav) sensibili al TTX nell'automaticità residua dei topi mutanti. L'inibizione farmacologica concomitante dei canali Nav sensibili a f-HCN e TTX ha rallentato l'automaticità atriale in wild-type e Cav3.1- -, mentre è stata arrestata in alcuni Cav1.3-/- e Cav1.3- /-/Cav3.1- -. Gli stessi risultati sono stati confermati in cellule di pacemaker SAN Cav1.3-/-/Cav3.1-/- isolate. L'eliminazione dei canali Cav1.3 e Cav3.1 interrompe la normale automaticità cardiaca inducendo bradicardia e alterando la conduzione cardiaca. Inoltre, con la doppia delezione dei Cav1.3 e Cav3.1, i canali f-HCN e i canali Nav sensibili al TTX sono i meccanismi predominanti a sostegno dell'attività del pacemaker. Part 1. Aim. Diabetic cardiomyopathy (DCM) is a multifactorial disease characterized by an early onset of diastolic dysfunction (DD). Mechanisms that can restore cardiac relaxation (lusitropic effect) improving intracellular Ca2+ dynamics, represent a promising therapeutic approach for cardiovascular diseases associated to DD. Istaroxime is a NaK ATPase (NKA) inhibitor with the property of accelerating Ca2+ re-uptake into sarcoplasmic reticulum (SR) through the SR Ca2+ pump (SERCA2a) stimulation. The project aims to characterize Istaroxime effects at a concentration mostly unaffecting NKA to isolate its effects dependent on SERCA2a only in a model of mild diabetes (type 1). Methods and results. Streptozotocin (STZ) treated rats were evaluated at 9 weeks after STZ injection in comparison to control (CTR) ones. SERCA2a-dependent Istaroxime effects were evaluated in cell-free system and in isolated left ventricular (LV) myocytes. STZ animals showed reduced SERCA2a protein level and activity and increased monomeric PLN/SERCA2a ratio. Intracellular Ca2+ handling and electrical activity were evaluated in isolated ventricular myocytes. In STZ myocytes, SERCA downregulation caused 1) increased diastolic Ca2+, 2) reduction in SR Ca2+ content and Ca2+ transient amplitude following control of membrane potential, 3) slower SR reloading process under Na/Ca exchanger (NCX) inhibition, 4) unchanged SR stability and Ca2+ sparks rate. Action potentials (APs) were significantly prolonged, resulting in an increased short-term variability (STV) of APD. Istaroxime (100 nM) significantly stimulated SERCA2a activity and reverted STZ-induced effects by 1) reducing diastolic Ca2+, 2) increasing Ca2+ transient amplitude and SR Ca2+ content, and 3) accelerating SR Ca2+ reuptake in STZ group. Moreover, Istaroxime, by stimulating SERCA2a, partially restored Ca2+ sparks characteristics and significantly accelerated Ca2+ sparks decay. Conclusions. SERCA2a stimulation by Istaroxime restores STZ-induced intracellular Ca2+ handling anomalies. Thus, SERCA2a stimulation can be considered a promising therapeutic approach for DD treatment. Part 2. Aim. Heart automaticity is generated in the sino-atrial node (SAN) by a functional interplay between ion channels of the plasma membrane and intracellular ryanodine receptor (RyR)-dependent Ca2+ release. SAN cells are characterized by the expression of voltage-gated L-type Cav1.3 and T-type Cav3.1 Ca2+ (Cav) channels in addition to L-type Cav1.2 channels, which are ubiquitously expressed in the heart. To investigate the significance of Cav expression for heart automaticity we used mutant mice carrying individual or concomitant genetic ablation of Cav1.3 and Cav3.1. Methods and results. Cav ablation additively reduced heart rate in mice. ECG recordings of intact Cav1.3-/-/Cav3.1-/- hearts showed atrioventricular rhythm dissociation and predominantly junctional, rather than SAN driven rhythmicity. Optical mapping of automaticity showed disruption of primary automaticity in Cav1.3-/-/Cav3.1-/- SAN and a shift of the leading pacemaker sites outside the SAN area. We also investigated the role of hyperpolarization-activated f-(HCN) channels, and TTX-sensitive Na+ (Nav) channels in residual automaticity of mutant mice. Concomitant pharmacologic inhibition of f-HCN and TTX-sensitive Nav channels slowed atrial automaticity in wild-type and Cav3.1-/-, while arrested it in 4/6 of Cav1.3-/-, 3/6 of Cav1.3-/-/Cav3.1-/-. Same results were confirmed in isolated Cav1.3-/-/Cav3.1-/- SAN pacemaker cells. Conclusions. Cav1.3 and Cav3.1 Ca2+ channels deletion disrupts normal heart automaticity by inducing bradycardia and altering cardiac conduction. Moreover, in the concomitant absence of Cav1.3 and Cav3.1 channels, f-HCN channels and TTX-sensitive Nav channels are the predominant mechanisms sustaining pacemaker activity.

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Brügmann, Tobias [Verfasser]. "Optogenetics in striated muscle: defibrillation of the heart and direct stimulation of skeletal muscles with light / Tobias Brügmann." Bonn : Universitäts- und Landesbibliothek Bonn, 2019. http://d-nb.info/1201727839/34.

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Davids, Ashraf. "The phenomenon of 'second window of protection' : effect of beta-adrenergic stimulation and melatonin." Thesis, Stellenbosch : Stellenbosch University, 2004. http://hdl.handle.net/10019.1/50171.

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DiPeri, Timothy P. "Neuromodulation Therapy Mitigates Heart Failure Induced Hippocampal Damage." Digital Commons @ East Tennessee State University, 2014. https://dc.etsu.edu/honors/208.

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Cardiovascular disease (CVD) is the leading cause of death in the United States. Nearly half of the people diagnosed with heart failure (HF) die within 5 years of diagnosis. Brain abnormalities secondary to CVD have been observed in many discrete regions, including the hippocampus. Nearly 25% of patients with CVD also have major depressive disorder (MDD), and hippocampal dysfunction is a characteristic of both diseases. In this study, the hippocampus and an area of the hippocampal formation, the dentate gyrus (DG), were studied in a canine model of HF. Using this canine HF model previously, we have determined that myocardial infarction with mitral valve regurgitation (MI/MR) + spinal cord stimulation (SCS) can preserve cardiac function. The goal of this study was to determine if the SCS can also protect the brain in a similar fashion. Both the entire hippocampus and the DG tissues were dissected from canine brains and analyzed. These findings provide strong evidence that, in addition to the cardioprotective effects observed previously, SCS following MI/MR induces neuroprotective effects in the brain.

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Brittsan, Angela Gail. "TRANSGENIC APPROACHES TO ELUCIDATE THE ROLE OF PHOSPHOLAMBAN IN BASAL CONTRACTILITY AND DURING BETA-ADRENERGIC STIMULATION OF THE HEART." University of Cincinnati / OhioLINK, 2000. http://rave.ohiolink.edu/etdc/view?acc_num=ucin960908353.

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Misra, Kiran B. "Stimulation by carnitine of Branched-chain ?-keto acid dehydrogenase in intact heart mitochondria of sedentary and exercise- trained rats /." The Ohio State University, 1991. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487759055156936.

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Mantovani, G. "STIMULATION OF THE HEALTH AND PRODUCTIVITY OF NURSING AND WEANED PIGLETS." Doctoral thesis, Università degli Studi di Milano, 2011. http://hdl.handle.net/2434/153538.

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Summary: Worldwide the swine industries are under pressure to reduce the use of antibiotics while maintaining animal health and performance. In 2006 all the AGP (antibiotic growth promoters) and some feed additives with growth promoting activities were banned (Cu, Zn). Since the first restrictive measures were taken, and due to the beginning of the negative consequences of the ban, numerous efforts have been done to find alternatives or replacement strategies to maintain pig growth performance and controlling enteric bacterial diseases. Therefore, the following studies aimed to find ways to control additive efficacy with due consideration to animal welfare and consumers requirements. The main objective of this thesis was to improve our knowledge on the properties of new additives as feeding strategy and oral vaccination to improve general and gut health in young pigs with the aim to substitute antibiotics growth promoters. To achieve these objectives, three different trials were designed to study different strategies to improve the gut health of the post-weaning piglets. I) Evaluation of the immune response against ovalbumin (OVA) in pigs orally vaccinated with OVA in tablets containing carboxymethyl high amylose starch (CM-HAS), flagellin and sow’s milk. This trial was designed with the aim to determine the effects of a new delivery system designed for oral vaccination or delivery of bioactive molecule in the gut. The trial was also designed to evaluate the potential of the sow’s milk to modulate the systemic as well as local immune response against the antigen ovalbumin incorporated in the vaccine. Sixteen piglets of 28 days (d) of age were divided into 4 groups of 4 animals each. The first group was vaccinated with compressed tablets containing only ovalbumin (OVA); the second group was immunized with tablets containing ovalbumin and the B subunit of the flagellin from Salmonella enterica Typhimurium (OVA-FLA); the 3rd and 4th groups were immunized with tablets containing ovalbumin pre-incubated in sow milk with or without flagellin, respectively (OVA-LT or OVA-LT-FLA). The oral vaccination was performed in two periods of three days; the 1st period being from day 28 to day 30 of age (D1-D3 of the trial) and the 2nd from 42 d to 45 d of age ( D14-D16). Blood samples were collected at days 1, 14, 21, 28 and 42 of the trial to determine, by ELISA, serum antibody titre against OVA. Feces samples were also collected before the first immunization and intestinal content from the ileum was collected at slaughtering to evaluate level of IgA anti-OVA by ELISA. All the animals were euthanized 42 days post-immunization to collect blood, mesenteric lymph nodes (MLN) and ileum content. The immune cells were isolated from the MLN and from blood and cultured with OVA to evaluate the lymphocyte proliferative response by flow cytometry (CFSE cell proliferation kit) and production of the main cytokine produced in adaptative immune response such as Interleukine-2 (IL-2) , IL-4, IL-10 and interferon-gamma (IFN-γ). Experimental animal studies have indicated that oral administration of antigens targets the systemic T cell compartment, diminishes cell-mediated immune responses, and induces tolerance. This phenomenon might lead to the induction of cytokines such as Transforming Growth Factor beta (TGF–β) and IL-10, and consequently enhance antigen-specific antibodies such as IgA and IgG. While the humoral immune response is critical in the control of some mucosal pathogens, those effects might be inappropriate on other mucosal pathogens where cell mediated immune responses may play a larger role. II) Milk rice in piglet nutrition: benefits or not? Rice milk has been shown to contain a high sugar level and antioxidants such as Ɣ-Oryzanol. For this reason the effects on growth performance and health status of piglets have been studied on 36 litters from (Landrace x LargeWhite) x Penerland sows. At 10 days after birth 18 litters were supplemented with rice milk (T) until weaning while the others 18 received creep feed (C). At 21 days a total of 288 piglets were weaned. Half from each group (72 piglets) were randomly assigned to either control (C) or treated (T), so there were four experimental piglet groups: C-C, C-T, T-C and T-T. All the animals received a pre-starter (0-14 d post weaning) and a starter (14-42 d pw) diets. Piglets from C-T and T-T groups were also supplemented with rice milk from weaning to 14 days pw. Piglets of T-C group had significantly higher weight at 42 d pw (P<0.01), an higher average daily gain (ADG) and dry matter feed intake (DMFI) (P< 0.01). Rice milk supplementation had no influence in glucose, urea, total protein and lysozyme. Reactive oxygen metabolites (ROMs) levels resulted lower in T-T piglets than C-C and C-T groups at 14 d-post w. (P<0.05). Total antioxidant capacity was higher in C-C and C-T than TC piglets at 14 d after weaning (P<0.05). The data from this trial suggest that rice milk was associated with greater post weaning growth and health status when supplementation was given only during the nursing period. III) Effects of plant polyphenols and mannan oligosaccharide on growth performance, antioxidant defense system and gut health in Escherichia coli Challenged piglets Objective of the current study was to evaluate the effects of plant polyphenols (PP) and/or, mannan oligosaccharide (MOS) on growth performance, plasma antioxidant capacity and health in E. Coli-challenged weaned piglets. Ninety-six piglets (7.43 + 0.89 kg L.W., 21 d age) were randomly allotted into 4 dietary treatments: control (basal diet), 0.1% PP, 0.1 % MOS or PP+MOS in a 5 weeks study. At 21 and 25 d on trial half piglets of each group were orally inoculated with 4 ml of E.coli (1×109 cfu/ml) and half with the same amount of saline water. No difference was observed in growth. Plasma urea was markedly increased in PP+MOS group compared to PP group (P< 0.05), and lysozyme content was significantly decreased in PP+MOS group compared to groups on d 7 (P< 0.05). PP+MOS dietary supplementation decreased intestinal lipase and trypsin compared to PP on d 21 (P< 0.05). Plasma malondialdehyde content (MAD) increased, while plasma total antioxidant capacity (TAOC) and catalase (CAT) activities decreased in piglets 6 days after infection. Challenged piglets fed PP and those fed MOS showed higher TAOC than challenged piglets fed PP in combination with MOS. CAT activity resulted higher in challenged piglets fed diet supplemented with PP or PP+MOS than control or MOS at d 13 after infection (P< 0.05). The results showed that dietary PP or MOS had the potential to improve enhance systemic antioxidant capacity. However no synergic effect was observed when PP and MOS were combined. General conclusions During the weaning period, several factors affecting the welfare and health of piglets with a consequently effect on the productive performance of the animals. One of the key factors for high growth performance is the maintenance of a healthy gut. The presence of a balanced enteric microflora which may protect the piglets from weaning common bacterial infections, has a general beneficial effect on the health of the animal. What we tried to demonstrate with this thesis is that we are running the correct way to find alternatives substances to protect the gut health of our piglets, but more research will be needed to understand different techniques such the oral vaccination of the animals.

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Johnson, Luke A. "Locus Coeruleus and Hippocampal Tyrosine Hydroxylase Levels in a Pressure-Overload Model of Heart Disease." Digital Commons @ East Tennessee State University, 2013. https://dc.etsu.edu/honors/288.

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Studies have indicated that approximately 30% of people with heart disease experience major depressive disorder (MDD). Despite strong clinical evidence of a link between the two diseases, the neurobiological processes involved in the relationship are poorly understood. A growing number of studies are revealing similar neuroanatomical and neurochemical abnormalities resulting from both depression and heart disease. The locus coeruleus (LC) is a group of neurons in the pons that synthesize and release norepinephrine, and that is known to play a significant role in depression pathobiology. For example, there is evidence that tyrosine hydroxylase (TH) is elevated in the LC in depression. In addition, there is evidence that the LC plays a role in cardiovascular autonomic regulation. The hippocampus is another region that exhibits abnormalities in both depression and heart disease. In this study, the levels of TH in the hippocampus and LC were examined in the guinea pig pressure-overload model of heart disease. TH levels were also measured in the pressure-overload model treated with vagal nerve stimulation, a new investigational therapeutic intervention in heart disease. This study found that there were no changes in TH levels in the LC or the hippocampus of the pressure-overload model or in the pressure-overload model treated with vagal nerve stimulation.

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BULGHERONI, MARA. "Effetti della stimolazione meccanica plantare ripetuta sul profilo autonomico, sui parametri cardiovascolari e di movimento nei pazienti affetti da malattia di Parkinson." Doctoral thesis, Università degli Studi di Milano, 2018. http://hdl.handle.net/2434/598526.

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Introduction: Parkinson’s disease (PD) is spread worldwide; the incidence rapidly increases over the age of 60 years. The cause for the neuronal degeneration tipical of Parkinson disease is not known, nor there are any effective treatment; at the moment only symptomatic treatments are available. Among them there is foot mechanical stimulation which, in a preliminary study, showed an improvement of motor function and performance, enhancement of vagal modulation and reduction of sympathetic modulation, with a concurrent reduction of clinostatic blood pressure after one session of stimulation. The purpose of this study was to evaluate the effects of repeated foot mechanical stimulation on the autonomic, hemodinamic and motor assesment in patients affected by idiopathic PD Material and methods: We enrolled 23 patients with idiopatic PD, from 50 and 80 years old. Each patient underwent a cardiovascular assessment, autonomic status, neurologic and motor profile assessment on the first day, on the second day and on the sixteenth day (the last day of the study). Foot mechanical stimulation was performed the first day, the second day and three times per 72 hours distance. Data were then collected and analyzed. Results: Our study showed how repeated foot stimulation on two specific points on the sole of the foot can lead to a significant reduction of sympathetic modulation and to an enhancement, albeit not statistically significant, of vagal modulation - revealed by both spectral analysis and by symbolic analysis. Moreover, between the start and the end of the study, there was a statistically significant reduction of both SAP and DAP measured in clinostatic position and a clear motor improvement. Conclusions: Repeated foot stimulation may be used in patients affected by Parkinson disease, coupled with the usual treatments, to improve motor function (and so patients’ quality of life), and to treat clinostatic hypertension. That can lead to a reduction in pharmacological antihypertensive therapies and to a better management of orthostatic hypotension, reducing the risk of falls and of disabilities.

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Jewett, Benjamin E. "Inverse Changes in Ghrelin and A2A Receptor Gene Expression Levels in the Hippocampus of Heart Failure Canines Following Spinal Cord Stimulation." Digital Commons @ East Tennessee State University, 2015. https://dc.etsu.edu/honors/262.

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Myocardial infarction (MI), often referred to as a heart attack, is a serious health issue in the United States. There is a well-documented link between MI and major depressive disorder (MDD), with a high incidence of MDD occurring after an MI. Overlapping pathologies have been observed within the hippocampus of the brain in animal models of MI and depression. These observations suggest that pathobiological cross-talk between the heart and brain could have a role in the etiology of MDD that occurs after an MI. Spinal cord stimulation (SCS) has previously been shown to have both cardioprotective and neuroprotective effects post-MI, and hence may protect individuals from developing depression post-MI. In this study, we examined the potential biochemical mechanisms that might underlie the neuroprotective actions of SCS following MI. Brain tissues were obtained from three groups of canines: sham-operated animals, animals subjected to experimental myocardial infarction/mitral regurgitation (MI/MR), and animals subjected to MI/MR that were simultaneously administered SCS. The whole hippocampus and hippocampal dentate gyrus were dissected from frozen brains. Quantitative endpoint-PCR and RT-qPCR techniques were employed to measure select biochemical mediators of neuroprotection, i.e. adenosine A2A receptor, ghrelin, and ghrelin receptor expression in hippocampal samples. SCS induced a significant decrease in A2A receptor expression and a dramatic increase in ghrelin expression in MI/MR canines as compared to the MI/MR group without SCS. These findings suggest that adenosine receptors and ghrelin may play a biochemical role in SCS-induced neuroprotection of the hippocampus. Understanding the neuroprotective actions of SCS has the potential to aid the development of new treatments or preventative measures for depression following a heart attack.

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Suever, Jonathan D. "MRI methods for predicting response to cardiac resynchronization therapy." Diss., Georgia Institute of Technology, 2013. http://hdl.handle.net/1853/50224.

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Cardiac Resynchronization Therapy (CRT) is a treatment option for heart failure patients with ventricular dyssynchrony. CRT corrects for dyssynchrony by electrically stimulating the septal and lateral walls of the left ventricle (LV), forcing synchronous con- traction and improving cardiac output. Current selection criteria for CRT rely upon the QRS duration, measured from a surface electrocardiogram, as a marker of electrical dyssynchrony. Unfortunately, 30-40% of patients undergoing CRT fail to benefit from the treatment. A multitude of studies have shown that presence of mechanical dyssynchrony in the LV is an important factor in determining if a patient will benefit from CRT. Furthermore, recent evidence suggests that patient response can be improved by placing the LV pacing lead in the most dyssynchronous or latest contracting segment. The overall goal of this project was to develop methods that allow for accurate assessment and display of regional mechanical dyssynchrony throughout the LV and at the site of the LV pacing lead. To accomplish this goal, we developed a method for quantifying regional dyssynchrony from standard short-axis cine magnetic resonance (MR) images. To assess the effects of LV lead placement, we developed a registration method that allows us to project the LV lead location from dual-plane fluoroscopy onto MR measurements of cardiac function. By applying these techniques in patients undergoing CRT, we were able to investigate the relationship between regional dyssynchrony, LV pacing lead location, and CRT response.

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